A common culprit behind severe gum disease may also stiffen and narrow the heart's aortic valve, preliminary research suggests. This may help explain links between gum problems and poor heart health.

Scientists have long linked severe gum disease to inflammation throughout the body and a higher risk of heart problems, including coronary artery disease, which can raise the risk of heart attack. Studies have also found that treating gum disease can improve blood-vessel health.

Now, researchers suggest that Porphyromonas gingivalis, one of the main bacteria involved in severe gum disease, may also contribute to calcific aortic valve disease (CAVD), a condition in which calcium builds up in the heart's aortic valve. The findings were presented in July at a meeting of the American Heart Association in Boston and have not been peer-reviewed yet.

Dr. Elena Aikawa, a professor of medicine at Harvard Medical School who was not involved in the study, said the findings "fit well with our current understanding of calcific aortic valve disease as an active, inflammation-driven disease rather than simply wear and tear of the valve."

Periodontal disease is likely just one contributor among many, rather than the sole cause of CAVD, she added. But the study does identify a biologically plausible pathway linking oral health to heart health that could open new opportunities for prevention and treatment.

How mouth bacteria harm the heart

CAVD affects millions of people worldwide, and there are no approved drugs that slow or stop its progression. As the disease worsens, people may develop fatigue, shortness of breath and chest pain, and in severe cases, they often require valve-replacement surgery.

Meanwhile, prior to the new research, it was known that bacteria and inflammatory signals from the mouth can sometimes enter the bloodstream and affect distant tissues, said Richard Lamont, chair of oral immunology and infectious diseases at the University of Louisville School of Dentistry, who was not involved in the study. Over time, these effects can accrue and gradually reshape how the immune system behaves, he said.

P. gingivalis is known to be particularly destructive to gum tissue, causing lots of inflammation, and it's been tied to cardiovascular disease in the past. To see if the bacterium might be directly impacting heart health, researchers at Fuwai Hospital in Beijing looked for P. gingivalis in aortic valve tissue removed during valve-replacement surgery. They compared this diseased tissue to valves that weren't calcified.

The calcified valves contained much higher levels of P. gingivalis DNA and proteins made by the bacterium. "P. gingivalis was about 30 times more abundant in calcified valves than in non-calcified valves," study first author Dr. Chenyang Li, a doctoral candidate at Fuwai Hospital, told Live Science in an email.

To test whether the bacteria might directly contribute to valve damage, Li and colleagues injected live P. gingivalis into the bloodstreams of healthy lab mice. The bacteria reached the animals' aortic valves, triggering inflammation, calcium buildup and narrowing of the valve.

"We were surprised to see valve calcification even in mice without high cholesterol," Li said. "This suggests P. gingivalis may directly contribute to valve disease, beyond traditional cardiovascular risk factors."

A comparison group of mice was given antibiotics before the injection and had less bacteria in their aortic valves and slower disease progression. Meanwhile, mice injected with dead P. gingivalis bacteria did not show any changes in their aortic valves.

The researchers traced the changes in the mice's hearts to interleukin-1 beta, a signalling molecule that normally helps the body fight infections. Exposure to P. gingivalis ramped up the production of this molecule, and in turn, the immune signal switched on genes that pushed healthy valve cells to behave more like bone-building cells, which is a hallmark of CAVD. This switch causes the cells to lay down calcium in the surrounding valve tissue.

When the scientists blocked interleukin-1 beta in some mice, the animals developed much less valve calcification even when the bacteria reached the valve. Lamont said that the mouse experiments strengthen the case that there's a biological mechanism directly linking gum and heart diseases. However, he cautioned that mice have very different oral microbiomes than humans, making it difficult to know whether the exact same process occurs in people.

That said, the team also saw the same pattern in human valve cells grown in the lab. Exposure to P. gingivalis increased inflammation and calcium buildup among the cells, while blocking interleukin-1 beta blunted those effects.

Both Aikawa and Lamont said more research is needed to confirm the relationship in humans. The findings give researchers a new pathway to explore for future treatments, raising questions of whether targeting inflammatory signals like interleukin-1 beta could help slow the progression of this widespread heart disease.

This article is for informational purposes only and is not meant to offer medical advice.

What do you know about the body's hardest-working muscle? Find out with our heart quiz!

Scientists have invented a soft robotic heart that could give them a new way to study a mysterious condition that accounts for roughly half of all heart failure cases.

This form of heart failure, called heart failure with preserved ejection fraction (HFpEF), is a condition in which the heart pumps out a normal amount of blood but becomes too stiff to relax and refill properly between beats. Over 3 million Americans have the condition, but researchers still don't fully understand why it develops, making it difficult to design treatments that directly target the disease.

The new device, described June 1 in the journal Nature Communications, is the first soft robotic heart model that can actively adjust how it responds to changes in pressure. It tightens or relaxes its artificial muscles, enabling researchers to control how stiff the heart becomes. This allows it to better mimic a diseased human heart.

Current laboratory models of HFpEF have drawbacks. Traditional "mock circulation loops" use rigid pumps and tubing to recreate blood flow but don't physically resemble a beating heart. Lab animals capture more realistic biology but are expensive and don't perfectly mirror human disease, said study co-author Thanh Nho Do, a biomedical engineer and associate professor at the University of New South Wales in Australia.

"HFpEF has been notoriously difficult to study and treat," Nho Do told Live Science in an email.

Earlier versions of the robotic heart could realistically recreate cardiac movement, but they followed present commands that didn't adapt to changing conditions. The new system attempts to solve that limitation by allowing the artificial muscle fibers to "feel" the pressure created by the fluid they are pumping and dynamically contract or relax against it.

That feedback is critical for reproducing HFpEF, in which abnormal stiffness — rather than weakened pumping — lies at the core of the disease.

The researchers built a silicone replica of the left side of the human heart and wrapped it in artificial muscle fibers made from rubber tubes reinforced with spring coils. The model continuously senses the pressure generated by the fluid flowing through it and adjusts the force of its artificial muscles in response. By changing how much the muscles resist being stretched as the heart fills, researchers can dial in different levels of stiffness.

Instead of modeling a single snapshot of HFpEF, the researchers recreated several stages of the disease's progression. In early stages, patients' hearts start to show impaired relaxation between beats, while in more advanced forms, the heat is so stiff that it can't adequately fill with blood before the next contraction.

"If we can model its progression pathway, we might be able to use models like ours to develop medical devices that interrupt that trajectory, rather than just treating end-stage disease," Nho Do said.

Current treatment for HFpEF focuses largely on managing symptoms and associated conditions, such as high blood pressure, obesity and diabetes. In recent years, drugs known as SGLT2 inhibitors have been shown to reduce the risk of hospitalization in many patients by reducing excess fluid in the body. But there are still few therapies that directly target the stiffening of the heart muscle.

The researchers hope their new model might pave the way, but they emphasized that the work is an early proof of concept. Looking ahead, they hope to develop increasingly sophisticated robot heart models that can complement other data on HFpEF, including that from computer simulations, animal studies and clinical testing.

"We hope the biggest impact will be in understanding HFpEF mechanisms and improving the way we develop cardiovascular devices," Nho Do said.

Heart quiz: What do you know about the body's hardest-working muscle?

Scientists uncovered a link between mild heart trouble and microscopic signs of brain damage that may raise the risk of memory problems down the line.

The new study, published Monday (July 6) in The Journal of Neuroscience, did not prove that the heart issues directly caused memory problems. But it "adds to the overall picture that preserving healthy brain-heart communication is key for healthy aging," said Dr. Jan Scheitz, a consultant stroke neurologist and head of the Brain-Heart Lab at the Charité University Hospital in Germany, who was not involved in the study.

"A healthy lifestyle that protects the cardiovascular system will not only benefit the heart but also the brain," he told Live Science in an email.

The work could one day help doctors identify patients at risk of memory problems early on through routine heart-function tests, said study co-author Dr. Xia Zhang, a doctoral researcher at the Max Planck Institute for Human Cognitive and Brain Sciences in Germany.

"The broader implication is that the brain may show subtle tissue-level changes related to cardiac dysfunction before we see obvious brain shrinkage or clinical dementia," Zhang told Live Science in an email.

Early warning signs

Researchers already knew that heart and brain function are closely interconnected. Heart diseases such as heart failure, atrial fibrillation and heart attack impair communication between the heart and the brain. This can contribute to thinking problems and dementia by restricting blood flow to the brain and causing chronic inflammation.

So far, though, scientists have only studied changes in the brain in people already diagnosed with heart conditions. They haven't necessarily assessed the changes that take place earlier on.

In the new study, researchers followed 73 patients who had sought care for heart-related symptoms at the Heart Center Leipzig in Germany, some of whom had confirmed coronary artery disease and/or heart failure. They also assessed 95 people without any heart-related symptoms. The researchers measured heart function at the start of the study. Then, about 3.5 years later, they performed cognitive testing and an MRI scan of the brain to take a snapshot of its structure.

Among all 168 study participants, those whose hearts pumped blood less efficiently at the start of the study showed greater signs of tissue damage in their gray matter years later. This was true regardless of whether or not they had diagnosed heart failure.

The cognitive tests were given only to the heart-disease patients, and they assessed attention, executive function, learning and memory. Only memory showed a link to weaker heart pumping. The participants with weaker heart pumping showed more microscopic damage in memory-related brain regions, and those brain changes correlated with worse memory scores.

The degree of brain damage also correlated with the levels of stress hormones released by the heart, but this link was only seen in patients who already had heart failure.

"What surprised us most" was that subtle reductions in the heart's ability to pump were tied to later brain changes, even in patients who did not meet clinical criteria for heart failure, Zhang said.

One limitation of the study is that the researchers didn't take MRI scans at the start. That means "we do not know whether some changes were already present at the beginning of the study period," Scheitz noted. This is something that Zhang and her colleagues plan to test in future studies.

"The next step for the field is replication in larger cohorts with multiple time points, so that cardiac function, brain microstructure, and cognition can be followed more precisely over time," she said.

The brain damage flagged in the 73 patients happened in parts of the brain that are important for memory and are vulnerable in Alzheimer's disease. "These regions helped identify a possible brain pathway through which poorer cardiac function may contribute to later memory problems," Zhang said.

However, until this idea is tested directly in future studies, it is too soon to say if the heart function-related brain changes seen on the MRI scans point to a higher risk of Alzheimer's, Zhang cautioned. The team did not measure proteins related to Alzheimer's, so they cannot conclude that the patients with measurable brain changes are developing Alzheimer's disease.

The study also did not directly test the effect of exercise on heart and brain health, but the findings may help explain why regular exercise is often linked to better brain health and cognitive aging, Zhang said.

"Regular exercise supports cardiovascular function, vascular health, and cerebral blood-flow regulation," she said, "all of which may help protect brain tissue over time."

This article is for informational purposes only and is not meant to offer medical advice.

What do you know about the body's hardest-working muscle? Find out with our heart quiz!

For Sarah Hall, every mealtime was dangerous.

She has a rare condition called cardioinhibitory syncope, which causes overactive nerve signals to tell the heart to stop beating in response to subconscious bodily processes, such as swallowing. Swallowing food caused Hall's heart to stop beating up to 12 times a day, often making her faint.

Hall's condition wasn't improving with any treatments, but an innovative procedure has changed her life, as well as the lives of dozens of others.

In work presented at the British Cardiovascular Society's annual conference, scientists reported that 25 people with the condition dramatically improved after an experimental procedure. The early findings, which have not been peer-reviewed yet, are promising but require validation.

"It's important to note that this is still a relatively new therapy and that larger studies and longer-term follow-ups are still needed to provide a better understanding of its durability and help identify which patients benefit most," said Dr. Sirisha Vadali, a cardiologist at HonorHealth who was not involved in the research.

When "rest and digest" goes haywire

The autonomic nervous system handles the electrical signals the body relies on to complete subconscious, everyday processes, like eating or sleeping. This includes the body's complementary "fight-or-flight" and "rest-and-digest" responses.

The latter system send the bulk of its signaling through the vagus nerve, which starts in the brainstem and extends through the chest and abdomen. As the body senses changes, like food entering the throat or the legs bending into a crouch, the vagus nerve updates the brain on what's happening, enabling it to subtly alter digestion, breathing and heart rate in response.

In some animals, vagal activation is involved in a more dramatic bodily process: hibernation. Hibernating mammals, like bears, experience a strong wave of signaling through the vagus nerve when they enter their winter den, which lowers their metabolic rate for weeks.

People with cardioinhibitory syncope "go into a hibernation response" because their vagus nerve signals are too strong, Dr. Boon Lim, a consultant cardiologist at Imperial College Healthcare NHS Trust who led the new work, told Live Science.

The vagus nerve transmits signals to the ganglionated plexi, a web of nerve endings on the surface of the heart. The signals then reach the body’s built-in system for maintaining heart rate — and when they're too strong, it briefly shortcircuits this system, causing the heart beat to pause entirely.

There are many ways this hyperactive vagal response can be triggered. For 50-year-old Hall, the trigger was swallowing, while for others with the condition, sudden abdominal pain can flip the switch.

Why we faint

Syncope, the medical term for fainting, is common. Lim estimates that 40% of people faint at some point in their lifetimes, and for most, it is because signals from the vagus nerve temporarily reduce their blood pressure. Without enough blood flowing to the brain, people briefly lose consciousness.

But in cardioinhibitory syncope, the heart pauses entirely for a few seconds due to hyperactive vagal signaling. The strength of the vagus nerve's signaling to the heart is determined largely by genetics. Fewer than 5% of people who seek treatment for syncope have cardioinhibitory syncope.

The condition generally isn't life-threatening, Vadali said, but its unpredictability is highly disruptive. "Many patients may experience anxiety about when the next episode might occur," she said.

Boon described a patient named Rob, who had reported frequent fainting episodes. A diagram tracking the waves of Rob's pulse on a normal afternoon showed the churning rhythm of his heartbeat becoming still ‪—‬ one of several daily episodes. "It suddenly pauses for close to five seconds for no reason," Lim said.

For people with cardioinhibitory syncope, the best option previously had been to have a pacemaker implanted, Lim said. But this isn't a permanent solution; pacemaker batteries need to be replaced every decade or so. Patients who get pacemakers at younger ages can face long-term health risks as the devices deteriorate, and battery replacement operations can cause infections.

Now, Lim and colleagues have shown that a procedure called cardioneuroablation could drastically improve the lives of patients like Rob.

In the procedure, Lim snaked a thin wire through Rob's body that eventually reached his heart, specifically the ganglionated plexi on the organ's surface. Lim then delivered a pulse of radio-frequency energy to the plexi, which destroyed the tissue, thus reducing disruption of the heart's built-in pacemaker.

Lim's team carried out the procedure on 25 people at Imperial College London between 2013 and 2023. On average, the patients had had fewer than one fainting episode in the following year. This translated to significant improvements in the patients' quality of life, they reported.

Three patients required additional procedures, because the ganglionated plexi can sometimes regrow. The procedure is fairly invasive, but compared to repeated pacemaker maintenance, it could still offer a more appealing solution to patients, the researchers say.

By now, Lim's team has used cardioneuroablation to treat 52 people. Vadali said the early data presented at the conference is promising but more research is needed to see how well its effects last.

For Hall, the procedure changed her life. She has not fainted since, even at mealtimes.

"I can drive; I can work," she said in a statement. "It feels like everything has come full-circle."

What do you know about the body's hardest-working muscle? Find out with our heart quiz!

Researchers have developed a system that uses short videos of the eye to estimate a person's levels of red blood cells — no needles required.

The technology, described in a paper published April 8 in the journal npj Digital Medicine, correctly identified anemia more than 80% of the time in a trial involving 224 participants.

This technology isn't ready to replace standard blood draws, the researchers behind the study cautioned. But they think it could potentially serve as a screening tool to flag people who may need a full blood test. This could be especially useful in low-income countries where access to laboratory testing can be scarce.

"Its potential utility may lie in enabling frequent, noninvasive longitudinal monitoring or early identification of patients requiring further investigation," said Dr. Christine Kiire, a consultant ophthalmologist at Oxford Eye Hospital and a visiting researcher in the artificial medical intelligence lab at the University College London Institute of Ophthalmology. If validated and made affordable, the system could make blood monitoring more accessible in resource-limited environments, Kiire, who was not involved in the study, told Live Science in an email.

The method could be useful in settings where it's burdensome to draw and analyze blood repeatedly, said Dr. Theodore Leng, an ophthalmologist and vitreoretinal surgeon at Stanford University who wasn't involved in the study. This could include outpatient screening, home monitoring, follow-up appointments for dialysis and cancer treatments, or pediatrics, he said in an email.

That said, the system is not ready for prime time yet. "It's great research but will take a lot of steps to be clinically available," Dr. Peter Campbell, an ophthalmologist at Oregon Health & Science University who wasn't involved in the study, said in an email.

How the needle-free system works

Noninvasive blood sensors already exist. In 2021, the Food and Drug Administration (FDA) approved a device, the Pronto-7, that measures levels of hemoglobin in the blood by shining light through the fingernail. Hemoglobin carries oxygen inside blood cells.

Unfortunately, Pronto-7's readings can be influenced by skin tone, meaning they're less accurate for people with dark skin. The white part of the eye, in contrast, contains very little pigment and looks roughly the same across different populations.

The new screening technique takes advantage of this. To build it, researchers used a microscope camera at 50x magnification to record 10-second videos of the whites of study participants' eyes. A software called Video-to-Vessels cleans the footage ‪—‬ removing blinks, eye movements and lighting changes ‪—‬ and converts the videos into time-lapse snapshots of the blood vessels within the eye.

Then, an AI model called VesselNet, which was trained on blood vessel snapshots paired with lab results regarding blood count, predicts the person's hemoglobin level and red blood cell count by analyzing patterns in the flow of blood cells.

"This paper is unique because it describes images of the front surface of the eye, rather than the retinal vasculature (at the back of the eye)," Campbell said. "So in theory it could be applied without expensive retinal cameras ‪—‬ even a smartphone."

The researchers tested the method on 224 people, including cancer patients with blood disorders and healthy volunteers, at Sheba Medical Center in Israel. They compared the model's predicted hemoglobin values with actual hemoglobin values measured using standard blood tests, finding that the model correctly identified whether a person had low hemoglobin about 83% of the time.

This falls short of what's needed for real-world use, Kiire said. For context, Pronto-7 scores between 80% and 88% for detecting low hemoglobin in men, and 84% to 87% in women.

"In practical terms, this sounds more like a great screening tool, rather than a technology ready to support dosing, transfusion decisions, or definitive hematology management," Leng said.

Additionally, whereas the eye-based method measures only two things — hemoglobin and red blood cell count — a standard blood test measures many more, Kiire said. The study authors think they may be able to count white blood cells, as well, if they design a camera with higher resolution and magnification.

Kiire also noted that certain conditions, such as pink eye and dry eye disease, as well as drugs such as medicated eye drops, may affect blood vessels in the eye and lead to false readings. On a practical level, getting good results "requires careful patient positioning and sufficient optical focus,"which aren't easy skills for clinicians to master and may limit the usability of the new method, she added.

The researchers plan to do studies involving larger and more diverse cohorts, including patients with iron-deficiency anemia, which were underrepresented in this study. They also aim to do repeated testing of their method, to validate and extend their findings.

This article is for informational purposes only and is not meant to offer medical advice.

A low resting heart rate is often seen as a sign of good health, but now, a large study suggests that both very low and very high heart rates may be linked to an increased risk of stroke.

The findings, presented May 6 at the European Stroke Organisation Conference 2026 in Maastricht, Netherlands, are based on data from nearly 460,000 people whose data is included in the UK Biobank, a large repository of health data from U.K. adults. On average, each person was monitored for 14 years, and researchers recorded more than 12,000 cases of stroke among the participants.

The researchers identified a U-shaped association between resting heart rate and stroke risk.

"When we looked across the data, the lowest risk was in the middle, around 60 to 69 beats per minute, and increased at both ends," said first author Dr. Dexter Penn, a clinical fellow in cerebrovascular disease at Imperial College London. "The common idea is that the higher the heart rate, the higher the stroke risk, but the relationship isn't as linear as it seems," he told Live Science.

The study included people ages 40 to 69. Compared with the people whose heart rates were in the middle range, people with heart rates at or above 90 beats per minute (bpm) had a 45% higher stroke risk. Those with heart rates below 50 bpm had a 25% higher risk, even after the researchers adjusted for other factors that affect the likelihood of stroke, such as age, blood pressure and atrial fibrillation (AFib), a common form of irregular heart rhythm.

So the U-shaped pattern was seen in people without any history of AFib.

"That's likely because atrial fibrillation itself is such a strong risk factor that it masks any additional signal from heart rate," said study co-author Alastair Webb, a stroke medicine researcher at Imperial College London. "In people without AF[ib], resting heart rate may act as a marker of underlying risk, though we need more data to confirm how reliable it is."

Dr. Sanskriti Mishra, director of the Comprehensive Stroke Center within the Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Center, said the results are clinically relevant because resting heart rate is easy to measure. "It may help flag cardiovascular risk in patients at either extreme," said Mishra, who was not involved in the work.

However, she emphasized that the findings are observational, meaning they cannot show that high or low heart rate directly causes stroke. More research is needed to confirm the exact relationship between the two.

When the data was broken down by stroke type, very low heart rates were linked specifically to ischemic stroke, which is caused by blocked blood flow to the brain. High heart rates were associated with both ischemic and hemorrhagic strokes, the latter of which involves bleeding in the brain.

It may be that lower heart rates stretch the pause between heartbeats, potentially reducing steady blood flow to small brain vessels and making blockages more likely, Penn suggested. Meanwhile, higher heart rates may increase stress on blood vessel walls, making them more vulnerable to both blockages and bleeds. "But these are still hypotheses," he said.

Webb cautioned that the findings should not cause anyone to panic.

"A low resting heart rate can still mean good fitness, particularly in physically active people," he said. "But in others, it may be a useful signal worth considering alongside traditional risk factors."

Mishra agreed that a low heart rate is often normal in both healthy adults and athletes. "Still, I would advise people to mention it to their doctor and continue managing established cardiovascular risk factors, such as high blood pressure, diabetes and high cholesterol," she said.

The findings of the new study have not been published in a peer-reviewed journal yet.

Editor's note: This article was updated on May 8, 2026, to adjust Dr. Sanskriti Mishra's title and affiliation.

This article is for informational purposes only and is not meant to offer medical advice.

What do you know about the body's hardest-working muscle? Find out with our heart quiz!

The patient: A 29-year-old man in Queens, New York

The symptoms: As the man was walking home one night, he suddenly started feeling heart palpitations — accelerated heartbeats at irregular intervals — that alarmed him, prompting an immediate visit to the emergency room.

What happened next: The man told the hospital doctors that he had no history of heart trouble. He was not experiencing symptoms that are normally associated with a heart attack, such as chest pain or pressure, difficulty breathing, dizziness, a cold sweat or shortness of breath. Nor did he have a history of drug use or illness that could have triggered palpitations, the attending physician wrote in a report of the case.

The diagnosis: Although palpitations are typically fleeting and harmless, according to the Mayo Clinic, they can sometimes be a symptom of serious heart conditions such as arrhythmia, in which electrical signals that regulate the heartbeat are repeatedly disrupted. This can cause the heart to pump blood less efficiently through the body, which can starve tissues of blood and oxygen.

At the hospital, doctors performed an electrocardiogram (EKG), which monitors the heart's electrical activity and rhythm. The test showed signs of atrial fibrillation (AFib), a common type of arrhythmia in which the heart's upper and lower chambers are out of sync. As a result, less blood fills the lower chambers and less blood reaches the lungs and the rest of the body.

AFib is sometimes associated with congestive heart failure, a chronic condition in which the heart doesn't pump blood efficiently, as well as strokes, which are caused by blocked or damaged blood vessels. Although the exact causes of AFib are unknown, the condition has been linked to digestive problems and overactivity of the parasympathetic nervous system, according to the report. (Also known as the "rest and digest" system, the parasympathetic nervous system balances out the activity of the "fight or flight" system.)

It was unclear what was causing the patient's AFib in this case. Doctors admitted the man to the hospital and prepared to perform a cardioversion, a procedure to restore regularity to a disrupted heartbeat.

The treatment: Before receiving the cardioversion, the patient required an anticoagulant to prevent the formation of blood clots. But first, doctors needed to make sure the patient did not have gastrointestinal bleeding, so a physician performed a digital rectal exam to check for blood in the patient's stool. At the time, the man's heartbeat was measured at 140 beats per minute (bpm); the average resting heart rate for an adult is 60 to 100 bpm.

When the rectal exam was over, the doctors noted that the patient's heartbeat had slowed to 80 bpm, and further examination showed that the irregularity in his heartbeat had disappeared. He was discharged from the hospital, and when he came back for a follow-up visit three months later, he said the palpitations had not returned.

What makes the case unique: Treatment for AFib typically involves medications that slow the heart rate and regulate its rhythm, or the use of cardioversion to "reset" the heartbeat. If the patient is at risk of a blockage in a blood vessel, doctors may prescribe an anticoagulant, as well.

Medication usually restores the heart's normal rhythm within hours — but in this case, the rectal exam achieved a similar result instantly.

The author of the report proposed that the exam affected the man's autonomic nervous system, which controls involuntary bodily processes like heartbeat. He suspected that this change was due to the stimulation of the vagus nerve, a structure of the nervous system that extends from the brainstem into organs of the chest and abdomen and is involved in heartbeat regulation.

Notably, during the rectal exam, the patient was instructed to bear down and strain without exhaling, a technique called the "Valsalva maneuver." It's also used to clear pressure from the middle ear and is known to increase activity in the vagus nerve.

Stimulation of the vagus nerve is known to increase activity in the parasympathetic nervous system and slow electricity conduction in heart tissue, the patient's doctor wrote in the report. In this patient, stimulation of his vagus nerve likely counteracted the signals causing the arrhythmia, the doctor suspected.

This type of rectal procedure could be an additional method for treating some patients with AFib, the author concluded, though he added that it should not replace more traditional treatments. More research would be needed to justify adding the procedure to standard practice.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

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Some people hit their stride in the morning, while others feel most awake and productive at night. But a growing body of evidence suggests that being part of the latter group, the "night owls," could be linked to poorer heart health.

Now, a large study published Jan. 28 in the Journal of the American Heart Association adds weight to the idea.

Pulling from the UK Biobank, a massive repository of data from U.K. adults, researchers followed more than 322,000 adults ages 39 to 74 for nearly 14 years. They examined how "chronotype" — whether someone is a morning or evening person — relates to their cardiovascular disease risk.

The participants reported their preferred sleep-wake schedules and were classified as morning, intermediate or evening types. Heart health was assessed using the American Heart Association's Life's Essential 8 score, which rates heart health on a scale of 0 to 100 based on eight factors: smoking, diet, exercise, blood sugar, body weight, blood pressure, cholesterol and sleep quality. Higher scores indicate better cardiovascular health.

Compared with intermediate sleepers, "definite evening" types were 79% more likely to have poor overall scores and had a 16% higher risk of heart attack or stroke over about 14 years of follow-up. "Definite morning" types were 5% less likely than intermediate sleepers to have poor scores.

But what's behind this link? Does something about night owls' lifestyles set them up for worse heart health, or is there something unique about their biology that plays a role?

How lifestyle may factor in

The night owls scored worse on various lifestyle-related factors, compared to the intermediate sleepers in the biobank study. For example, they had 54% higher nicotine exposure, 42% poorer sleep, 19% lower physical activity, and 8% poorer diet. In contrast, the morning people generally had lower nicotine use and better diets than intermediate types did.

When these differences were taken into account, about 75% of the increased cardiovascular risk observed in night owls appeared to be linked to lifestyle factors, rather than to the chronotype itself. Among these factors, smoking contributed the most (34%), followed by poor sleep (14%), high blood sugar (12%), and diet and body weight (11% each).

"The drivers of overall cardiovascular health are modifiable, including nicotine exposure," study lead author Sina Kianersi, a postdoctoral research fellow at Brigham and Women's Hospital and Harvard Medical School, told Live Science in an email. Other influential lifestyle factors included physical activity levels, blood pressure and cholesterol, he added.

"So for people who identify as night owls, it is a good reason to be even more proactive about those basics," he said.

Prior studies have suggested that night owls often experience social jet lag, a mismatch between their internal clock and their daily routines. This mismatch may be associated with habits like late-night eating, skipped breakfasts, irregular sleep and a greater reliance on caffeine or nicotine. In turn, these behaviors have been linked to factors that raise heart disease risk, such as higher body mass index (BMI), elevated blood sugar, higher insulin resistance, and lower levels of good cholesterol.

Past research also indicates that, even if they get a decent amount of sleep overall, adults with irregular sleep patterns have a 26% higher risk of stroke, heart attack, or heart failure than those with regular sleep patterns.

"Fragmented or insufficient sleep can raise blood pressure, cholesterol, and blood sugar, often with weight gain," Dr. Bibhu Mohanty, an associate professor at the University of South Florida who was not involved in the research, told Live Science in an email. "This is largely driven by [the stress hormone] cortisol, which mobilizes sugar and fat in ways that can make disease harder to reverse, once it is established."

The biology of night owls

Being a night owl isn't a choice — it's partly written in people's genes.

Studies have linked hundreds of genetic variants to chronotype. Many of the highlighted genes are involved in regulating the body's 24-hour clocks, or circadian rhythms. These rhythms help control sleep, appetite, hormone cycles and heart function throughout the day and night.

People with late chronotypes often have delayed circadian rhythms. That means their levels of melatonin, the sleep-promoting hormone, rise later in the evening than they do in early chronotypes. In turn, their cortisol, which helps wake up the body, rises later in the morning than usual.

This shift can throw the body out of sync with the normal day-night cycle, making the body’s fight-or-flight system overactive. As a result, blood pressure can stay high at night, and inflammation and oxidative stress increase. Over time, these changes can damage blood vessels, disrupt blood sugar, and promote plaque buildup in the arteries, which may manifest as heart disease, studies suggest.

Many of the genes involved in determining chronotype also directly affect lipid and glucose metabolism, or how the body breaks down fats and sugars. Studies show that evening types show altered expression of these "clock genes" alongside elevated inflammation markers and triglycerides, a type of fat, compared to morning types. These patterns may contribute to metabolic issues like insulin resistance and poor cholesterol, which are known heart disease risks, though more research is needed to confirm the direct link.

Early evidence also suggests subtle differences in heart structure and function in night owls, though the long-term effects of these differences are still being studied.

Questions to address

Some data from the UK Biobank study suggest the link between night owls and poorer heart health may be stronger in females than in males. Female night owls were 96% more likely, and male night owls 67% more likely, than their intermediate chronotype counterparts to have a poor overall cardiovascular health profile, according to the LE8 score.

Kianersi said, "This difference could reflect social pressures, biology, or both. It's a signal that deserves further study."

Even though the UK Biobank study found a link between the chronotype and poorer heart health, being a night owl doesn't doom you to cardiovascular disease.

"We need studies that get closer to cause and effect, using approaches like genetics as well as intervention research," Kianersi said. "And it will be important to see if these patterns hold in younger adults and in other populations with different work schedules and environments."

For night owls looking to protect their hearts, Mohanty advises focusing on improving lifestyle habits whenever possible.

"That means developing healthier sleep routines, exercising, making healthy dietary choices, avoiding unnecessary snacking and smoking, and potentially using medication to reduce risk if needed," he said. Approaching heart health holistically is "probably the best approach to limit risk."

This article is for informational purposes only and is not meant to offer medical advice.

The deceased: A 39-year-old man in the United States

The autopsy findings: Medical examiners evaluated the man after a deadly fight, during which a stab wound had punctured a vein in his lungs. They noted that the man's heart was slightly enlarged and that he had moderate atherosclerotic coronary artery disease (CAD) in two vessels. CAD is caused by plaque buildup in the walls of arteries that lead to the heart.

Upon dissecting the man's heart, the examiners noticed an unusual lump around the atrioventricular node, which coordinates electrical signals between the heart's top and bottom chambers. When examiners sliced the node and surrounding tissue into thin sections to investigate the lump, they uncovered a "boomerang-shaped, bony structure" about the size of a black bean, according to a report of the case.

They identified this structure as the os cordis — a "cardiac bone" rarely, if ever, seen in humans.

What makes the case unique: The os cordis has long been observed in nonhuman mammals, including ruminants such as cows and camels. In animals, it is believed to support the cardiac valves that direct the flow of blood within the heart.

The structure was only recently described in primates, in a report published in 2020, just five years before the case study described above. In that 2020 report, scientists examined 16 chimpanzee hearts and found that three contained an os cordis. Those three chimps also had heart-tissue scarring, leading the researchers to suggest that the development of the bony structure might have been linked to such tissue damage.

Also in 2020, a similar structure was described in seven humans by Dr. Jorge Trainini, a cardiac surgeon and professor at the National University of Avellaneda in Argentina. He and his co-authors dubbed their discovery the "cardiac fulcrum," emphasizing its proposed role in stabilizing heart muscles as they pump against the forces of gravity.

They reported that, unlike the os cordis they saw in cow hearts, the adult human fulcrum was made of cartilage and tendon, not bone. That said, in the team's own analysis, they found that a heart from a 10-year-old did contain bone tissue, and they suggested that the structure might lose its bony nature with age. (The 10-year-old had cardiomyopathy, or disease of the heart muscle, and had undergone a heart transplant. The bony tissue was found in the explanted heart.)

Trainini told Live Science in an interview that the os cordis and the cardiac fulcrum are the same structure. But the case report authors disagreed. They acknowledged Trainini's previous findings, but they maintained that the structure they found in the 39-year-old man was distinct because it was made of bone.

However, the case report authors come to a similar conclusion as Trainini, stating that such a structure may be more common among humans than is currently recognized. They suggested that, since they found the os cordis during a dissection of the heart tissue that was not standard for an autopsy, the feature may typically go unnoticed.

Tranini went so far as to argue that all humans likely have a cardiac fulcrum based on his subsequent investigations of around 100 human hearts.

Though the case report authors didn't know the man's full medical history, they noted that the formation of an os cordis might be linked to his apparent cardiac disease. It's known that age and disease can influence this structure in other animals, too, they added.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

Men tend to develop cardiovascular disease about seven years earlier than women do, according to a new study.

The difference is driven largely by coronary heart disease, which is caused by plaque buildup in the arteries within the heart. It appears roughly a decade sooner in men than in women.

Cardiovascular disease is an umbrella term that includes conditions such as coronary heart disease, heart failure and stroke. It remains the leading cause of death for both men and women in the United States, but it doesn't manifest at the same time in both sexes.

The new research, published Jan. 28 in the Journal of the American Heart Association, drew on data from the Coronary Artery Risk Development in Young Adults (CARDIA) study, which followed more than 5,000 Black and white adults across the United States for over 30 years.

The researchers found that the risk of cardiovascular disease for men and women begins to diverge around age 35. From that point through middle age, men consistently had a higher risk of cardiovascular disease than women did. That remained true even when the researchers adjusted for common risk factors, such as body mass index (BMI), blood pressure, blood sugar levels, physical activity, smoking status, diet quality and levels of non-HDL cholesterol (the "bad" kind).

This suggests that some other biological or social factors may contribute to making men more vulnerable to heart disease at younger ages, the study authors say.

"The study supports that men waiting until middle age to assess cardiovascular risk miss a critical window for prevention," said Dr. Brett Sealove, chair of cardiology at Hackensack Meridian Jersey Shore University Medical Center, who was not involved in the study. Men should begin routine heart health screenings in their 30s and focus on managing modifiable risk factors, such as their diet, exercise habits and smoking, he told Live Science in an email.

However, Sealove noted that these new findings should not lead clinicians or patients to overlook women's risk of developing heart disease before age 65.

Dr. Kim Eagle, a cardiologist and director of the University of Michigan Health Frankel Cardiovascular Center, echoed that concern. "The study is not practice-changing and I worry that many may conclude that heart disease is predominantly a male problem," Eagle, who was not involved in the study, told Live Science in an email.

Eagle pointed out that the study found little to no difference between the age at which men and women developed heart failure or stroke. Furthermore, "it is likely that women have an acceleration of heart disease after menopause compared to men which is not captured in this study," he said. "Heart disease kills more women than any other illness. We should not downplay its importance."

The timeline of heart disease

The CARDIA cohort included 5,115 participants from four U.S. cities: Chicago; Minneapolis; Birmingham, Alabama; and Oakland, California. The participants were between 18 and 30 years old when the study began, between 1985 and 1986, and they were followed until August 2020, making the oldest participants about 65 by the end. The researchers collected health information through medical exams and surveys at baseline and then at two, five, seven, 10, 15, 20, 25 and 30 years into the study.

About 5% of the men had developed some form of cardiovascular diseases by age 50, but for women, that same incidence rate was reached around age 57. The largest sex-based gap appeared in coronary heart disease: Men reached a 2% risk of having coronary heart disease 10 years earlier than women did.

By contrast, the researchers found little to no difference between men and women in the age at which stroke occurred. Their heart failure risk was also similar for much of adulthood..

"The long duration of the study coupled with some diversity of people and the fairly large cohort provides us with valuable data on how cardiovascular health changes from the start of adulthood to middle age," Sealove said.

That said, as an observational study, the research cannot prove what factors cause men to develop heart disease earlier than women do, Sealove noted. Rather, it can only draw a link between sex and heart disease risk. In addition, public health guidelines, diagnostic tools and treatments changed substantially over the study period, which could have influenced when the disease was detected or treated, he noted.

Additionally, Eagle found the study's sample size small, and he also pointed out that it did not account for pregnancy-related complications or menopause, or for forms of heart disease that disproportionately affect women, such as conditions involving the smaller coronary arteries. (The authors didn't explicitly note how many of the women in the study were menopausal by its end.)

The study authors suggested that differences in health care use may contribute to the difference in heart disease seen between the sexes. For example, women ages 18 to 44 attend roughly four times as many preventive health care visits as men do, in part due to seeking gynecologic and obstetric care, they wrote in the paper. Encouraging preventive care among young adult men may represent an important opportunity to reduce cardiovascular risk earlier in life, they suggested.

"The relationship between gender and heart disease risk is complex and changes over a lifetime," Sealove said. While men appear to be more vulnerable to earlier heart disease, women's risk rises sharply after menopause as levels of protective estrogen decline.

"The study doesn't show that one gender is more at risk overall," he said. Rather, it highlights when risk peaks across a lifetime.

"At the end of the day, it is important to know that cardiovascular disease is the leading cause of death and disability in women and men," Sealove said, "and everyone should receive regular health screenings and live a heart healthy lifestyle."

This article is for informational purposes only and is not meant to offer medical advice.

Not all fat is created equal — while one type of fat in the body raises blood pressure, another helps keep it in check, a study in mice suggests.

In people, excess body fat has long been tied to high blood pressure, or hypertension, and a number of other cardiovascular problems. But the body carries two types of fat: "brown" fat, which burns energy and helps keep the body warm, and "white" fat, which stores excess calories.

For a long time, it was thought that brown fat withers away after childhood, said senior study author Dr. Paul Cohen, a cardiologist and physician-scientist at The Rockefeller University in New York. However, about 15 years ago, it was discovered that adult humans retain some amount of brown fat, which gets activated primarily by cold exposure. Moreover, Cohen has since shown that higher levels of brown fat are linked to a lower prevalence of obesity and hypertension.

"We wanted to better understand how brown fat might do this," Cohen told Live Science.

Now, in a new study published Jan. 15 in the journal Science, Cohen and his team showed that eliminating the gene that makes "beige" fat — the mouse equivalent of adult human brown fat — converted all the beige fat around blood vessels into white fat. This, in turn, caused mice to develop high blood pressure.

The team traced the effect to an enzyme released by fat cells. Normally kept in check by beige fat cells, the enzyme's levels spiked when beige fat was converted into white fat, the study showed. This triggered excessive tightening of blood vessels and higher blood pressure.

This is an important study that, for the first time, establishes how beige fat directly affects cardiovascular health, said Lawrence Kazak, an associate professor at McGill University who studies the energy expenditure of brown fat and was not involved in the work.

It's well documented that obesity influences blood pressure and cardiometabolic health on a system level, Kazak told Live Science. But this work highlights a "niche role" for beige fat and the mechanism behind its "local effects" on the blood vessels, he said.

How fat controls blood pressure

Cohen's team began their study by deleting the Prdm16 gene from the fat cells of lab mice, turning the beige fat around their blood vessels white. This gene is known to be highly active in beige fat, acting as a master regulator that helps them maintain an energy-burning function rather than becoming white fat.

This change was visible just by looking at the tissue, said first study author Mascha Koenen, a postdoctoral fellow at Cohen's lab. Beige-fat-laden tissue, which normally looks dusky and speckled with tiny droplets, turned pale, resembling ordinary white fat.

The researchers observed that the animals that lacked beige fat also developed higher blood pressure, and their blood vessels became stiffer and accumulated more fibrous tissue, making it harder for them to relax as the blood surged through them.

The team then treated the mice's blood vessels with a hormone called angiotensin II, which is known to raise blood pressure by tightening arteries, similar to how pinching a hose restricts the flow of water. Blood vessels from mice lacking beige fat constricted more strongly in response to the hormone, compared with vessels from normal mice.

To identify the mechanism behind this, the team sifted through molecular signals released by fat cells near the blood vessels and identified an enzyme called QSOX1. This enzyme stiffens the connective tissue around blood vessels and makes it harder for them to relax.

Normally, the protein encoded by the Prdm16 gene keeps the production of this enzyme in check. But without beige fat, the levels of QSOX1 surge, leading to stiff blood vessels and high blood pressure, the team concluded.

Importantly, the researchers found that deleting both beige fat and QSOX1 from mice prevented this chain reaction, and those mice did not develop high blood pressure, suggesting that QSOX1 is essential for driving this mechanism, they concluded.

Beige fat in mice and brown fat in humans are known for their heat production; they contain high numbers of mitochondria, which are the cells' energy factories and impart the tissue its brown color. However, Koenen noted that this heat-producing function is not related to the QSOX1 mechanism they identified. Their study instead highlights an additional role of beige fat as "secretory" cells, which release important proteins into the blood.

Even if the beige fat cells are small, "they can have this huge impact on whole body physiology," Koenen told Live Science. And the study could point to new ways of treating high blood pressure.

"You can imagine that molecules that can inhibit QSOX1 could be potentially therapeutically beneficial," Kazak suggested.

Cohen also believes that targeting QSOX1 could help scientists develop precision therapies for hypertension in the future. This would require them to first learn more about this mechanism in order to counter it, he noted. Nonetheless, the research points to a "pathway forward" for studying the effects of QSOX1 inhibitors in humans.

Heart disease is the leading cause of death in the United States.

Since researchers first established the link between diet, cholesterol and heart disease in the 1950s, risk for heart disease has been partly assessed based on a patient’s cholesterol levels, which can be routinely measured via blood work at the doctor’s office.

However, accumulating evidence over the past two decades demonstrates that a biomarker called C-reactive protein – which signals the presence of low-grade inflammation – is a better predictor of risk for heart disease than cholesterol.

As a result, in September 2025, the American College of Cardiology published new recommendations for universal screening of C-reactive protein levels in all patients, alongside measuring cholesterol levels.

What is C-reactive protein?

C-reactive protein is created by the liver in response to infections, tissue damage, chronic inflammatory states from conditions like autoimmune diseases, and metabolic disturbances like obesity and diabetes. Essentially, it is a marker of inflammation – meaning immune system activation – in the body.

C-reactive protein can be easily measured with blood work at the doctor’s office. A low C-reactive protein level – under 1 milligram per deciliter – signifies minimal inflammation in the body, which is protective against heart disease. An elevated C-reactive protein level of greater than 3 milligrams per deciliter, signifies increased levels of inflammation and thus increased risk for heart disease. About 52% of Americans have an elevated level of C-reactive protein in their blood.

Research shows that C-reactive protein is a better predictive marker for heart attacks and strokes than “bad,” or LDL cholesterol, short for low-density lipoprotein, as well as another commonly measured genetically inherited biomarker called lipoprotein(a). One study found that C-reactive protein can predict heart disease just as well as blood pressure can.

Why does inflammation matter in heart disease?

Inflammation plays a crucial role at every stage in the development and buildup of fatty plaque in the arteries, which causes a condition called atherosclerosis that can lead to heart attacks and strokes.

From the moment a blood vessel is damaged, be it from high blood sugar or cigarette smoke, immune cells immediately infiltrate the area. Those immune cells subsequently engulf cholesterol particles that are typically floating around in the blood stream to form a fatty plaque that resides in the wall of the vessel.

This process continues for decades until eventually, one day, immune mediators rupture the cap that encloses the plaque. This triggers the formation of a blood clot that obstructs blood flow, starves the surrounding tissues of oxygen and ultimately causes a heart attack or stroke.

Hence, cholesterol is only part of the story; it is, in fact, the immune system that facilitates each step in the processes that drive heart disease.

Can diet influence C-reactive protein levels?

Lifestyle can significantly influence the amount of C-reactive protein produced by the liver.

Numerous foods and nutrients have been shown to lower C-reactive protein levels, including dietary fiber from foods like beans, vegetables, nuts and seeds, as well as berries, olive oil, green tea, chia seeds and flaxseeds.

Weight loss and exercise can also reduce C-reactive protein levels.

Does cholesterol still matter for heart disease risk?

Though cholesterol may not be the most important predictor of risk for heart disease, it does remain highly relevant.

However, it’s not just the amount of cholesterol – or more specifically the amount of bad, or LDL, cholesterol – that matters. Two people with the same cholesterol level don’t necessarily have the same risk for heart disease. This is because risk is determined more so by the number of particles that the bad cholesterol is packaged into, as opposed to the total mass of bad cholesterol that’s floating around. More particles means higher risk.

That is why a blood test known as apolipoprotein B, which measures the number of cholesterol particles, is a better predictor of risk for heart disease than measurements of total amounts of bad cholesterol.

Like cholesterol and C-reactive protein, apolipoprotein B is also influenced by lifestyle factors like exercise, weight loss and diet. Nutrients like fiber, nuts and omega-3 fatty acids are associated with a decreased number of cholesterol particles, while increased sugar intake is associated with a larger number of cholesterol particles.

Furthermore, lipoprotein(a), a protein that lives in the wall surrounding cholesterol particles, is another marker that can predict heart disease more accurately than cholesterol levels. This is because the presence of lipoprotein(a) makes cholesterol particles sticky, so to speak, and thus more likely to get trapped in an atherosclerotic plaque.

However, unlike other risk factors, lipoprotein(a) levels are purely genetic, thus not influenced by lifestyle, and need only be measured once in a lifetime.

What’s the best way to prevent heart disease?

Ultimately, heart disease is the product of many risk factors and their interactions over a lifetime.

Therefore, preventing heart disease is way more complicated than simply eating a cholesterol-free diet, as once thought.

Knowing your LDL cholesterol level alongside your C-reactive protein, apolipoprotein B and lipoprotein (a) levels paints a comprehensive picture of risk that can hopefully help motivate long-term commitment to the fundamentals of heart disease prevention. These include eating well, exercising consistently, getting adequate sleep, managing stress productively, maintaining healthy weight and, if applicable, quitting smoking.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Hospitals may soon be able to rely on a "self-driving" machine to help patients recover from heart attacks. This machine would deliver treatments to the patient, collect data on how their body responds, and then adjust their medications to stabilize the patient within parameters preset by their doctor.

This is the vision for the Autonomous Closed-Loop Intervention System (ACIS), a device being developed by scientists at NTT Research, an arm of global technology company NTT. The device has been tested in animal experiments but not in human patients yet.

The researchers' eventual goal is to allow the heart to rest and minimize its oxygen use in that critical recovery window after a patient experiences a cardiac emergency. The jobs that would be handled by ACIS are usually done by medical providers — but the idea is that the device could standardize and optimize the process to deliver better outcomes while relieving strain on doctors' already-limited resources.

"We think that this system will outperform the standard of care," said Dr. Joe Alexander, director of NTT Research's Medical and Health Informatics (MEI) lab.

ACIS stemmed from a larger effort spearheaded by the MEI Lab known as the Bio Digital Twin program. Its aim is to construct advanced virtual models of organ systems that can be personalized with an individual patient's data, providing a detailed and dynamic representation of their medical status and a testable model for developing treatment plans.

Live Science spoke with Alexander about Digital Twins, ACIS and his vision for how they might transform health care.

Nicoletta Lanese: When we're talking about a Bio Digital Twin, is it fair to say it's a virtual copy of the patient?

Dr. Joe Alexander: Probably the layperson would think of a Bio Digital Twin as a copy of the person. But actually, it's just a system of equations, modeling and simulation to represent a person to the extent that is relevant for the disease. It's a very specific application, so there's no single Bio Digital Twin representing the [whole] person.

In our case, although we set out to build a family of Bio Digital Twins to represent different organ systems for different types of important diseases, we're starting with the cardiovascular system. So when I talk about a Cardiovascular Bio Digital Twin, I'm not talking about even a copy of the heart; I'm talking about a mathematical representation of all of the systems necessary for looking at the cardiovascular system in a particular patient.

In the case of ACIS, we're looking at acute heart failure and acute myocardial infarction [colloquially known as a heart attack].

NL: Could you talk about what kind of data goes into the model?

JA: This Cardiovascular Bio Digital Twin is representing pressures and flows throughout the cardiovascular system, including pressures and flows generated by all four chambers of the heart. … We are able to represent the cardiovascular system dynamics in pressures, flows and volumes.

NL: And how do you make that actionable for an individual patient?

JA: We're in the early stages of it, but we have a road map for how to do it. Basically, we first go after representing the "normal" cardiovascular system for patients. So, if we can get data around "normal," then that's very good. [Editor's note: The MEI Lab is working with partners such as the National Cerebral and Cardiovascular Center in Japan to get access to this kind of data.]

But probably what's most important is finding populations that are relevant to the particular patient — so, in this case, patients with cardiovascular disease or patients with heart failure. So we go after that population-level data; let's say for heart failure. Then, from that data, we can estimate parameters for our cardiovascular model that represent the general population of patients with heart failure.

Within that population, as you know, there's a lot of variability. So are there other characteristics specific to our patient that we can use? Maybe results from echocardiogram [EKG]; maybe age; maybe comorbidities [other medical conditions]; sex, male or female; or environment. And if there is genetic information available, then we can find a subpopulation that's even more relevant to the patient.

Now, with ACIS, we [would] actually hook up a patient to the "first guess" of our Cardiovascular Bio Digital Twin for what would match that patient based on population-level data. Since it's a feedback control system, the feedback will automatically adjust the parameter values to deliver the necessary drugs or device therapies that that particular patient needs for some prespecified cardiac output. In that way, we can further fine-tune the Digital Twin for that patient.

NL: Can you describe how ACIS and its feedback loop work?

JA: The idea is that it's a "self-driving" therapeutic, just like a self-driving car. But in this case, "self-driving" is delivering the appropriate drugs or, in severe cases, medical-device therapies that a patient may need.

We have a system where we specify — just type in the keyboard — the desired cardiac output, heart rate, left atrial pressure, arterial pressure that we want the patient to achieve. Then, syringes that are filled with the appropriate drugs to create those changes are driven by our model, or "best guess" for that particular patient. This is all after a patient has had the primary lesion [like a blood vessel blockage] treated in the cath lab.

Let's say they had a vessel that was occluded; it's already been opened up or a stent has been placed, and they go to the ICU [intensive care unit] or CCU [coronary care unit] in order to recover. Recovery means that the heart needs an opportunity to rest. That means letting the heart work as little as possible to maintain the desired cardiac output.

We have a certain regimen of drugs that are given. Catecholamines improve the ability of the heart to contract. Nitrates reduce afterload of the heart so it doesn't have to work against such a high load when it tries to inject into the arterial system. Diuretics decrease the circulating blood volume and remove blood from the lungs, which has built up due to the acute failure.

These drugs are typically given by a physician; they'll give one drug and look at the response, give another drug, the response, and manage that patient over several days. When our system achieves proper function — and we're almost there, I think — all those drugs can be given at once if we know how the system will respond. That saves us a lot of time in treating the patient.

The drugs are delivered by these autonomously controlled syringes; then the patient responds to them, and that response is fed back in this system. Those values are compared to the ones that we typed in the keyboard, and if there's a difference, then feedback systems work to reduce that difference. It also gives information to our Digital Twin for that patient, so that in the future, we have better representations of those resistors and capacitors in the model.

NL: What stage of development has ACIS reached at this point?

JA: So, in animal experiments in dogs, last year for the first time, we experimentally induced acute heart failure and we were able to let this autonomous system correct the cardiac output, arterial pressure autonomously, while minimizing myocardial [heart muscle] oxygen consumption.

Since that first successful experiment about a year ago, we've had several other successful [animal] experiments, all the while improving our feedback system to be more complex, making it so that it can operate based on intermittent data, so you don't have to be continuously sampling. You can do it episodically.

We have several more years of work in optimizing this system, we think, in animal experimentation — probably about three years more. And then we'll be ready for first-in-human studies where ACIS will be used but with a clinician in the loop [for the initial human tests]. What ACIS would do is tell the physician what doses of these various drugs to deliver, and the physician would then make a decision whether to do it or not, as a safety measure.

Now, what I've been describing so far has mostly been about drugs, but the same algorithms work for medical devices, such as left ventricular assist devices [LVAD, a type of mechanical pump] or extracorporeal membrane oxygenation devices [ECMO, which circulates the blood to let the heart and lungs rest]. This is all within the scope of what we expect to achieve in experimental animals within the next three years before going to first-in-human studies.

NL: What are the next steps toward getting ACIS approved? What might the trials look like?

JA: It would be kind of like [testing] an autonomous or self-driving vehicle — level 1 through 4 degrees, or stages, of autonomy.

In other words, allowing the system to have increasing responsibility and watching the performance until settling into acceptance of an autonomous system where then, still, probably a specialist would monitor it — like someone sitting in the seat of a self-driving car, ready to take over if things go wrong. I see that kind of progression, similar to the self-driving vehicle.

NL: And in the long run, would ACIS always have some kind of clinician supervision?

JA: I still hold to the concept of "autonomous," but I suspect that there will be a cardiologist somewhere roaming around, monitoring, perhaps, a number of patients at once.

I'm very committed to the idea that the device that we conceive of can actually outperform the cardiologist. And I know that we'll rub some cardiologists the wrong way. But we expect to demonstrate that point, or strongly suggest that that's true, by doing experiments in animals where we compare the ACIS system to clinically trained cardiologists. We expect reduced infarct size [degree of heart tissue death] from ACIS compared to the standard of care from cardiologists.

NL: Assuming this device gets approved in the future, where do you see it having the most benefit?

JA: There's the so-called Quintuple Aim of Health Care, which says to improve the patient experience, improve the physician experience, improve population health, reduce the cost of care, and improve health equity. These aims, I think, are all addressed by ACIS.

The patient would have more attention and minute-to-minute care — you wouldn't have a resident trying to juggle many patients at once. You could have a less-specialized clinical caretaker who is watching the behavior of the device, and so that would improve not only the patient experience and quality of the patient's care but also the health care provider's experience. They wouldn't have to be overworked to such an extent.

We think that this system will outperform the standard of care because [on paper] you more rapidly converge on the minimization of myocardial oxygen consumption and have better recovery during the hospital stay. So the patients have fewer readmissions and complications after being released. There's always some injury to the heart [with these cardiac events], and maybe, there may be some infarction of the heart. So we think that this level of care could reduce infarct size, so you preserve more of the heart, during treatment.

NL: And when you eventually hand off ACIS for clinical testing, what would the next project be?

JA: For us, the natural progression within the next 10 years, probably within the next five years, would be chronic heart failure. In chronic heart failure, you have to deal with more complexity, such as [tissue] remodeling, where the ventricles get thicker or get dilated. That kind of remodeling changes the mechanics.

You also have to deal with data from patients who are not in the hospital. We plan on building registries of patients [with Digital Twins] who would have been acutely ill to have access to that data for treating them outside. But then we have to also rely on things like wearable technologies, and we've been working on that as well. We have collaborations with folks at the Technical University of Munich who are developing special biosensors and biomaterials and implantable sensors and so forth that could help provide the data that would be important to doing predictive health maintenance in patients with chronic heart failure.

And in chronic heart failure, we have to deal with comorbidities and complications like kidney failure … and anemia. The combination of fluid overload and anemia all due to renal failure really makes the heart suffer from a lack of oxygen and causes slow deterioration.

I'm sure that complexity alone will keep me busy for the rest of my life. We have a lot of work to do with chronic heart failure; that would be next for sure.

Editor's note: This interview has been lightly edited for length and clarity.

For decades, cardiologists have observed that heart attacks cause more damage when they occur during the day than when they happen at night — and understanding why could be key to treating the condition, a new study finds.

There are many theories as to why daytime heart attacks are more harmful; some point to daily fluctuations in stress hormones and blood pressure as possible culprits. But the role of the immune system has remained less clear.

Earlier research showed that immune cells called neutrophils, which act as first responders to injury, cause more inflammation and collateral tissue damage at injury sites during the day. They are relatively calmer at night.

Now, in the new study, published Dec. 12 in the Journal of Experimental Medicine, scientists connected the dots between daytime heart attacks and aggressive neutrophils.

More damaging by day

By analyzing clinical records from more than 2,000 heart attack patients, the team found that patients admitted during daytime hours showed higher neutrophil counts and greater heart damage, suggesting neutrophils themselves might play a role in worsening the injury. They then confirmed the same pattern in experiments with mice.

The researchers split their lab mice into two groups: one with normal neutrophil levels and one whose neutrophil levels were depleted with an antibody treatment. Then, they induced heart attack in the mice at different times of the day and night.

In the first set of mice, they observed a pronounced rhythm of greater heart injury in the morning than at night, similar to what was seen in the human data. However, in the mice with low neutrophil counts, this rhythm disappeared and the heart attacks caused less damage overall.

To test the idea further, the researchers genetically disabled a gene that helps control the circadian clock, a regulator of 24-hour cycles in the body. As they expected, the rhythm again disappeared and the overall heart damage was reduced in these modified mice.

Importantly, although depleting neutrophils hobbles the immune system, deleting just the clock gene didn't impair the mice's ability to fight infections, the scientists found.

"This makes the study really interesting," Tim Lammermann, an immunologist at the University of Münster in Germany who was not involved in the work, told Live Science. That's because it was always believed that immune protection and inflammatory damage caused by neutrophils "cannot be disconnected from each other."

Putting neutrophils in 'night mode'

Next, the scientists wanted to test whether there might be another way to control this gene and mimic the body's natural nighttime calming of neutrophils without diminishing the cells' numbers. They focused on a receptor on neutrophils called CXCR4, which typically responds to signals that slow down neutrophil activity at night.

They genetically engineered mice to carry really high concentrations of this receptor. This calmed the cells down even during the daytime, so the heart injury was again alleviated and the rhythmic pattern disappeared.

Finally, using a drug that activates this receptor, the researchers toned down neutrophil activity during the day, pushing the cells into their nighttime state. Treatment with this drug prior to heart attack reduced tissue damage and improved heart function weeks after the event, they found.

What's more, in mouse models of sickle cell disease, in which neutrophils clog blood vessels and trigger rampant inflammation, the drug reduced blockages and improved blood flow.

It's surprising that controlling just one type of immune cell offered significant protection against these inflammatory injuries, senior study author Andrés Hidalgo, an immunologist at Yale University, told Live Science.

Lammermann noted that the experiments with the drug were particularly significant, providing evidence that the compound reduced the inflammatory response of neutrophils while keeping their defense mechanisms intact.

The researchers also uncovered an interesting pattern behind the neutrophil action: In skin wounds and heart tissue alike, daytime neutrophils tend to spread into neighboring uninjured areas, enlarging the injury site, Hidalgo explained. Calmer, nighttime neutrophils, on the other hand, stay confined to the center of the damaged zone.

The findings suggest there could be ways to fine-tune neutrophils and tone down their aggressiveness without compromising their defense capability. However, translating this approach to humans will require careful study. The ways in which CXCR4 signaling affects other types of cells would also need to be carefully considered, Lammermann cautioned.

A drug that calms down inflammation without compromising immunity would be the holy grail of immune therapy. However, human trials for such a drug would need to assess many factors, such as the timing of when it should be given in the event of a heart attack, and if there are any potential risks involved, he added.

This article is for informational purposes only and is not meant to offer medical advice.

Your heart pumps blood from your head to your toes, provides cells with fresh oxygen, and removes waste products. Located in the middle of your chest and tilted slightly to the left, your heart pushes out about 1.5 gallons (5.7 liters) of blood every minute to over 60,000 miles (97,000 kilometers) of blood vessels.

When things go wrong with the heart and circulatory system, the consequences can be dire. Cardiovascular disease is the leading cause of death for both men and women in the U.S., where about 1 in 3 deaths is attributable to heart disease. In the U.S. alone, one person dies every 34 seconds from cardiovascular disease, and heart disease costs the country over $400 billion annually.

The heart is undoubtedly one of the most important organs in the human body, and there's a lot to learn about it. So don't skip a beat, and take our quiz to test your knowledge of the heart.

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Research has long pointed to a link between poor gum health and a higher risk of cardiovascular disease — and now, a new trial suggests that treating severe gum disease may reduce the narrowing of a major artery over time in otherwise healthy people.

Likely by reducing inflammation, this routine oral hygiene procedure may be an unsung way of minimizing declines in blood vessel functioning.

"I was very overwhelmed when I looked at the data the first time," study co-author Dr. Marco Orlandi, a clinical research periodontist at University College London, told Live Science.

Around 40% of U.S. adults ages 30 and older have some level of gum disease, known as periodontitis, a chronic inflammatory condition whose progression leads to wobbly teeth, tooth loss and persistent bad breath. As the disease worsens, small pockets around the teeth that cannot be reached by a toothbrush or floss expand and fill with plaque and bacteria.

There is now an abundance of research linking periodontitis to a higher risk of various health outcomes, including Alzheimer's disease, colon cancer and rheumatoid arthritis. A key area with mounting evidence is the association between severe gum disease and cardiovascular disease, with previous studies finding that the management of gum disease is linked to improved blood vessel function.

Now, a clinical trial published Aug. 19 in the European Heart Journal has found that treating periodontitis slows the thickening of the inner two layers of the carotid arteries, found on each side of the neck, in otherwise healthy adults. The thickness of those artery walls is a key marker for cardiovascular disease risk.

Related: Keratin extracted from sheep's wool repairs teeth in breakthrough

By targeting inflammation rather than other artery health factors, like cholesterol, "the impact of what we are doing comes without going through the classic risk pathway" for cardiovascular disease, Orlandi said.

To test whether treating periodontitis actually causes the carotid arteries to thicken less over time, Orlandi and his team of periodontists and cardiologists conducted a gold-standard trial at a dental hospital in central London. The trial was randomized, meaning participants were randomly placed in a treatment group or a comparison group that didn't receive the intensive gum treatment.

First, the researchers took ultrasounds of the carotid arteries of 135 people with severe periodontitis, to establish a baseline level of thickness. They also measured how much the arteries dilated when blood flow increased — a measure of blood vessel functioning — and took blood samples to pinpoint markers of inflammatory and oxidative stress. All of the individuals were healthy besides having gum disease.

Next, the participants were randomly divided into either the treatment group or the control group. Care was taken to ensure there was a roughly even split between the two groups in terms of the participants' periodontitis severity, smoking status and family history of cardiovascular disease.

In the treatment group, patients received intensive periodontitis treatment: a thorough clean of the whole mouth and a deep clean below the gumline to remove plaque and tartar. The control group received a simple scale and polish, more akin to a regular dental cleaning that doesn't include a deep clean of the gums.

The participants were then followed for two years, and they each received further dental treatments at regular intervals throughout that time. The researchers also reassessed the carotid artery at the one-year and two-year marks, and took blood samples and measured blood-vessel function at five time points.

They found that the thickness of the carotid arteries' innermost linings was lower for individuals who received intensive treatment than for those in the control group. This difference was "comparable to what has been seen with lifestyle interventions and some pharmacological agents in similar populations," study co-author Dr. Francesco D'Aiuto, a clinical research periodontist at University College London, told Live Science in an email.

The treated patients also had better blood vessel function and lower levels of inflammatory and oxidative stress markers in their blood, which are known to contribute to the narrowing of artery walls — a condition called atherosclerosis.

Although many factors drive atherosclerosis, "our results reinforce the view that untreated periodontitis is a modifiable risk factor for vascular ageing and possibly cardiovascular events," D'Aiuto said.

However, a key limitation of the research is that it was conducted in only one location, so there is a chance that the findings partly come down to quirks of the location or the people in the sample, Orlandi said.

Another limitation, said Dr. Maurizio Tonetti, a clinical and research periodontist at the University of Hong Kong who was not involved in the research, is that all of the participants in the trial were healthy other than having periodontitis. As such, these results should not be interpreted as evidence that if someone with atherosclerosis has their gum disease treated, the health of their arteries will improve, he told Live Science.

Even so, the findings "are bringing the concept of these [intensive gum disease] interventions into the preservation of wellness," Tonetti said.

"For many, many years, dentists have been focusing on the teeth, forgetting the rest of the body, and physicians have been focusing on the body, forgetting that there are teeth," he said. "They are really two worlds that have been separated and need to go back together for the benefit of patients."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 65-year-old woman in Austria

The symptoms: The patient had been experiencing shortness of breath during physical activity for several weeks when she went to a hospital for evaluation. She also had a history of passing unusually dark urine, which had been happening since childhood, and in her 40s, she'd had total hip and knee replacements on both sides due to arthritis.

What happened next: The woman's doctors checked her heart function with an echocardiogram, which uses ultrasound to visualize blood flow through the heart's valves and chambers. They also used cardiac catheterization, which involves guiding a long, thin tube through the blood vessels and into the heart to further examine its valves and look for blockages and narrowed arteries.

The diagnosis: The evaluations revealed that the woman had severe aortic stenosis, in which the heart's aortic valve is narrowed or blocked. This valve normally opens to allow oxygen-rich blood to flow from the heart to the rest of the body, so stenosis hinders that crucial blood flow.

The treatment: The patient underwent open heart surgery to have her aortic valve replaced. Thirteen days later, she was discharged from the hospital. In a report of the case, one of the woman's doctors noted that, three years after the surgery, the patient remained free of cardiovascular symptoms.

What makes the case unique: Common risk factors for aortic stenosis include having high cholesterol, high blood pressure or a history of smoking. The condition often coincides with coronary artery disease, which is characterized by plaque buildup in one or more of the arteries that supply blood to the heart. In this patient's case, the coronary arteries appeared normal, but doctors discovered something unusual during her open heart surgery: "black pigmentation" and calcified "dark black" tissues in her aorta and aortic valve, respectively.

The tissue removed during the surgery was further examined under a microscope. This examination revealed "brown pigment deposition" within hardened areas of the aortic valve and in some of the noncalcified tissues in the structure. Within the hardened valve tissue, the team also found signs of chronic inflammation, including the presence of "pigment-laden" immune cells. There was also degeneration within the connective tissues of the valve.

Based on these findings, as well as the patient's medical history, the doctors determined that she had a rare genetic condition called alkaptonuria. Globally, the inherited disease is thought to affect 1 in 250,000 to 1 in 100,000 people, although the prevalence varies widely among countries.

Alkaptonuria is caused by mutations in a gene called HGD, which carries instructions for an enzyme that helps break down two protein building blocks in the body: phenylalanine and tyrosine. These mutations make the enzyme less effective, which causes a buildup of a byproduct of phenylalanine and tyrosine. The byproduct, homogentisic acid, is excreted in urine, which causes pee to darken when it's exposed to air. And in people with alkaptonuria, there's too much homogentisic acid for the body to excrete, so the substance builds up in connective tissues.

The accumulating acid becomes an "ochronotic pigment," which essentially stains the tissues where it accumulates and eventually calcifies, or hardens. Many people with alkaptonuria require joint replacements because their joints have calcified, and in some people, this calcification also affects the heart. This was the case for the 65-year-old woman.

"It is difficult to assess the incidence of cardiac ochronosis accurately because of its rarity," the case report author noted. "Cardiac ochronosis is a very rare disease, but cardiac surgeons and pathologists should be aware of this condition since they might be confronted with the typical signs during elective cardiac surgery and histological examination of excised specimens."

This article is for informational purposes only and is not meant to offer medical advice.

Heart rate tracking is increasingly common among fitness enthusiasts, and understandably so. Whether it is a rugged outdoor smartwatch or a discreet smart ring, smart wearables can help you determine if you exercised hard enough, rested well during sleep or stressed too much during the day — simply by listening to your heartbeat.

Some of the best fitness trackers can even use machine learning to give you detailed exercise recommendations based on how your health metrics change over time — not to mention that smart wearables can be invaluable tools for endurance athletes. But how do fitness trackers measure your heart rate, exactly? And how accurate are these measurements? We asked the experts.

Most fitness watches and smart rings depend on a technique called photoplethysmography (PPG). While its name may sound scarily complex, this technology is based on a relatively simple concept — light absorption by the body tissues.

How does photoplethysmography work?

PPG uses optical sensors that detect heart rate by measuring changes in the volume of blood flowing through tiny blood vessels in the skin and underlying connective tissue, Dr. Peter Sogaard, professor of cardiology at Aalborg University in Denmark and chief medical officer at VentriJect, a company which has developed a novel device for measuring cardiorespiratory fitness, told Live Science by email.

With each heartbeat, the heart muscle contracts and relaxes, to force the next portion of blood into circulation. Contracting causes a temporary spike in blood volume and increased pressure on the artery walls, and it is often referred to as the systolic phase of the cardiac cycle. When the heart relaxes between beats, the blood flow decreases — this is known as the diastolic phase. PPG sensors measure these changes in blood volume and pulse pressure (the difference between systolic and diastolic pressure), and then convert these metrics into heart rate measurements, Sogaard said.

PPG sensors detect these changes in blood movement by emitting light at specific wavelengths into the skin. Blood components like hemoglobin, the protein in red blood cells, absorb some of that light. The tracker's photodetector then measures the amount of light reflected back. The more light absorbed by the blood, the higher its volume in the blood vessels — and this is what fitness trackers interpret as a heartbeat, Sogaard said.

"The most commonly used light sources are infrared and green LED," Sogaard said. That is because these wavelengths of light tend to be the most effective at penetrating the skin tissue, according to a 2022 review published in the Frontiers of Physiology. Generally, the accuracy of PPG increases with the light wavelength, the review authors noted. Some optical sensors even combine several wavelengths to improve accuracy.

That is the theory. But how accurate are optical sensors in practice? The answer is less clear.

How accurate is photoplethysmography?

"Multiple factors can affect the accuracy of PPG, from tracker placement and body temperature to skin thickness, motion artifact [distortions caused by movement] and cardiovascular disorders like arrhythmia and peripheral vascular disease [a condition in which the arteries outside of the brain and the heart become blocked or narrowed]," Dr. Masaki Nakamura, a cardiothoracic surgeon at Baptist Health Miami Cardiac & Vascular Institute, told Live Science by email.

For example, optical sensors tend to provide more reliable heart rate measurements during rest and sleep than they do during exercise, according to a 2020 meta-analysis in the Journal of Sports Sciences. Scientists compiled 44 studies that compared the accuracy of PPG fitness to more precise ECG (electrocardiogram) and chest-strap heart rate monitors and found that the biggest discrepancies could be observed with weightlifting, cycling and other high-intensity sports. While most modern fitness trackers use accelerometer-based algorithms to account for rapid movements, motion artifacts can still affect their tracking accuracy.

Skin contact is another factor that can have an impact on PPG measurements, Sogaard said. For example, a device that is too loose or too tight will not allow the optical sensors to get a good reading. Skin temperature can also interfere with PPG. "If the patient has a low temperature, vessels are contracted and measurements become inaccurate," Sogaard said.

Moreover, optical sensors may struggle with detecting heart rate in people with darker skin tones or tattoos. That is because both melanin, the dark pigment in the skin, and tattoo ink can absorb light and reduce the amount of light reflected back to the tracker, according to a 2023 review published in the Journal of Racial and Ethnic Health Disparities.

People with obesity may also struggle with obtaining accurate heart rate measurements. Excess body fat can lead to changes in skin thickness and blood flow, which is why it may affect the accuracy of optical sensors, according to a 2021 review published in the journal Biosensors. The good news is that scientists are working on developing new technologies that would make PPG more accessible for these population groups.

While not without limitations, PPG fitness trackers can be useful for monitoring heart rate in people with certain cardiovascular conditions, according to Nakamura. "Continuous heart rate and blood pressure monitoring can be crucial for cardiac patients to prevent future events like a heart attack, stroke or acute heart failure. The current industry gold standards of blood pressure and heart rate assessment are the manual sphygmomanometer (BP cuff) and the electrocardiogram. However, both these exams can only be measured intermittently and can be affected by factors such as white coat syndrome [a condition when a person's blood pressure is high only when measured in a health care setting], caffeine or stress," Nakamura said.

That said, experts agree that PPG-based heart rate readings should never be regarded as a substitute for clinically validated tests conducted by healthcare professionals.

This article is for informational purposes only and is not meant to offer medical advice.

A woman with a failing heart has been kept alive with the help of a new "breakthrough" stem-cell technology, scientists report.

The 46-year-old woman had experienced a heart attack in 2016 and subsequently developed severe heart failure, in which the heart cannot pump blood efficiently enough to meet the body's needs. The patient was awaiting a heart transplant when she underwent the experimental stem-cell procedure as part of a clinical trial.

During the surgery, the woman's heart was implanted with tiny patches of heart muscle cells, which had been grown from stem cells in a lab. These 10 patches, each comprised of about 400 million heart cells, kept the woman stable until she could receive a heart transplant three months later, according to a paper published Wednesday (Jan. 29) in the journal Nature.

"We now have, for the first time, a laboratory-grown biological transplant available which has the potential to stabilize and strengthen the heart muscle," study co-author Dr. Ingo Kutschka, a heart surgeon at University Medical Center Göttingen in Germany, said in a press conference, Nature News reported.

Related: In a 1st, baby's heart defect successfully treated with injected stem cells

Unlike many other cell types, such as skin cells, heart muscle cells cannot easily regrow or repair themselves if they are damaged by an insult like a heart attack. Such damage to the heart can lead to heart failure, which affects around 6.7 million adults ages 20 and older in the United States, according to the Centers for Disease Control and Prevention (CDC). Heart failure was listed as a contributing or primary cause of death on more than 450,000 death certificates in the U.S. in 2022, the CDC reported.

Over half of people with severe heart failure die within a year unless they receive a heart transplant, but there are limited donor hearts available, Nature News reported.

To supplement these limited heart transplants, scientists have experimented with transplanting heart muscle cells instead. In the new Nature paper, the researchers describe a method of growing heart tissue from stem cells known as induced pluripotent stem cells (iPSCs). Scientists create these stem cells by gathering normal adult cells and then reprogramming them back into a "pluripotent" state, from which they can develop into almost any cell type in the body.

The scientists encouraged these iPSCs to develop into heart muscle cells and connective tissue in the lab; the researchers then mixed the resulting tissue with collagen to create tiny patches that could be implanted onto the surface of the heart.

"The graft is basically outside of the heart," Dr. Jianyi Zhang, an iPSC bioengineering expert at the University of Alabama at Birmingham who was not involved in this study, told Nature. "It's quite a breakthrough."

The scientists first tested similar patches on rhesus macaque monkeys (Macaca mulatta) with heart failure; the patches tested on monkeys were grown with monkey stem cells. Six months later, several of the monkeys grew thicker heart walls that could pump up to 10% more blood per heartbeat than a group of untreated monkeys.

During the patch procedure, the monkeys were all given immunosuppressant drugs, to prevent their immune systems from rejecting the grafts. Additionally, none of the monkeys developed tumors or irregular heartbeats, which had been a problem in similar studies conducted in the past.

The success of the monkey trial enabled the trial in human volunteers, one of whom was the 46-year-old woman. After the woman underwent her heart transplant, the researchers examined her old heart and saw that the implanted patches had grown minuscule blood vessels, indicating that they were receiving blood and oxygen from the body.

"This is clear now, that you can add muscle to the failing heart, and that we can do that without safety concerns," study co-author Wolfram-Hubertus Zimmermann, a pharmacologist at University Medical Center Göttingen, said in the press conference.

The eventual hope is that this approach will help people stay alive for long enough to receive a donor heart; it's not intended as a complete alternative to transplants.

In an ongoing trial, the scientists have so far implanted the patches in 15 other people. They are also experimenting with more macaques to find a way to minimize the use of immunosuppressant drugs, which help prevent rejection but can leave a patient vulnerable to infection and other health problems.

The patient: A 60-year-old woman in Be'er Sheva, Israel

The symptoms: While enjoying the food at a wedding, the woman began feeling a painful pressure in her chest that then radiated into her arms. This sensation persisted for several hours, although the pain subsided enough that she opted to stay at the reception. The next day, lingering chest pain, discomfort and generalized feelings of weakness prompted her to seek medical care.

What happened next: Emergency room physicians performed an ultrasound and detected abnormal activity in the patient's left ventricle, the part of the heart that performs most of the organ's pumping action. Some segments of the heart muscle were not contracting at all, and contraction in other segments was reduced. This disruption was "moderate to severe," doctors wrote in a report of the case.

The diagnosis: Doctors determined that the woman was experiencing a condition called takotsubo cardiomyopathy, also known as "broken heart syndrome," which produces symptoms mimicking those of a heart attack, such as chest pain and difficulty breathing. "Takotsubo" refers to a type of Japanese jar used for trapping octopuses; the condition distorts the muscles of the left ventricle, making it resemble a narrow-necked octopus-catching jar.

The treatment: The woman received steroids and medications for lowering blood pressure, including ACE inhibitors, which relax arteries and veins, and beta-blockers, which block the effects of stress hormones on the heart. The doctors referred her to a cardiac rehabilitation center. After one month, an echocardiogram showed that the patient's heart activity had returned to normal.

What makes the case unique: Prior to this case, scientific studies had linked takotsubo cardiomyopathy to drug use, neurological disease, physical or emotional stress, and allergic reactions to certain foods. But this case had a cause that had never been documented before: Minutes before developing symptoms, the woman had mistaken wasabi for avocado and swallowed a teaspoon-sized helping.

This is the first example of wasabi consumption causing broken heart syndrome. While some compounds in wasabi are likely beneficial to health, such as cancer-fighting agents, swallowing an unusually large amount may have triggered an extreme stress reaction in the patient, thus leading to disruption of her normal heart function.

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

More than 100 years ago, Dr. Karl Landsteiner discovered that not all red blood cells are alike. He found that, when different people's blood was mixed, it would often clump up and curdle, destroying the cells within it. His work on the different types of red blood cells led to the discovery of the ABO blood group system, which won him the 1930 Nobel Prize in physiology or medicine and also helped make blood transfusion a safe, reliable practice that saves millions of lives every year.

Many people know where they fit into the classic ABO blood typing system, which designates blood as type A, B, AB or O. But these four basic blood groups aren't the end of the story.

So how many blood types are there, really?

Depending on how deep you dig, the answer could number in the hundreds or more — and the list is still growing.

Related: What's the rarest blood type?

Blood types exist because red blood cells, which relay oxygen through the bloodstream, carry different proteins and sugars on their surfaces. These are called antigens. Each person has a specific combination of antigens on the surfaces of their blood cells, and that combination determines their blood type.

Landsteiner's ABO blood group system categorizes a person's blood based on whether they have one, both or neither of the antigens known as A and B. ABO blood type is determined by a single gene, one copy of which is passed down by each parent.

O is the most common version of that gene — but it's recessive, so a person needs to inherit two copies to have an O blood type. Both the A and B versions of the gene are dominant, so they overpower any copy of the O gene. Having one copy of A or B will lead to an A or B blood type, respectively, and a person will have an AB blood type if both A and B are present.

"The ABO blood group system is the most important blood group to consider during a blood transfusion," Dr. Emily Coberly, divisional chief medical officer at the Red Cross, told Live Science in an email. "We all make antibodies against the ABO antigens that aren't on our own red blood cells."

For example, if you have type A blood, you'll have antibodies, or protective immune proteins, that attack B antigens. So you wouldn't want type B blood in your body. (This handy graphic from the Red Cross illustrates the idea.)

You also may have heard of blood types being "positive" or "negative." This categorization comes down to another antigen, called the Rh factor. People with the Rh factor on their cells have Rh-positive blood, whereas people without the Rh factor are Rh-negative. The Rh factor is controlled by a cluster of genes influencing multiple antigens, so the genetics are more complicated than in the ABO system, but being Rh-positive is both a dominant trait and more common in the population.

The various combinations of the ABO system and Rh factor create the eight main blood groups. In most cases, knowing which of these blood groups a person fits into is enough to provide them a safe transfusion.

But certain diseases can complicate things, and blood types get even more complex when you consider the hundreds of other antigens present on the surface of red blood cells.

What are the other blood types?

Besides the A, B and Rh factor antigens, there are at least 350 other known antigens on red blood cells, Coberly said. That number is still going up as researchers identify important new proteins. If cells build just one of these antigens differently than other cells do, that justifies labeling a new, unique blood type. So, theoretically, there are as many blood types as there are combinations of surface antigens on the red blood cell.

As of 2024, the International Society of Blood Transfusion recognizes 47 blood group systems. Each of these blood group systems can encompass multiple blood types, just as the ABO system includes A, B, AB and O.

Coberly said some examples of these rarer blood types include the McLeod phenotype, in which a person's red blood cells don't express a protein called Kx; the Kidd-null phenotype, in which cells don't express a group of proteins known as the Kidd group; and the Bombay phenotype, in which cells don't express a protein called the H antigen.

Like the ABO group and Rh factor, these rare blood types are genetic. They may also be associated with various health conditions and symptoms; for example, the McLeod phenotype is associated with the neurological disorder McLeod syndrome. And because of the genetic component, they may be tied to certain racial or ethnic backgrounds.

For example, sickle cell disease (SCD), a condition that causes red blood cells to form in a crescent-moon shape, primarily affects people of African or Hispanic descent. People affected by SCD often need repeated blood transfusions, which can lead the immune systems to become sensitized to the donor blood. This causes about half of those treated for the disease to develop antibodies against the myriad antigens present on the donor blood cells. That happens even when the donated blood is matched to the patients' ABO type and Rh factor.

After developing antibodies, these patients require meticulously matched blood that accounts for these additional immune proteins. Otherwise, their immune systems may attack and destroy the donor blood, which can quickly lead to life-threatening complications.

These complexities in blood types are one reason why blood banks always need new donors, Coberly emphasized.

"This is why it is so important that we maintain a diverse blood supply from blood donors of all backgrounds," she said. "Blood will be available for all patients when they need it, including those that need blood that is more closely matched to them."

Some scientists are trying to bypass this issue entirely by creating universal donor blood — whether it's by growing red blood cells from scratch or removing antigens from existing donated blood.

A simple difference in the genetic code — two X chromosomes versus one X chromosome and one Y chromosome — can lead to major differences in heart disease. It turns out that these genetic differences influence more than just sex organs and sex assigned at birth — they fundamentally alter the way cardiovascular disease develops and presents.

While sex influences the mechanisms behind how cardiovascular disease develops, gender plays a role in how health care providers recognize and manage it. Sex refers to biological characteristics such as genetics, hormones, anatomy and physiology, while gender refers to social, psychological and cultural constructs. Women are more likely to die after a first heart attack or stroke than men. Women are also more likely to have additional or different heart attack symptoms that go beyond chest pain, such as nausea, jaw pain, dizziness and fatigue. It is often difficult to fully disentangle the influences of sex on cardiovascular disease outcomes versus the influences of gender.

While women who haven't entered menopause have a lower risk of cardiovascular disease than men, their cardiovascular risk accelerates dramatically after menopause. In addition, if a woman has Type 2 diabetes, her risk of heart attack accelerates to be equivalent to that of men, even if the woman with diabetes has not yet gone through menopause. Further data is needed to better understand differences in cardiovascular disease risk among nonbinary and transgender patients.

Despite these differences, one key thing is the same: Heart attack, stroke and other forms of cardiovascular disease are the leading cause of death for all people, regardless of sex or gender.

We are researchers who study women's health and the way cardiovascular disease develops and presents differently in women and men. Our work has identified a crucial need to update medical guidelines with more sex-specific approaches to diagnosis and treatment in order to improve health outcomes for all.

Related: 9 heart disease risk factors, according to experts

Gender differences in heart disease

The reasons behind sex and gender differences in cardiovascular disease are not completely known. Nor are the distinct biological effects of sex, such as hormonal and genetic factors, versus gender, such as social, cultural and psychological factors, clearly differentiated.

What researchers do know is that the accumulated evidence of what good heart care should look like for women compared with men has as many holes in it as Swiss cheese. Medical evidence for treating cardiovascular disease often comes from trials that excluded women, since women for the most part weren't included in scientific research until the NIH Revitalization Act of 1993. For example, current guidelines to treat cardiovascular risk factors such as high blood pressure are based primarily on data from men. This is despite evidence that differences in the way that cardiovascular disease develops leads women to experience cardiovascular disease differently.

In addition to sex differences, implicit gender biases among providers and gendered social norms among patients lead clinicians to underestimate the risk of cardiac events in women compared with men. These biases play a role in why women are more likely than men to die from cardiac events. For example, for patients with symptoms that are borderline for cardiovascular disease, clinicians tend to be more aggressive in ordering artery imaging for men than for women. One study linked this tendency to order less aggressive tests for women partly to a gender bias that men are more open than women to taking risks.

In a study of about 3,000 patients with a recent heart attack, women were less likely than men to think that their heart attack symptoms were due to a heart condition. Additionally, most women do not know that cardiovascular disease is the No. 1 cause of death among women. Overall, women's misperceptions of their own risk may hold them back from getting a doctor to check out possible symptoms of a heart attack or stroke.

These issues are further exacerbated for women of color. Lack of access to health care and additional challenges drive health disparities among underrepresented racial and ethnic minority populations.

Sex difference in heart disease

Cardiovascular disease physically looks different for women and men, specifically in the plaque buildup on artery walls that contributes to illness.

Women have fewer cholesterol crystals and fewer calcium deposits in their artery plaque than men do. Physiological differences in the smallest blood vessels feeding the heart also play a role in cardiovascular outcomes.

Women are more likely than men to have cardiovascular disease that presents as multiple narrowed arteries that are not fully "clogged," resulting in chest pain because blood flow can't ratchet up enough to meet higher oxygen demands with exercise, much like a low-flow showerhead. When chest pain presents in this way, doctors call this condition ischemia and no obstructive coronary arteries. In comparison, men are more likely to have a "clogged" artery in a concentrated area that can be opened up with a stent or with cardiac bypass surgery. Options for multiple narrowed arteries have lagged behind treatment options for typical "clogged" arteries, which puts women at a disadvantage.

In addition, in the early stages of a heart attack, the levels of blood markers that indicate damage to the heart are lower in women than in men. This can lead to more missed diagnoses of coronary artery disease in women compared with men.

The reasons for these differences are not fully clear. Some potential factors include differences in artery plaque composition that make men's plaque more likely to rupture or burst and women's plaque more likely to erode. Women also have lower heart mass and smaller arteries than men even after taking body size into consideration.

Reducing sex disparities

Too often, women with symptoms of cardiovascular disease are sent away from doctor's offices because of gender biases that "women don't get heart disease."

Considering how symptoms of cardiovascular disease vary by sex and gender could help doctors better care for all patients.

One way that the rubber is meeting the road is with regard to better approaches to diagnosing heart attacks for women and men. Specifically, when diagnosing heart attacks, using sex-specific cutoffs for blood tests that measure heart damage — called high-sensitivity troponin tests — can improve their accuracy, decreasing missed diagnoses, or false negatives, in women while also decreasing overdiagnoses, or false positives, in men.

Our research laboratory's leaders, collaborators and other internationally recognized research colleagues — some of whom partner with our Ludeman Family Center for Women's Health Research on the University of Colorado Anschutz Medical Campus — will continue this important work to close this gap between the sexes in health care. Research in this field is critical to shine a light on ways clinicians can better address sex-specific symptoms and to bring forward more tailored treatments.

The Biden administration's recent executive order to advance women's health research is paving the way for research to go beyond just understanding what causes sex differences in cardiovascular disease. Developing and testing right-sized approaches to care for each patient can help achieve better health for all.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Women are more likely than men to die of complications from high-risk cardiovascular surgery, a new study finds.

These life-threatening complications, such as heart attacks and infections, were more likely to be recognized too late in women than in men, resulting in the higher death rate seen in women. Not recognizing or responding quickly enough to complications is referred to as "failure to rescue" by doctors.

The new study, published Oct. 16 in the journal JAMA, analyzed the medical records of more than 860,000 patients who had undergone high-risk surgical procedures between October 2015 and February 2020. All of the procedures involved the heart or blood vessels, including surgeries to repair aneurysms, heart bypass surgeries, and heart-valve replacements.

Overall, about 15% of these patients experienced some complication following their procedure; a similar rate of complications was seen in men and women. But, of the overall group, nearly 11% of the women died of complications, compared with 8.6% of the men. The researchers concluded that this difference was likely caused by delays in doctors recognizing and treating women's complications, which included heart attacks, blood clots in the lungs, kidney failure, lung failure, pneumonia, hemorrhage and surgical-site infections.

Related: Scientists developing new 'heart-on-a-chip'

Dr. Mario Gaudino, a cardiac surgeon at Weill Cornell Medical Center and New York Presbyterian Hospital who was not involved in the research, described the study as a "wake-up call" to the long-overlooked disparities in men's and women's outcomes after major surgeries.

Notably, women in the study were also more likely to receive care at teaching hospitals and larger, high-volume hospitals, compared with men. These types of facilities are associated with better-quality care than other medical centers, such as low-volume hospitals — however, women's higher death rate was consistent across all the different facilities.

"If anything, these results show how pervasive the problem is," said Dr. Catherine Wagner, a cardiac surgery resident at the University of Michigan and lead author of the study. "This suggests there is a systemic problem contributing to the under-recognition and under-treatment of women's postoperative complications," Wagner told Live Science in an email.

The study does not draw any definitive conclusions about the factors that might be driving this disparity. Previous research has focused on women's tendency to get surgery at older ages than men, which means they may be dealing with more underlying medical conditions and be at a more advanced stage of disease. These characteristics were reflected in the women in the new study, who, on average, were a bit older and had a slightly higher rate of comorbidities than the men.

However, while these are relevant factors, they fail to fully account for the study's results, which found a much higher death rate among women despite men and women having similar rates and types of complications, said Dr. Andrei Churyla, a cardiac surgeon at Northwestern Medical Group in Chicago who was not involved in the study.

Unconscious bias against women may be one possible explanation, he said. There's a tendency for medical providers to dismiss women's pain, which can delay, or even preclude, proper diagnosis and treatment. A 2022 study in the Journal of the American Heart Association found that young women who complained of chest pain had a 29% longer wait time for heart-attack evaluation than young men, for example.

A lack of understanding of the female heart also may factor into patients' outcomes, Gaudino suggested. "As cardiovascular physicians, I think we've had the wrong approach of thinking that women were actually like men, or just small men," he said. "The mistake we make is to keep treating women with approaches we know work for men."

Until recently, much of the research on cardiac surgery has focused overwhelmingly on male populations, and few studies have been conducted specifically in female patients, Gaudino said.

Additionally, the diagnostic criteria for complications were developed based on data from male patients, so these may fail to account for differences in women's baseline physiology and how these complications manifest in them. As an example, high levels of troponin, a protein in heart muscles, signal a heart attack is coming on — but the cutoff for what counts as "high" was derived mostly from men, who have higher baseline troponin levels than women, he said.

Gaudino suspects the female body is still misunderstood by physicians and that this means complications that would be flagged easily in male patients are more likely to go unnoticed, and thus untreated, in female patients.

There's been a recent effort to shore up research in this area to better understand and address the gap in surgical outcomes between men and women.

"I think we have to constantly remind ourselves that women are different from men," said Dr. Brittany Zwischenberger, a cardiac surgeon at Duke Health in Durham, North Carolina. "And our current focus on sex and gender will hopefully result in tailored approaches to surgery and their postoperative course, and ultimately reduce disparities. But really, this [study] is an opportunity for us to improve postoperative care for all patients."

This article is for informational purposes only and is not meant to offer medical advice.

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More than any other organ in the body, the heart inspires the imagination. Throughout human history, people around the world have written, spoken and sung about the heart in thousands of languages, describing it as the seat of love, kindness and courage.

But the heart's primary function is to keep us alive. This fist-size muscular organ drives the circulatory system, pumping oxygenated blood throughout the body. It may speed up or slow down depending on our emotions or physical exertion, or due to injury or disease. But in general, a healthy heart thumps steadily and reliably.

So how many heartbeats does that add up to in a single day, or over the course of a human life span?

There's a lot of variation to how fast your heart beats in a day; whether you're sitting at a desk, walking to the store, or running on a treadmill, your heart responds to different energy requirements by beating faster or slower. Heartbeat intervals even slow down and speed up by about 100 milliseconds every time you inhale and exhale, said Dr. Partho Sengupta, chief of cardiovascular medicine for Robert Wood Johnson Medical School at Rutgers University in New Jersey.

"The most interesting aspect of the heart is its ability to modulate its rate and its function depending upon the metabolic needs of the body," he told Live Science. "The physiology is continuously adapting — it almost has its own brain to sense the body's needs."

Estimating a lifetime of heartbeats begins with timing your ticker minute by minute, and then seeing if your average resting heart rate falls within a certain range. Heart rate is measured in beats per minute (BPM). The range for a healthy adult is 60 to 100 BPM while at rest, though the rate for most adults is between 55 and 85 BPM, according to Harvard Medical School. By comparison, the average resting heart rate for a newborn is 70 to 190 beats per minute, per the University of California San Francisco Benioff Children's Hospitals, to meet the energy demands of a faster metabolism.

Related: Can foxgloves really give you a heart attack?

In adults, a resting BPM that falls outside the normal range warns cardiologists of pathologies, Sengupta told Live Science. "We diagnose conditions based upon faster heart rate, when it becomes more than 100, or low heart rate, when it's becoming lower than 60," he said.

A person's heart rate typically slows somewhat with age, as time exacts its toll on heart muscles, said Dr. Salvatore Savona, a specialist in cardiovascular disease and a clinical assistant professor of internal medicine at The Ohio State University Wexner Medical Center in Columbus.

For example, aging can bring the development of fibrosis — growth of excess tissue that impedes beating — or an abnormal heart rhythm like atrial fibrillation, the most common heart rhythm disorder, Savona told Live Science. "That can affect how fast and how slow the heart goes," Savona said.

Listen to your heart

How do heartbeats add up over time? A person with an average resting heart rate of 70 BPM, for example, would generate 100,800 heartbeats in one day. In a year, that would add up to approximately 36.8 million beats. Average life expectancy in the U.S. (as of 2022) is 77.5 years, according to a 2022 report by the Centers for Disease Control and Prevention.

That means in a lifetime, that person's heart beats around 2.85 billion times.

Is there a threshold for how many beats a heart has in it before it wears out and simply stops beating? Or, to paraphrase the Celine Dion song, will your heart go on?

Factors such as age, genetics, injury and disease can gradually erode the heart's performance. But the better we take care of this hardworking organ, the longer and more effectively it will function, said Sengupta.

While aging is a fact of life and all of our body's capabilities diminish over time, "we have an ability to at least reduce the wear and tear that is happening because of stress," he told Live Science.

For example, is restful sleep a priority? How about a healthy diet and regular exercise? "These are questions we need to ask, about how we are responding to our body's needs and are we taking care of ourselves," Sengupta said.

Contrary to popular belief, placing defibrillator pads on the front and back of the body rather than on the front and side may boost the chances of restoring a person's heartbeat, a new study hints.

The research looked at cases in which defibrillator pads were used following an out-of-hospital cardiac arrest. It suggests that back-and-front placement more than doubles the chance of success, compared to front-only placement.

The new study assessed the influence of pad placement on the survival outcomes of more than 250 patients with cardiac arrest. Cardiac arrests occur when the heart suddenly stops beating because of an electrical malfunction. (That's opposed to a heart attack, or myocardial infarction, which is caused by impaired blood circulation to the heart.)

"The key is, you want energy that goes from one pad to the other through the heart," Dr. Mohamud Daya, study co-author and a professor of emergency medicine at the Oregon Health and Science University, said in a statement. While the research provides early hints that pad placement makes a difference, it has limitations and thus bears confirmation in more extensive studies.

Related: Heart attacks fell dramatically during the pandemic — and they're still dropping

Each year in the U.S., more than 350,000 people experience cardiac arrest outside of a hospital, and less than 10% of them survive.

Two of the most treatable causes of cardiac arrest are ventricular fibrillation (an irregular heartbeat) and pulseless ventricular tachycardia (when the heart beats too fast to adequately pump blood around the body). In these cases, defibrillation, which delivers an electrical current to the heart via two pads that are placed on the body, can restore a normal heartbeat and increase survival rates — if it's performed quickly enough.

Defibrillator pads are usually placed on the chest — one on the upper-right side below the collarbone and the other on the left side underneath the armpit. However, the pads can also "sandwich" the body, with one placed on the front of the body and one on the back. Until now, medical professionals have generally assumed that both pad placements are equally effective at treating cardiac arrests, the study authors noted.

However, in their new study, the researchers looked at 255 adults in Oregon who'd had an out-of-hospital cardiac arrest caused by either ventricular fibrillation or pulseless ventricular tachycardia. The 192 male and 63 female patients, who had an average age of 66, each received defibrillation from emergency medical services: 158 with front-and-back pad placement and 97 with front-and-side placement.

Overall, the researchers found that patients with front-and-back placement were 2.64 times more likely to experience return of spontaneous circulation (ROSC) — when the heart starts beating again — than those whose pads were placed only on their chest. They described their findings in a paper published Sept. 9 in the journal JAMA Network Open.

The findings hint that placing the pads at the front and back improves the flow of electrical current to the heart by coming at the organ from either side, the authors say.

However, the new study was fairly small in size and only observational, meaning the researchers looked retrospectively at events that already happened. They weren't testing each method side-by-side in a well-controlled study, so they cannot prove that pad placement itself actually influences defibrillation outcomes. It may be that other factors — such as a person's age or sex — made the difference. To rule these out, a gold-standard clinical trial is needed to test both pad placements.

The researchers also didn't find any statistically significant difference between the groups in terms of several other critical outcomes of a cardiac arrest — such as survival rate. The two groups' survival rates both before hospital admission and at point of discharge were very similar. It's unclear exactly why this would be the case, so that would need to be clarified before this study is used to change clinical practice.

Front-and-back positioning is also not always possible. For, instance if someone has overweight or is positioned in such a way that it is difficult to move them, it may not be feasible.

"It can be hard to roll people," Daya said. "Emergency medical responders can often do it, but the lay public may not be able to move a person."

This article is for informational purposes only and is not meant to offer medical advice.

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The COVID-19 pandemic heralded a 35% drop in hospital admissions for heart attacks in the U.S. — but even now, that rate is continuing to fall. Why?

New research suggests that, although people avoiding medical care during the pandemic contributed to the decline in the short term, better heart-attack prevention is the bigger reason for this downward trend.

A heart attack, or acute myocardial infarction (AMI), happens when there's a blockage of blood flow to the heart that causes some of the heart's muscle tissue to die. The symptoms — including chest pain, arm or shoulder pain, shortness of breath, tiredness and nausea — are fairly well known, and most people are aware that heart attacks need immediate medical care in a hospital setting.

However, the pandemic came with an unusual dip in AMI hospitalizations.

Related: Young women may be likelier to die after heart attacks than men

Since 2020, researchers have debated the reasons for this drop. For instance, did patients who were experiencing heart-attack symptoms avoid medical care? Or did patients who might have otherwise had a heart attack die of COVID-19 first?

To investigate these questions, researchers analyzed 7.5 years of Medicare claims data collected between January 2016 and June 2023. They looked at the rates of AMI-related emergency room visits and hospitalizations and the characteristics of the affected patients.

The study, published July 31 in the journal JAMA Cardiology, found that AMI visits and hospitalizations were lowest when the pandemic was at its peak, as measured by COVID-19 death rates. The same was true for other urgent or painful conditions, such as kidney stones. This suggests that people who normally might have sought care chose to stay home when COVID-19 infection risk was high.

The scientists tried correcting for factors such as excess COVID-19 deaths, meaning those over and above the number of deaths that would be expected under typical conditions. However, that adjustment didn't explain the drop in hospital visits, so the researchers concluded that care avoidance was the main cause of the pandemic-related reduction.

"Although there were more deaths overall during the pandemic, we have to appreciate that only some of those patients would have had an AMI over the same time period," said study first author Andrew Wilcock, an assistant professor at the University of Vermont Larner College of Medicine and a visiting fellow at Harvard Medical School.

The effects of excess deaths or changes in Medicare enrollment were "so slight on expected [AMI] rates that they could not explain the shortfalls we observed," Wilcock told Live Science in an email.

But even after pandemic-related restrictions were lifted, AMI visits and hospitalizations stayed lower than they had been before the pandemic. This reflects a broader and sustained decline in heart-attack rates. The researchers propose a combination of reasons for this trend, including that fewer people are smoking, people may be eating healthier, and there is better treatment for underlying conditions such as high cholesterol and high blood pressure.

"It's not just one thing, but a constellation of factors," Wilcock said. "Lifestyle changes and better drugs are compelling explanations for the downward trend in AMI hospitalizations."

There's still room for progress, though.

"We've made improvements, but we still have a lot to do in terms of smoking cessation, exercise, diet, blood pressure and cholesterol control, and so forth," said Dr. Robert Bonow, a professor of cardiology at Northwestern University who was not involved in the research. "Cardiovascular disease remains the leading cause of death worldwide. It would be nice to see it drop to number two."

The study authors noted that their research had some limitations. For instance, using Medicare claims meant that most of the data came from people with disabilities or chronic illnesses, or who were 65 or older. As a result, AMIs in younger people or those with different health care coverage weren't included in the numbers.

In addition, the authors noted that they lacked data on patients' longer-term outcomes. For example, they can't say whether the drop in AMI-related health care visits at the height of the pandemic led to higher rates of heart attack-related disabilities down the line.

"Although AMIs returned to their expected trends, overall hospitalization incidence hasn't returned to pre-pandemic levels," Wilcock said. "The new, post-pandemic normal in use of the hospital is something we would like to understand better."

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Blood clotting, also called coagulation, is a vital process the body uses after an injury to stop bleeding and help prevent infections. But sometimes, blood clots form inside an artery or vein, where they can cause damage or even lead to death.

So what causes blood clots? And what makes them more likely to form?

A blood clot can form when a blood vessel is injured. This kicks off a chain of events that causes a protein called thrombin to accumulate nearby. The thrombin then activates bits of cells called platelets in the blood, causing them to form a plug that covers the injury site.

These platelets also bind fibrinogen, another bloodborne protein. Thrombin converts this fibrinogen into a tough protein called fibrin, which forms a mesh that bridges the platelets to reinforce the plug. Once the wound has healed, these clots dissolve.

Related: What's the rarest blood type?

In some cases, though, blood clots can form when there isn't an acute injury. This happens when factors in the blood make it more likely to clot; blood vessel linings are damaged over time by disease; or blood flow is restricted, for example, by plaque buildup caused by coronary artery disease.

Medically known as a thrombus, a blood clot that forms in one of these ways may stay in the blood vessel without dissolving and block the passage of blood. This can cause tissue damage if the clot cuts off blood flow completely. If thrombi form in the heart, they can lead to heart attacks. If they form in the brain, they can cause stroke.

If some or all of the clot breaks loose from its original site, it is called an embolus. Broadly, emboli are masses that travel through the bloodstream and can get stuck if they reach a vessel that's too narrow.

Such roving clots are especially dangerous because they can travel to any part of the body. In a condition called deep vein thrombosis (DVT), a clot forms in a large vein, often in the legs, and can break off and travel to the lungs. That is then called a pulmonary embolism, which is a life-threatening medical emergency.

"I cannot stress how important it is to recognize the symptoms of a blood clot," Dr. Rachel Rosovsky, director of thrombosis research in the Division of Hematology at Massachusetts General Hospital, told Live Science. "If you have a DVT, it could be leg pain, redness or swelling. For a pulmonary embolism, it could be chest pain, pressure, shortness of breath or a fast heart rate."

It's important not to ignore these symptoms, especially if you are at risk of a blood clot, because a successful recovery often depends on quick treatment.

Some diseases make blood more likely to clot. There are genetic conditions that increase the levels of clotting proteins in the blood; reduce the levels of proteins that prevent or dissolve clots; or otherwise impair those proteins' functions.

Other conditions — including cancer, autoimmune diseases, high blood pressure and infections like COVID-19 — may also throw off the body's delicate balance of coagulation factors. In COVID-19, a combination of excessive inflammation and rogue antibodies are thought to increase the blood's propensity to clot.

Related: If blood is red, why do veins look bluish?

Both pregnancy and hormonal treatments, such as some forms of birth control and hormone replacement therapies, are tied to an increased risk of blood clots. Research suggests that anxiety and depression may boost the risk of DVT by increasing stress-related neural activity tied to clot formation.

Lifestyle factors also contribute to a person's risk of blood clots. Smoking raises the risk by increasing inflammation in the body and making platelets more reactive. Obesity is also tied to a higher risk of blood clots; this may be partly because signaling molecules made by fat cells can boost levels of clotting factors and make platelets stickier.

By limiting a person's mobility, long-haul travel, injuries such as bone fractures, and major surgeries can all temporarily increase the risk of dangerous clots. That's because less movement means less blood flow, more inflammation and more activation of clotting factors in response to that inflammation.

Some of these risk factors can be mitigated, though.

"If you sit at a desk all day, get up and walk around every hour," Rosovsky said, adding that seated travelers should wear compression stockings or take regular movement breaks during their journeys. She also recommended that, in general, people stay well hydrated, maintain a healthy weight, engage in physical activity and avoid smoking.

"Right now, someone dies of a blood clot every six minutes," Rosovsky said. As many as 100,000 die of blood clots each year in the U.S. Rosovsky stressed that it's important to know your risk factors and how to mitigate them, but also, to be aware of the signs and symptoms of blood clots and seek medical attention if you experience them.

This article is for informational purposes only and is not meant to offer medical advice.

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Having anxiety or depression may increase the risk of potentially life-threatening blood clots, known as deep vein thrombosis (DVT).

With DVT, a blood clot forms in a deep vein, usually in the legs. DVT can cause damage by limiting blood flow to the site of the clot and increasing pressure in veins. A larger danger arises if some or all of that clot breaks loose and then travels to the lungs, where it can block blood flow, causing shortness of breath, chest pain and even death.

Within the last decade, scientists have uncovered links between people's mental health and their risk of these blood clots. However, conflicting study results and complicating factors — such as some study subjects' medication use and histories of high blood pressure — have made it difficult to determine exactly how the two are connected. 

Now, a study published July 4 in the American Journal of Hematology has examined not only how much anxiety or depression can raise a person's risk of DVT but also why.

Related: Rare clotting effect of early COVID shots finally explained

"My research comes from my patients," Dr. Rachel Rosovsky, lead study author and director of thrombosis research in the Division of Hematology at Massachusetts General Hospital, told Live Science. "When I realized the association between long-term anxiety and depression and blood clots, I started to think about whether those conditions could affect a patient's risk of developing a clot."

To investigate the link, the researchers looked retrospectively at data from almost 119,000 people. The data included measurements of stress-related brain activity obtained using positron emission tomography (PET). PET scans reveal the activity levels and energy use of different parts of the brain. 

The researchers compared the activity of the amygdala — a brain region that processes and responds to potential threats — to that of the ventromedial prefrontal cortex, which helps regulate the amygdala and thus control emotional responses. In that way, the researchers got a snapshot of stress-related neural activity, or SNA. 

The data also included measures of high-sensitivity C-reactive protein, a marker of inflammation, and heart rate variability, a measure of adaptability. The higher your heart rate variability, the better your body can cope with stressful situations.

Of the overall group, about 106,450 had a diagnosis of anxiety, while 108,790 had depression; there's overlap in these groups as many participants had both conditions. 

Over an average follow-up time of 3.6 years, about 1,780 study participants experienced DVT. Those with a history of anxiety or depression were 53% and 48% more likely to experience DVT, respectively, compared with those with no history of either condition. Similar trends were seen among people with both conditions.

Related: 6 distinct forms of depression identified by AI in brain study

Furthermore, of 1,520 people who got PET scans, those with anxiety or depression showed higher SNA than those without either condition. People with higher-than-normal levels of this activity were 30% more likely to experience DVT than those with normal levels.

"We first showed that anxiety and depression were significantly associated with increased SNA," Rosovsky said. Then, the team found that SNA was associated with increased leukopoietic activity, meaning the creation of white blood cells — a driver of inflammation. 

This had previously been shown to "promote clotting through many different mechanisms," she said. And now, the team has connected the dots from anxiety and depression to SNA and on to DVT risk. 

Three potential mechanisms connect anxiety and depression to DVT: higher SNA, higher inflammation and reduced heart rate variability. It appears that the more stress a person experiences, the higher their risk of DVT, the researchers concluded.

This "intriguing study" sheds light on how SNA influences the production of blood in the body, said Kamran Mirza, a professor of hematopathology at the University of Michigan who was not involved in the study. It reveals a "potential connection between mental health and increased clotting risk that warrants further investigation," Mirza told Live Science.

Notably, the researchers were limited to data that had already been collected. Prospective studies that follow people over time would enable scientists to track changes in stress and inflammation and see how they relate to DVT. The team plans to examine how treating anxiety or depression might affect DVT rates, and they also want to see if somehow reducing SNA could reduce risk.

"If you have depression or anxiety, be aware that those are potential risk factors for blood clots," Rosovsky said. "But also think about whether you have other risk factors and what you can do about those to reduce your risk."

This article is for informational purposes only and is not meant to offer medical advice.

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Bacteria present in some people's guts may help break down cholesterol, making them less susceptible to heart disease, a new study suggests.

The link between a high diversity of gut microbes and a lower chance of cardiovascular disease is well established. Previous research has shown that people with heart-related diseases, such as atherosclerosis, carry different kinds of microbes in their guts than people without the conditions. Researchers thought this may be related to a microbe-made enzyme called IsmA that breaks down cholesterol.

People whose gut bacteria made IsmA had less cholesterol in their blood than those whose gut bacteria didn't make this enzyme. However, the specific species of bacteria that make cholesterol-gobbling enzymes were not known.

Now, a study published April 2 in the journal Cell has shown that bacteria in the genus Oscillibacter break down cholesterol and that people who carry more of those bacteria have lower cholesterol levels than people with fewer of those microbes.

Related: 9 heart disease risk factors, according to experts

Uncovering the bacteria that metabolize cholesterol is "very interesting and exciting," Daoming Wang, a researcher at the University of Groningen in the Netherlands, told Live Science in an email. Wang, a bioinformatician who studies the human gut microbiome, wasn't involved in the new study.

To understand how gut bacteria influence heart health, the researchers examined stool and blood samples collected from more than 1,400 people in the Framingham Heart Study, a decades-long study of heart disease risk factors.

The team used different techniques to profile the microbial DNA in the stool samples. They also analyzed metabolites — the byproducts left over when chemicals like cholesterol break down. For each participant, the team then correlated these findings with known markers of heart health, like blood-borne cholesterol and triglyceride levels.

People with lower triglyceride and cholesterol levels had an abundance of Oscillibacter bacteria in their poop, the team found. They checked whether this correlation showed up in another, independent set of people and found that it did.

To confirm that Oscillibacter indeed metabolized cholesterol, the researchers grew the bacteria in the lab and exposed them to cholesterol marked with fluorescent tags. Using microscopy, the team looked for fluorescence within the bacterial cells, to see if the microbes sucked up the cholesterol — and they did.

The researchers then tracked the fate of the gobbled cholesterol and found that different bacterial species broke it down into various steroids. These steroids could be absorbed by other gut bacteria, resulting in decreased cholesterol levels overall.

To figure out which genes and proteins might help Oscillibacter break down cholesterol, the team used a machine-learning algorithm. The algorithm analyzes features of genes to predict how proteins encoded by these genes will look. This analysis revealed that genes that encoded proteins similar to IsmA were likely responsible for metabolizing cholesterol.

These results take us closer to understanding the "dark matter" of the microbiome, meaning the large number of gut microbial genes whose functions aren't yet known, Wang said. "This dark matter hinders us from seeing the whole picture of gut bacterial functionality."

In theory, tweaking the gut microbiome to boost cholesterol breakdown could be a strategy to reduce people's cholesterol levels, the study authors proposed. But before that can be done, we need follow-up investigations to better understand exactly how these bacteria break down cholesterol and how this can be used as a therapy, Wang said. We need detailed studies in lab animals, followed by clinical trials in humans, he said.

Nonetheless, Wang added, "it's very exciting to further explore the potential of manipulating Oscillibacter species as therapeutic interventions for managing cholesterol levels."

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Scientists just published the most detailed map of the developing human heart to date.

The atlas includes 75 types of heart cells, including cell types in the heart's valves and the muscles that fuel its beats that have never been seen before. It shows how these and other cells organize to form the different internal structures of the heart in the womb. The research, which was released Wednesday (March 13) in the journal Nature, also reveals how the different cells interact during heart development.

"For the first time, we can view how the cardiac cells organize to form the different structures of the heart at high resolution, akin to zooming in on individual houses in Google Maps," Elie Farah, the study's first author and a postdoctoral scholar in the Neil Chi Research Laboratory at the University of California, San Diego (UCSD), told Live Science in an email.

To chart their map, Farah and his colleagues studied whole human hearts that had been donated to the UCSD Perinatal Biorepository, a bank of tissues used to study human pregnancy. The hearts in the study were donated between weeks 9 and 16 of fetal development. At this stage, the heart has already progressed from being a simple tube to developing four distinct chambers, but it is still much smaller than an adult heart. 

Related: Scientists unveil new 'heart-on-a-chip'  

One technique the researchers used was single-cell RNA sequencing, which enabled them to look at a type of genetic material called RNA inside each heart cell. RNA carries blueprints stored in genes over to a cell's protein-construction factories, so analyzing RNA can help scientists identify different types of cells.

The other technique used in this study is called "multiplexed error-robust fluorescence in situ hybridization," or MERFISH for short. It was introduced in 2019 by Quan Zhu, associate director of UCSD's Center for Epigenomics and a co-senior author of the new paper. This method allows researchers to detect and quantify RNA transcripts — the copied blueprints — of hundreds of genes in each cell while recording the anatomical location of the cell in an organ.

Zhu teamed up with Chi's laboratory to use this cutting-edge technology to study how human hearts develop, becoming "the first research team to apply MERFISH technology to study the human developing heart with spatially resolved single cell resolution," Zhu told Live Science in an email. In other words, MERFISH enabled the team's map to capture the characteristics and coordinates of individual cells within the fetal heart.

"We not only are able to identify unexpected cell types special to the developing heart that are not in the adult heart, but also understand deeper why the left of our hearts are different from the right at a very early stage," Zhu added. For example, more layers of heart muscle cells were observed in the lower-left chamber, or left ventricle, than the right ventricle, indicating that the left ventricle develops earlier than the right.

In addition to analyzing whole hearts, the team conducted genetic mouse studies and laboratory tests with human stem cells. These demonstrated how different types of cells communicate with each other to drive the development of the heart's internal structures.

For example, they observed interactions between muscle cells in the heart's ventricles; fibroblasts, or cells that contribute to the formation of connective tissue; and endothelial cells, which line blood vessels. These interactions may play a role in the formation of the heart's ventricular walls.

"This is a landmark paper," Norbert Hübner, professor and group leader at Max Delbrück Center in Germany who was not involved in the study, told Live Science in an email. The way the researchers analyzed RNA "serves as a model for understanding organ function at the single-cell level and identifying clinically relevant cell states and niches in the developing heart," he said.

The comprehensive atlas of the developing heart has some very important applications.

"The data are crucial for future studies of congenital heart disease [heart defects people are born with] and to inform regenerative medicine approaches aiming to replace lost or dysfunctional myocardium [heart muscle]," Dr. Michela Noseda, a senior lecturer and group leader at Imperial College London who was not involved in the study, told Live Science in an email.

Although this atlas is unprecedented in its detail, even better versions are in the pipeline.

The next step is to create a full 3D model of the developing human heart, Farah said. Then, the researchers want to track the heart's development over time to create "a 4D atlas of the developing human heart" — basically a kind of "movie" of heart development that would give scientists a better understanding of this critical process.

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Exercise has long been recognized by clinicians, scientists and public health officials as an important way to maintain health throughout a person's lifespan. It improves overall fitness, helps build strong muscles and bones, reduces the risk of chronic disease, improves mood and slows physical decline.

Exercise can also significantly reduce the risk of developing conditions that negatively affect heart heath, such as high blood pressure, high cholesterol and obesity. But large amounts of exercise throughout life may also harm the heart, leading to the development of a condition called athletic heart.

As the sports cardiology director at the University of Colorado Anschutz Medical Campus, I'm often asked how much and what kind of exercise is necessary to get the benefits of exercise. Many people also wonder about the risks of exercise, and what happens if you exercise too much.

The American Heart Association generally recommends 150 minutes of moderate-intensity exercise, such as brisk walking, or 75 minutes of vigorous-intensity exercise, such as running, each week. It also recommends muscle strengthening exercises at least twice per week.

When people exceed these guidelines, the heart may remodel itself in response — that is, it begins to change its size and shape. As a result, heart function may also change. These changes in heart structure and function among people who engage in high levels of exercise are referred to as the athletic heart, or athlete's heart. Athletic heart doesn't necessarily cause problems, but in some people it can increase the risk of certain heart issues.

What is athletic heart?

To understand how exercise affects the heart, it's important to consider what kind of exercise you're participating in.

Exercise is generally divided into two broad categories: dynamic and static.

Dynamic exercises, like running, cross-country skiing and soccer, require the heart to pump an increased amount of blood, compared to the amount delivered to the body at rest, in order to sustain the activity. For example, when running, the amount of blood the heart pumps to the body may increase by threefold to fivefold compared to at rest.

Static exercises, like weightlifting, gymnastics or rock climbing, require the body to use skeletal muscle in order to push or pull heavy amounts of weight. While the heart does pump more blood to skeletal muscles that are working during these activities, these kinds of exercises depend on a muscle's ability to move the weight. For example, in order to do curls with dumbbells, the biceps must be strong enough to lift the desired weight.

Some exercises, like rowing or cycling, are both highly dynamic and highly static because they require the heart to pump large amounts of blood while simultaneously requiring a large amount of muscle strength to sustain effort.

It is important to distinguish between dynamic and static exercise because the heart adapts differently according to the type of exercise you engage in over time. Dynamic exercise increases the volume of blood pumping through the heart and can cause the heart to become enlarged, or dilated, over time. Static exercise increases the amount of pressure on the heart and can also cause it to become enlarged over time but with thickened walls.

Who develops athletic heart?

Exercise that exceeds guidelines, such as exercising more than an hour most days of the week, may lead to development of athletic heart. Athletic heart commonly occurs among endurance athletes, who regularly compete in activities like marathons or other long-duration events. Many exercise several hours per day and more than 12 to 15 hours per week.

Among runners, for example, the heart remodels itself in response to having to pump a high volume of blood. As a result, the chambers of the heart enlarge to hold and pump more blood. Among weightlifters, the heart remodels itself by thickening in response to the increase in pressure applied on the heart.

Exercise is good for the body, and athletic heart results from a lifelong commitment to an activity that promotes good health. But there may be some issues that arise from an athletic heart.

First, athletes with markedly enlarged hearts may be at risk of developing atrial fibrillation, which is abnormal heart rhythms that typically occur among older adults or people with high blood pressure or heart failure. Abnormal heart rhythms are worrisome because they may lead to a stroke.

There are many potential reasons atrial fibrillation occurs in athletes. A dilated atrium — the top chamber in the heart — may become inflamed and develop scar tissue, increasing the risk of atrial fibrillation. Stress and environmental factors may also work together to increase the risk of arrhythmia.

Coronary artery calcification, or CAC, is another concern among elite athletes. Coronary artery calcification, which commonly occurs in older adults or those with risk factors for coronary artery disease, increases the risk of having a heart attack or stroke. In recent years, doctors have been using imaging tests to monitor calcium buildup in the arteries of their patients to try to determine their risk of heart attack or stroke over time.

It is not entirely clear why elite athletes develop coronary artery calcification. Fortunately, it does not appear that athletes have an increased risk of heart attack, even among those with very high levels of CAC. For example, a large study of almost 22,000 participants found that even athletes who engaged in high amounts of exercise and had elevated levels of CAC did not have an increased risk of death from cardiovascular disease over a decade of follow-up.

Some athletes are appropriately concerned about having calcium buildup in their heart arteries and may wonder whether or not they should be taking medications like aspirin or statins. But risks vary from person to person, so anyone concerned about CAC should talk to their doctor.

Putting exercise in its place

Though elite athletes may have an increased risk of developing athletic heart, exercise undoubtedly remains one of, if not the best, methods to maintain a healthy lifestyle.

For example, if someone does not exercise routinely, their heart will become stiff and not pump blood as well as it once did. Routine exercise — especially dynamic exercise like running — maintains a compliant heart and prevents stiffening. A compliant heart will expand a lot more as it fills with blood and, in turn, pump out more blood with each heartbeat. A stiff heart has difficulty filling up with blood and has difficulty pumping blood through the body.

Generally, routine exercise throughout adulthood encourages the heart to remain strong and flexible even in old age. Even if someone were only to begin regularly exercising in their 40s to 50s, it is possible to reverse some of the effects of sedentary aging.

For example, a 2018 study of 53 sedentary people mostly in their early 50s found that those who participated in a two-year exercise training program using a combination of running, cycling and elliptical exercise had hearts that became more compliant compared to the hearts of those who did not exercise.

It is never too late to start exercising. Routinely following exercise guidelines can help promote physical and mental health and help your heart stay young throughout your life.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

The heart is a near-universal symbol of love and one of the most vital organs in the body. Now, to better understand the inner workings of the heart, scientists are recreating the organ's biology in a device the size of a credit card. 

The new "heart-on-a-chip" device, currently being developed by a team from the National Institute of Standards and Technology (NIST), mimics the interactions of cells within a human heart. The researchers say the technology could be used to study heart disease, which is the leading cause of death in the U.S.

Traditional animal experiments — which typically use lab rats and monkeys, among other animals — don't perfectly capture how a disease will progress or a drug will behave in the human body. Because of this, researchers are working to develop more accurate ways of mimicking the complexity and intricacy of human organs in the lab. This accuracy is especially important for drug development, as 90% of candidate drugs currently fail clinical trials in people.

New, human-like models that are being developed include organoids, or miniature organs grown from stem cells, and organ-on-a-chip models, in which cells found in specific tissues are grown on a chip that mimics the physiological conditions of an organ in the body. Many organs have been modeled in such chips, including the lungs, kidneys and the vagina. 

Scientists have developed heart-on-a-chip models, in particular, to study how the heart heals after injury, and heart disease, as well as to aid drug discovery. Hearts-on-a-chip have even been sent to space to study the effect of microgravity on the heart. 

Related: Tiny 'hearts' self-assemble in lab dishes and even beat like the real thing

In a statement released on Feb. 6, the team at NIST said this kind of technology, which includes their new heart-on-a-chip model, could streamline drug development, making it faster, safer and more precise. Importantly, these models would not replace human clinical trials — they would hopefully reduce or replace the animal testing needed before human trials begin. 

"This system could be considered for biomanufacturing and regenerative medicine of the heart and other organs on chips," Darwin Reyes, a biomedical engineer at NIST who led the development of the new chip, told Live Science in an email. 

These chips typically have transparent or semi-transparent covers, and by peering inside, researchers can see fluids running through tiny channels that interconnect like streams of water. In the case of NIST's chip, these channels imitate the blood vessels in the heart. Scientists grow human heart cells inside these channels and can study how the cells react to the addition of different drugs into the system. 

Unlike existing heart-on-a-chip models, the cells in the new NIST model can be arranged on opposite sides of a porous membrane, meaning that they can communicate with each other via signaling molecules, Reyes said. The next step for the team is to assess how these heart cells behave under normal and stress-induced conditions, he said. 

Different organ chips can also be linked together  — for example, a liver chip can be linked to a heart chip, which could enable scientists to study how these two organs interact after exposure to a certain drug. 

In a recent review of these technologies, published Feb. 6 in the journal Lab on a Chip, Reyes and a colleague emphasized that "significant work" is needed before organ-on-a-chip models can be used in preclinical drug tests. For instance, the heart cells used in these devices are grown from stem cells and often don't fully mature. So instead of resembling adult cells, they resemble cells found in a developing fetus. 

Certain materials used in heart-on-a-chip models also need to be refined. Polydimethylsiloxane, for instance, is a polymer commonly used to make the chip, but it's "relatively expensive" and readily absorbs small molecules. That easy absorption can skew scientists' drug tests, making them think that a substance brings about a certain effect or lacks signs of toxicity, when that isn't the case, the authors wrote. 

Nevertheless, with further honing, organ-on-a-chip models may cause a "paradigm shift" in the way that new drugs are developed and tested, the team said. The potential of these devices was recognized by the Food and Drug Administration last year, when the agency ruled that they could stand in place of traditional animal testing, as long as the data they generate is robust enough.  

Editor's note: This article was updated on May 3, 2024 after NIST issued an amendment to their original statement, clarifying that the model is still under development. The story was first published on Feb. 14, 2024.

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Scientists are working to build blood vessels from human cells using tiny ice sculptures — these frigid 3D forms twist and branch like real arteries and can be used as temporary scaffolds that later get melted away, to be replaced by living cells.

The researchers demonstrated the first step of this blood-vessel-building process in a recent study by creating the scaffolds using a 3D "ice printing" technique. The scaffolds were then coated in a gel that was embedded with human cells, which the team grew for about two weeks.

The ice printing technique could one day be used to make realistic, lab-grown blood vessels from human cells that capture the "complex geometries" of real vascular networks in the body, study researcher Feimo Yang, a doctoral candidate in mechanical engineering at Carnegie Mellon University, told Live Science.

"Currently, this is more of a proof of concept," Yang said, but with development, this technique might be useful for fabricating blood vessels that could be transplanted into a person when they need an artery or vein repaired, replaced or bypassed.

Related: 3D-printed human brain tissue works like the real thing

Doctors currently harvest blood vessels for transplant from elsewhere in a patient's body or from a donor. For some procedures, clinicians may use artificial blood vessels made from synthetic polymers; natural materials, such as proteins; or a mix of the two. However, these artificial blood vessels don't perfectly replicate real ones and can fail, in part because they're non-living.

That's where ice printing could provide an advantage; it could help scientists create more realistic structures from real human cells.

Ice printing at tiny scales could also be helpful for crafting so-called organ-on-a-chip devices, Yang added. Such devices use fluids that flow through many tiny channels to sustain the growth of cells, and they act as miniature models of organs in the human body.

The team's new work — which Yang will present at the 68th Biophysical Society Annual Meeting being held from Feb. 10 to 14 in Philadelphia — was built on the back of a printing technique called 3D-ICE, first described in a 2022 paper in the journal Advanced Science.

The printer uses water as its "ink" and works by dripping drops of water onto a cold copper surface, which is kept at minus 31 degrees Fahrenheit (minus 35 degrees Celsius). When a water drop strikes the surface, it quickly freezes, and each successive drop adds to the growing ice sculpture.

The printer spits out about 200 drops of water per second, Yang said. This rate is slow enough to enable one water drop to start to freeze before the next one hits but fast enough that the drops still freeze together in a smooth structure, rather than creating defined layers. If the drops fell too fast, one liquid water drop would merge into the next and spread out before freezing, Yang explained.

The drops themselves are about 50 micrometers in diameter, so the resulting structures can be made with micron-level details. And the printing technique is fast. The sculptures the team made stood about 0.1 inch (3 millimeters) tall and 0.008 inch (0.2 mm) in diameter, and "it takes maybe 20 seconds" to print, Yang said.

Related: 'Organ-on-chip' shows how uterus coaxes embryo to implant in early pregnancy

There are other ice printing techniques that build small sculptures layer by layer or volume by volume, but these are not great at creating smooth surfaces. 3D-ICE, by contrast, can create smooth, free-flowing shapes closer to what one sees in the human circulatory system.

After creating a tiny sculpture with their ice printer, Yang and colleagues coated the structure in a gelatin-based material. Because their printer specifically uses "heavy water" — in which the hydrogen atoms are replaced by deuterium — the ice stays frozen at above-freezing temperatures. That meant the researchers could work at temperatures where their gel stayed malleable while the ice remained frozen.

Using ultraviolet light, they melted the ice away and hardened the gel, leaving smooth channels that closely resemble blood vessels. The team then added cells that line blood vessels, called endothelial cells, to the gel and showed that they could grow the cells for two weeks. In the future, they'll experiment with growing the cells for longer.

While it will be some time before 3D-ICE could be used to craft blood vessels destined for a human patient's body, "hopefully, we'll be able to expand the use of this technology," Yang said.

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A baby became the world's first partial-heart transplant recipient in 2022, and now, more than a year later, the toddler's transplanted tissues still show "excellent" function and are growing along with his body, doctors report.

"This publication is proof that this technology works, this idea works, and can be used to help other children," Dr. Joseph Turek, who led the procedure as the chief of pediatric cardiac surgery at Duke Children's Hospital & Health Center in Durham, North Carolina, said in a statement.

Owen Monroe, the transplant recipient, underwent the groundbreaking procedure in Spring 2022, when he was 18 days old. Before birth, the baby was diagnosed with a heart malformation in which there's only one large blood vessel to carry blood out of the heart, rather than the two smaller ones typically found in human hearts.

Having only one outflow vessel increases the amount of blood dumped into the lungs, making it harder to breathe, and it also reduces the amount of blood that flows to the rest of the body. Owen's single outgoing blood vessel was also leaky, compounding the problem.

Related: 1st-of-its-kind heart transplant in infant could prevent organ rejection

Treating the malformation either required a full heart transplant — which might have required too much time to procure a donor organ — or the transplantation of heart valve implants that wouldn't grow with Owen's body. Such implants, typically taken from deceased organ donors, need to be replaced frequently, and each subsequent surgery puts the infant's life at risk.

Faced with these choices, Owen's doctors and parents opted for a third treatment option that had only ever been tried in pigs. So far, that decision has panned out very well, Turek and his colleagues reported Tuesday (Jan. 2) in JAMA.

The valves and arteries used in Owen's partial-heart transplant came from a 2-day-old baby girl who'd died soon after a complicated delivery and whose heart was donated immediately after death. The donor's heart muscles weren't healthy enough for a full transplant to be performed, but she had "structurally normal outflow valves with excellent function," the study authors noted.

These still-living heart tissues were transplanted into Owen in an eight-hour procedure. He was discharged from the hospital 30 days after the surgery. He needed a lower dose of immune-suppressing drugs than normally required for whole-heart transplants, his doctors noted. 

"Normal heart transplant patients go on two agents to manage their rejection issues," Turek told CNN. "And Owen is on one of those two agents, at basically half a dose." 

Since the procedure, Owen's transplanted valves have increased in size along with the rest of his heart, and their function has been excellent, his doctors reported in JAMA. The growing toddler has been hitting all his developmental milestones, such as crawling, standing, looking around for objects and starting to make sounds.

Since 2022, 13 additional partial-heart transplants like Owen's have been performed at four medical centers around the world, with the majority being done at Duke. Some of these have been "domino heart transplants," in which a patient with healthy valves but weak heart muscles receives a full heart transplant, and their healthy valves are then donated to another patient. 

"Of all the hearts that are donated, roughly half meet the criteria to go on to be used for full transplant, but we believe there's an equal number of hearts that could be used for valves," Turek said in the statement. "If you introduce the donated hearts that weren't being put to use into the supply chain and add the valves from domino heart transplants, that can create a substantial change."

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When a doctor listens to someone's heartbeat, they typically hear a characteristic sound: "lub-dub, lub-dub." In some people, though, this two-tone heartbeat is accompanied by whooshing or rasping noises, and these unusual sounds are called a heart murmur.

But what is a heart murmur, exactly, and what causes it?

A heart murmur indicates turbulent blood flow through the heart's valves, Dr. Kenneth Ellenbogen, a professor of cardiology and the director of clinical cardiac electrophysiology and pacing at the Virginia Commonwealth University School of Medicine, told Live Science by email.

"Murmurs may be benign and not indicate significant heart disease or may signify a valve problem requiring further evaluation and/or treatment," he said.

Related: What is a normal heart rate?

The typical "lub" and "dub" sounds of heartbeats are caused by different heart valves flapping shut as the heart muscle contracts.

Blood is pumped from the left and right atria, the chambers that receive blood from veins, to the left and right ventricles, which pump blood out to the body through arteries. Valves located between each atria-ventricle pair close to prevent the backflow of blood. This valve closure makes the "lub" sound.

After the blood leaves the ventricles, the valves that separate the heart from arteries close, generating the "dub" sound. When this blood flow is disrupted, the classic lub-dub can be accompanied by the whooshing, humming or rasping sounds that are characteristic of heart murmurs, and these noises can be detected when a doctor listens to the heart through a stethoscope.

Heart murmurs can be caused by an abnormal structure in the heart, such as a valve abnormality. For example, they may emerge when a valve doesn't close tightly enough, allowing blood to flow backward, or they might reflect a narrow or stiff valve.

Murmurs can also stem from a hole in the heart or a "cardiac shunt," meaning an irregular pattern of blood flow caused by a heart defect present at birth, Ellenbogen said. In addition, certain infectious diseases — such as bacterial endocarditis (an infection of the heart's lining) and rheumatic fever — can damage the heart and lead to heart murmurs, according to Yale Medicine.  

Heart murmurs that are not caused by structural abnormalities or diseases of the heart are referred to as "innocent" or "physiological." These result from a marked increase in blood flow through the ventricles, Ellenbogen said. 

Innocent heart murmurs are often diagnosed in babies and young people going through growth spurts, because to keep up with the body's rapid increase in weight and height, blood needs to flow more rapidly. Innocent heart murmurs are relatively common: about 10% of adults and 30% of children ages 3 to 7 experience them, according to Harvard Health.

Related: What's the rarest blood type? 

Such benign heart murmurs are also common in pregnancy. During gestation, pregnant people's blood volume increases in order to nourish the growing fetus. This can change the heart's sounds, particularly between weeks 12 to 20 of pregnancy, but these murmurs are typically harmless.

An overactive thyroid, untreated high blood pressure and heart-rate-raising exercise may also cause heart murmurs, according to the British Heart Foundation.

People with innocent heart murmurs don't tend to experience any symptoms. "Abnormal" heart murmurs — those tied to structural differences or heart disease — do not always cause symptoms but can be associated with trouble breathing, sweating, chest pain, weight gain, bulging neck veins and chronic cough. In babies and young children, symptoms of abnormal heart murmurs can also include feeding problems, poor growth and excessive fussiness, according to Yale Medicine.

Common risk factors for heart murmurs include intravenous drug use and family history of cardiac defects, according to Yale Medicine. Ellenbogen also noted that a person's existing heart murmur will become louder if they have a fever or anemia, meaning they have a deficiency in red blood cells or oxygen-carrying hemoglobin. That's because increased body temperature and low red blood cell count can affect the thickness of the blood, forcing the heart to pump blood faster, according to the medical resource StatPearls.

This article is for informational purposes only and is not meant to offer medical advice.

You stand up quickly from the couch, and for a few seconds, you struggle to see and maintain your balance as your surroundings suddenly plunge into darkness.

This common-yet-unnerving experience raises a question: Why do you sometimes get dizzy when you stand up, and why can your vision go dark?

It turns out that this reaction — known as postural or orthostatic hypotension — is caused by a rapid change in body positioning, and it's usually nothing to worry about. But if it happens frequently or lasts a long time when it occurs, that could be a sign of a chronic health condition, an expert told Live Science.

Visual changes, lightheadedness and dizziness that occur in the seconds after you stand up happen due to a sudden, temporary drop in blood pressure, Dr. Stephen Juraschek, an associate professor of medicine at Beth Israel Deaconess Medical Center of Harvard Medical School, told Live Science by email.

Related: What is normal blood pressure?

For a moment, the brain is not supplied with enough blood and oxygen, he said. And the oxygen supply for the light-sensing tissue of the retina also falls. Since the retina requires a lot of oxygen to function properly, even a small dip in its supply can lead to vision problems.

The process of maintaining stable blood pressure after standing up is controlled by the autonomic nervous system, a set of nerves that regulates involuntary bodily functions, such as heart rate, breathing and digestion, Juraschek said. "When people stand up, about 300-800cc [cubic centimeters] of blood gets pulled in the legs, leading to a temporary drop in blood pressure," he said; that's about 0.3 to 0.8 quarts of blood suddenly flowing into the legs.

This drop in blood pressure is detected by pressure-sensitive receptors in the arteries that supply blood to the brain and in the right atrium of the heart, which blood flows into after delivering oxygen to the body. These activated receptors then trigger a body-wide response that stabilizes the person's blood pressure — blood vessels constrict, the muscles of the legs and abdomen contract and heart rate increases, Juraschek said.

This does not usually cause noticeable effects. But in people who are dehydrated or experiencing an illness, like the flu, the drop in blood pressure may be more dramatic and might take longer to stabilize, Juraschek explained. People can also be prone to this dizziness if they take medications to reduce blood pressure, such as beta-blockers, he said.

Related: How much blood is in the human body?

And some people can be prone to the symptoms when getting out of bed in the morning, since their blood pressure is typically low at that time, and also when they're drinking alcohol or sweating a lot, according to Houston Methodist.

These short bouts of dizziness differ from chronic orthostatic hypotension, in which some individuals experience long-lasting or frequent loss of vision and balance after standing. This condition can interfere with their daily lives and cause falls, fainting and car accidents, and it's a risk factor for cardiovascular problems and kidney disease, Juraschek said.

"Postural hypotension may be particularly concerning if it persists beyond 3 minutes of standing," he noted.

Depending on what causes the condition, orthostatic hypotension can be either primary or secondary, according to the National Institute of Neurological Disorders and Stroke. Primary orthostatic hypotension is rare and caused by impairments to the autonomic nervous system, such as those caused by nerve damage.

Secondary postural hypotension, in which symptoms are caused by other medical conditions, is more common. This can be related to low heart rate (bradycardia), low blood sugar (hypoglycemia) and thyroid conditions, for instance, the Mayo Clinic states. Aging can also leave the pressure sensors in the neck and heart less reactive and the heart less able to quickly adjust its speed, leaving people ages 65 and older more prone to these dizzy spells.

This article is for informational purposes only and is not meant to offer medical advice.

Most people will take a blood test at some point in their life, and commonly, this requires blood to be drawn from the vein on the inside surface of the elbow. However, this simple procedure can sometimes become a bruise-inducing ordeal when health care providers struggle to locate patients' veins.

But why are some people's veins so "hard to find?"

There are several reasons why patients may have been told their veins are difficult to locate, including the depth and size of their veins, whether they were dehydrated and their stress levels, Dr. Mark Whiteley, a consultant venous surgeon and phlebologist at The Whiteley Clinic, a vein treatment center chain in England, told Live Science in an email.

However, people's veins can also be hard to find due to external factors, such as the technique used to draw blood or the temperature of the room, Whiteley said.

Related: If blood is red, why do veins look bluish?

"The standard technique for doing this [drawing blood] is to place a tourniquet on the upper arm around the biceps, with the aim to dilate the veins in the lower arm," he said. Once those veins are dilated, or widened, blood can be drawn using a "hypodermic" needle that's inserted beneath the skin, and a syringe. "However, if a tourniquet is placed too tight or too loose, veins may remain hidden," he said.

Arterial blood is pumped down the arms through the arteries at high pressure, while venous blood flows back out of the arms at a lower pressure. "If the tourniquet is too tight, no blood can get into the lower arm and so the veins do not fill," Whiteley said. "If the tourniquet is too loose, venous blood can leak out under the tourniquet … resulting in deflated veins."

Temperature is important because surface veins are part of the body's temperature control system. "When we are very hot, all of our veins dilate, helping us lose heat. When we are cold, our bodies secrete hormones to constrict the veins, reducing their diameter and making them virtually impossible to dilate," Whiteley said.

Setting these external factors aside, it is possible for a person's veins to be too small or too deep to be easily detected. "Patients who have veins that are deeper under the skin, particularly those with a high body mass, can make it very difficult for veins to be palpable through the skin," Whiteley said. In addition, some people have "rolling veins," meaning their veins move easily when touched and can change position during needle insertion, according to Cleveland Clinic.

People's stress and anxiety levels may make their veins difficult to spot because the blood vessels in the skin constrict as part of the "fight or flight" response, while the veins that supply muscles dilate. "Patients who are very nervous go pale, as all of the blood vessels in the skin constrict. As such, it is very difficult to dilate the veins to take blood," Whiteley said.

Veins may also be hard to find due to dehydration and other conditions that affect the volume of blood in the body, like surgical shock, he added. Past injuries can also make people's veins difficult to stick.

Related: Best water bottles 2023: 13 of the best reusable bottles to keep you hydrated

"Patients who have had a great many blood tests, or who have had drugs injected into veins, or who have had surgery affecting the veins in the arm can have scarred or even absent veins that are too damaged to take blood from," Whiteley said.

This article is for informational purposes only and is not meant to offer medical advice.

A trip to a local county fair ended with a young woman developing a stroke and being rushed to the hospital after going on a new ride. 

Halfway through the ride, which swings fairgoers rapidly in circles, the 37-year-old woman started to develop a headache and lost coordination of the muscles on the right side of her body. She also started to walk clumsily, due to the loss of muscle control. 

Her husband immediately rushed her to the emergency department, where she was diagnosed with vertigo — a condition in which problems with the inner ear or part of the brain cause dizziness — and sent home with a prescription for anti-nausea drugs. However, two days later her symptoms persisted and she was taken back to hospital. 

Doctors involved in the case, published Aug. 26 in the journal Cureus, found that her heart rate and breathing rate had soared, and her blood pressure, which was already historically high, was also extremely elevated. They took a computed tomography (CT) scan of her brain that revealed that she had an area of dead tissue near an artery that supplies the right side of the cerebellum, part of the brain that regulates muscle movements and controls balance. This suggested that she'd had a stroke. 

Related:Artificial sweetener may increase risk of heart attack and stroke, study finds

Strokes are the fifth leading cause of death in the U.S. and occur when blood flow to the brain is interrupted, depriving tissues of oxygen and causing them to die. Risk factors include having high blood pressure, obesity, smoking and having an inactive lifestyle. In this case, the woman had a 10-year history of smoking a pack of cigarettes a day, and she had untreated high blood pressure. 

Doctors couldn't find the exact source of the woman's stroke, although they suspected it was caused by an embolism, in which an artery is blocked by a blood clot that traveled from another part of the body. They prescribed her medications to control her post-stroke headaches and reduce her risk of developing heart disease, and her status was tracked through physical therapy follow-up appointments.

Over the next month, the woman didn't report any new symptoms of stroke and said she'd quit smoking. However, her coordination had worsened. A magnetic resonance imaging (MRI) scan of her brain showed no evidence of another stroke, but six months later, a scan of her head and neck revealed a bulge in the wall of an artery that supplies the right side of her cerebellum. The artery hadn't yet ruptured, but needed to be closely monitored, doctors concluded.

Based on previous cases of people having strokes on rollercoasters and other amusement park rides, the report authors suggest that hyperextension of the neck and tearing of blood vessels may lead to ride-induced strokes. Rides commonly display health warnings, for example, for people with high blood pressure, certain heart conditions and those who are pregnant. However, it is rare to see signs highlighting potential neurological risks, they wrote. 

"Healthcare providers need to be vigilant in identifying and managing these cases, and further research on specific risk factors in young individuals is crucial to improving prevention and safety measures in amusement park settings," they concluded.

In an extremely rare medical case, a scuba diver who descended deep into an underwater cave developed a deadly blood syndrome in which fluid leaked out of his blood vessels.  

The syndrome was a strange complication of decompression sickness, or "the bends," in which air bubbles form in the blood as people go from high pressure at depth to low pressure at the surface. The condition usually causes joint pain, dizziness and extreme fatigue. It can be fatal, but most people respond to treatment, which usually involves being placed in a hyperbaric chamber under high pressure and oxygen flow.

In the new case, described July 5 in the journal BMJ Case Reports, the diver developed systemic capillary leak syndrome (SCLS), but survived thanks to prompt treatment. 

The patient, a man in his 40s, presented at the emergency room with "worsening shortness of breath" following a deep cave dive to depths of "approximately [100-foot] 30 meter seawater" for "roughly 40 minutes" the day before, the report noted. 

Related: Free divers' heart rates can drop as low as 11 beats per minute

Dr. Ali Ataya, an associate professor of medicine at the University of Florida and an expert on capillary leak syndrome, helped treat the man and was able to recognize several symptoms of SCLS.

SCLS is a severe form of inflammation that causes all your blood vessels to leak a protein that normally keeps fluid inside. In response, fluid flows out of the cells, Ataya told Live Science. 

So what may have caused this rare complication?

"In the man's case, we think that the air bubbles that form from the ascent during decompression result in a pro-inflammatory cascade in the blood vessels which causes them to become more permeable, resulting in the leakage of protein and fluid that leads to SCLS," Ataya said.

SCLS is often deadly, but the fact that the team quickly diagnosed the problem, resuscitated the man and treated the inflammatory cascade may explain why the man recovered enough to leave the hospital in "just under a week," Ataya said.

Dr. Jeffrey Cooper, a professor in the department of emergency medicine at the University of Nebraska Medical Center told Live Science that the case may raise general awareness of the potential complications associated with deep diving. 

"If someone came into the emergency department like this man did, I might have considered decompression sickness but as the presentation was so unusual, I may have been misled and thought something else was going on, like sepsis or an allergy," he told Live Science.

Ataya emphasized the need for physicians to be aware of this potential complication.

"What we've learned from this case is that when someone presents in shock with an unclear cause that we should always consider SCLS as part of the diagnosis," he said. 

But divers shouldn't panic. Millions of people dive safely every year without getting this syndrome, he added.

People with heart disease often develop dreadful sleep problems, and now, scientists have identified a direct link between these conditions for the first time in a new study in mice and human tissues. 

Published Thursday (July 20) in the journal Science, the research shows that heart disease may derail the production of the sleep hormone melatonin in the brain due to damage to a group of nerves that innervate, or plug into, both organs — the superior cervical ganglion (SCG).

Found in the neck, these nerves are part of the autonomic nervous system, which regulates involuntary processes in the body, such as breathing and heart rate. Because nerves originating from the SCG connect to both the heart and the pineal gland — the tiny brain structure responsible for melatonin production — issues with the heart could explain why the body's melatonin-maker falls off track. 

"Imagine the ganglion as an electrical switchbox," senior author Stefan Engelhardt, a professor of pharmacology and toxicology at the Technical University of Munich, said in a statement. "In a patient suffering from sleep disturbances following a heart disease, you can think of a problem with one wire causing a fire to break out in the switchbox and then spreading to another wire."

Related: Irregular sleep may increase your risk of dying from cancer and heart disease 

The research is "important and timely," Brooke Aggarwal, an assistant professor of medical sciences at Columbia University who was not involved in the study, told Live Science in an email, noting that it "suggests a novel mechanism that may help to explain why those with heart disease are more prone to sleep disturbances." 

She went on to caution, though, that "future prospective studies need to be conducted, as well as clinical trials of any potential treatments stemming from this mechanism."

Struggling to sleep is a common side effect of heart disease — for example, up to 73% of people with heart failure experience symptoms of insomnia. Past studies have shown that melatonin levels are reduced in people with heart disease, but scientists didn't know why. 

In the new study, researchers analyzed human brain tissue samples from deceased heart disease patients and from people without heart disease. This postmortem analysis revealed a reduced number of nerve fiber, or axons in the SCG of people who had heart disease compared with the "heart-healthy" control group. The SCG of the individuals with heart disease were also markedly scarred and enlarged.

In supporting mouse experiments, the team found that immune cells called macrophages, which gobble up diseased and damaged cells, were present in the cervical ganglia of mice with heart disease, and the rodents' nerves showed signs of inflammation and scarring. The mice also had fewer axons in their pineal glands and less melatonin in their blood than healthy mice did. The rodents' circadian rhythms — the internal processes that regulate how the body responds to day and night — were also disrupted, as evidenced by changes in their metabolic rates and activity levels, for example.

Giving mice melatonin completely reversed this disruption, the team found. Additionally, when drugs were used to destroy the macrophages in the rodent's SCGs, their melatonin levels were restored.

Because these analyses were conducted in mice and only 16 humans, the findings "call for further studies" to reveal the mechanisms that drive immune cells to the SCG, the researchers noted in the paper. This may involve studying the nerve cells that link the heart and spinal cord, as well as messenger proteins called cytokines that summon macrophages.

In time, the team believes the study may pave the way for the development of new drugs to treat sleep disturbances caused by heart disease. 

"It will be now pivotal to obtain evidence in a randomized clinical trial to determine whether therapeutic melatonin is indeed effective in treating sleep disorders in patients with chronic heart disease," Engelhardt told Live Science in an email. If it proves effective, "then this could spare many patients the unnecessary side effects that come with standard sleeping pills."

A method for "reanimating" organ donors' hearts works just as well as the standard approach to collecting hearts for transplantation, new trial data shows. If widely applied, the method could increase the heart donor pool by an estimated 30%. 

"Honestly if we could snap our fingers and just get people to use this, I think it probably would go up even more than that," Dr. Jacob Schroder, a transplant surgeon at the Duke University School of Medicine who led the trial, told The Associated Press. "This really should be standard of care."

Most transplanted hearts come from brain-dead donors, who've died due to a complete loss of brain activity, rather than circulatory death, in which the heart stops. A brain-dead patient can be declared dead before their heart stops beating, and this allows doctors to remove the heart while it's still perfused with oxygen-rich blood and therefore not yet damaged by a lack of oxygen. The heart is then flushed with a preservation solution, placed in an ice-filled cooler and rushed to its recipient.

In the recent trial results, published Thursday (June 8) in The New England Journal of Medicine, doctors compared the survival rates of transplant recipients who got hearts from brain-dead donors with the survival rates of those who got hearts from donors who'd died of circulatory death. A total of 166 U.S.-based heart transplant patients were included in the primary analysis — 86 in the brain-death group and 80 in the circulatory-death group.   

Related: The 9 most interesting transplants 

Six months post-surgery, the brain-death group had a 90% survival rate and the circulatory-death group had a 94% survival rate, suggesting that donation after circulatory death, or DCD, is an equally viable approach to heart transplants.

DCD is made possible by "extracorporeal machine perfusion," which involves hooking up the donor organ to a machine that pumps blood and nutrients through its tissues. The new trial tested a perfusion system called Organ Care System Heart, made by TransMedics, the trial's funder. The system warms the blood that it pumps through the donor hearts, as compared with other perfusion systems, which still require the organ be cooled as part of the preservation process.

Although the two groups had similar survival rates at six months, compared with the traditional heart transplant group, the DCD group had slightly higher rates of moderate to severe primary graft dysfunction, in which one or both of the heart's ventricles show dangerous dysfunction within 24 hours of the transplantation surgery. However, none of the DCD patients had primary graft failure that resulted in retransplantation, while two people in the traditional transplant group did.

Overall, the rate of serious adverse events was very low and similar in both groups, as assessed out to 30 days post-surgery.  

The new trial involved multiple medical centers and builds upon previous evidence in favor of DCD, which mostly drew from isolated cases and small trials performed at single centers in Australia and the United Kingdom, the trial authors wrote.

Historically, though, one big hurdle to using perfusion systems on hearts and other donated organs is cost. Back in 2019, Dr. Brian Lima, director of cardiac transplantation at the Sandra Atlas Bass Heart Hospital in Manhasset, New York, told Live Science that few studies had compared perfusion with standard cold storage, so no "earth-shattering data" existed that could convince hospitals to make the expensive switch nationwide. 

However, at that time, doctors at Duke University Medical Center had just performed the nation's first adult heart transplant with a "reanimated" organ. Following that landmark procedure, Lima suggested that perfusion could soon become the standard of care. 

In the first known case of its kind, a man in Michigan developed recurrent deep vein thrombosis (DVT) in both legs after reportedly being bitten by a brown recluse spider.

Previously, "no case of deep vein thrombosis has been reported following a brown recluse spider bite," according to a new report of the unusual case, published in April in the journal Clinical Case Reports.

Brown recluse spiders (Loxosceles reclusa) aren't typically found in Michigan. However, rare, isolated populations have sometimes been identified in the state, and some studies suggest that the arachnids might spread northward from their native range as the planet warms. 

The six-eyed, solid-brown spiders are considered native to Kansas, Oklahoma, Texas, Louisiana, Arkansas, Missouri, Mississippi and Alabama, as well as parts of Georgia, Tennessee, Kentucky, Ohio, Indiana, Illinois, Iowa and Nebraska. 

Related: What is the deadliest spider in the world? 

The 45-year-old man in the new case report went to an emergency department in Michigan following the brown recluse bite. (The case report does not note how the spider's identity was verified, but in any case, there are no medical tests available to definitively identify a brown recluse bite.) 

The man was experiencing left calf pain, as well as swelling and ulcers around the bite site. Upon examining the patient, doctors also noted swelling, tenderness and fluid buildup (known as edema) in his right calf. Based on the results of various tests, the doctors made a provisional diagnosis of DVT, and treated the man with saline, morphine and a medicine to counter blood clotting. 

When the man's pain and swelling persisted, he underwent a balloon thrombectomy, a surgery to physically remove the blood clots, and had stents placed in several affected veins. He was then discharged with prescriptions for various medications to decrease the chance of further blood clotting.

However, the man was "noncompliant with medication" and returned to the emergency department four days later with discoloration, mild swelling and worsening leg pain, the case report authors wrote. He underwent another thrombectomy and was advised to continue his anti-blood-clotting medications.

At a follow-up visit the next month, "he complained of persistent leg pain and leg swelling despite medication compliance" and was treated with a venoplasty, a procedure that helps open a narrowed vein using a small balloon. But again, another month later, the man's symptoms persisted, and shortly after, he went to the emergency room for an acute episode of leg swelling and pain, the authors wrote. 

He was then sent to a venous thromboembolism clinic, where doctors discovered scar tissue in the patient's veins that likely contributed to his persistent symptoms. After that visit, the patient was advised to take anticoagulants for life and to use compression stockings and a compression pump for symptom relief, the authors wrote. He was then lost to follow-up, so long-term data are not available.

How could a brown recluse spider bite trigger such persistent DVT? It's possible that a molecule called phospholipase D (PLD), found in the spider's venom, could have partially driven the condition's development, the study authors suggested. PLD has been linked to "massive inflammation" and the accumulation of platelets, cell fragments that stick together to form blood clots.

"In our patient, we did not find any other cause which might have contributed to DVT," the authors wrote. "Hence, PLD can be attributed to the development of deep venous thrombosis." 

Brown recluse bites can cause mild to severe symptoms, Live Science previously reported. Most bites cause inflammation but ultimately resolve on their own. However, in people who are sensitive to the spiders' venom, bites can cause skin cells to rapidly die, leading to the development of circular "necrotic lesions" that sometimes linger for months. 

In rare, particularly severe cases, brown recluse bites can cause systemic loxoscelism, a body-wide immune reaction that can lead to blood clotting and the destruction of red blood cells.

A heart attack, or myocardial infarction (MI), is when blood flow to part of the heart muscle (myocardium) is blocked and that part of the organ does not get enough blood. 

When their blood supply is reduced, muscle cells in the heart get damaged and die. The more time that passes without blood flow, the greater the damage to the heart muscle. MIs are most often caused by blockages in the arteries that supply blood to the heart muscle, according to the American Heart Association (AHA). The buildup of plaque in these arteries is known as coronary artery disease (CAD), the most common type of heart disease in the U.S.

Every year, about 805,000 people in the United States have a heart attack. One in 5 heart attacks are "silent," meaning they go unnoticed due to the lack of overt symptoms, such as chest pain or shortness of breath, according to the Centers for Disease Control and Prevention (CDC). Silent heart attacks tend to affect more men than women, according to Harvard Health.

Approximately 12% of American adults who have a heart attack die within a month of the event, according to a 2019 study published in the journal JAMA Network Open; this death rate is based on data gathered from Medicare beneficiaries in 2014. 

Related: Do other animals get heart attacks? 

Heart attack is not the same as cardiac arrest. The former is caused by impaired blood circulation, whereas cardiac arrest happens when the heart suddenly stops beating due to an electrical malfunction in the organ, the AHA said.

What happens during a heart attack? 

A heart attack is a medical emergency experienced over minutes or hours, but the groundwork for that event is set years or decades in advance.

The heart is a muscular organ. The average adult heart beats 100,000 times daily, pushing about 1.5 gallons of oxygenated and nutrient-rich blood through the body each minute. Blood first travels from the heart to the lungs where it is re-oxygenated before it returns to the heart to be pumped out to arteries to supply oxygen and nutrients to the brain, digestive tract and rest of the body's tissues.

Most often in the leadup to an MI, the two primary coronary arteries that supply oxygen and nutrients to the heart muscle narrow over years to decades, largely due to atherosclerosis, a buildup of fatty plaques in the arterial walls, according to the AHA. Atherosclerotic plaques are hard on the outside and soft on the inside and cause arteries to become rigid, according to the Cleveland Clinic.

Sometimes, the plaques' hard outer surface can crack and blood components called platelets will stick to the cracks, forming blood clots that further narrow the artery.  

If the arteries have already been narrowed due to years of atherosclerosis, the clot can completely block the blood supply downstream to the heart. Bits of the plaques can also break off and move through the artery, causing the blockage to rapidly worsen. Such blockages can lead to a heart attack, and within a few minutes, muscle cells in the heart undergo damage and begin to die. 

Less commonly, a sudden spasm or contraction of the walls of the coronary arteries can block blood flow to the myocardium and trigger a heart attack, according to Penn Medicine. These spasms occur most often in people who smoke and in people with high cholesterol or high blood pressure, and the spasms can sometimes be driven by alcohol withdrawal or stimulant use, among other triggers.  

What are the warning signs of a heart attack? 

According to the CDC, the warning signs of a heart attack include:

• Chest pain or discomfort. Most heart attacks involve a feeling of uncomfortable pressure, squeezing, fullness or pain in the center or left side of the chest. This discomfort typically lasts for more than a few minutes before subsiding, or sometimes, it emerges, goes away and then comes back.
• Pain or discomfort in other areas of the upper body, such as jaw, neck, back, arms or shoulders.
• Shortness of breath.
• Feeling weak, light-headed or faint.
• Unusual or unexplained tiredness.
• Nausea or vomiting.

Heart attack symptoms may vary between men and women, although chest pain or discomfort is the primary symptom for both sexes. However, women are more likely to experience other symptoms that are typically less associated with heart attack, such as unusual or unexplained tiredness and nausea or vomiting, according to the CDC.

MIs are more common in the winter months, compared with other times of the year, and they can be triggered by both physical and emotional stressors, such as vigorous exercise, intense fear or anger, according to a 2009 review published in the journal Cardiology in Review. 

Genetic factors, tobacco smoking and sedentary lifestyle can increase the risk of a heart attack, the AHA said. Long-term exposure to air pollution may also increase the risk of MI, according to a 2021 meta-analysis published in the journal Frontiers in Medicine.

What is the first treatment for a heart attack? 

The first treatment for a heart attack involves removing the blood clot or plaque that's blocking the artery to limit the damage to the heart muscle, according to the National Heart, Lung and Blood Institute (NHLBI). 

Time is a critical factor. If a patient gets to a hospital quickly, doctors can restore the heart's blood supply and prevent or limit the damage. 

Blood flow can be restored through angioplasty (a non-invasive nonsurgical procedure used to widen narrowed or obstructed arteries), stenting (inserting a small mesh tube that holds open weak or narrow arteries) or coronary artery bypass grafting (an open-heart surgery used to restore blood flow in severe heart attacks). Patients may also be given medications to prevent further blood clotting, such as aspirin, the NHLBI says.  

Additional treatments can include nitroglycerin, or nitrates, which improve blood flow in the coronary arteries and ease chest pain, as well as thrombolytic medicines, which help dissolve blood clots, according to NHLBI. 

This article is for informational purposes only and is not meant to offer medical advice.

Coronary artery disease (CAD) is the most common type of heart disease and occurs when plaque buildup narrows or blocks one or more of the arteries that supply blood to the heart. The term is often used interchangeably with coronary heart disease (CHD). 

Specifically, CAD is a problem of one or more arteries supplying the myocardium, the muscular layer of the heart. This is the thickest layer of tissue in the organ and consumes more oxygen than the rest of the heart, consequently requiring the most blood flow.

According to the Centers for Disease Control and Prevention (CDC), 382,820 people in the United States died from CAD in 2020, while 20.1 million adults ages 20 and older live with the condition.

What causes coronary artery disease?

CAD is caused by a process known as atherosclerosis, in which plaque builds up in the inner walls of arteries, causing them to narrow and become rigid. This blocks blood flow, and the blockage can rapidly worsen if a piece of plaque breaks off and causes a blood clot. 

One factor that increases the likelihood of atherosclerosis is the long-term presence of high concentrations of low-density lipoprotein (LDL) cholesterol in the blood. These high levels can result from a relative deficiency of LDL receptors, which are proteins on the membranes of various body cells, especially liver cells. LDL receptors capture LDL from the blood, causing its contents — cholesterol and fat molecules called triglycerides — to be taken inside the cell and out of the blood. Thus, a lack of these receptors causes LDL cholesterol levels to be higher in the blood. 

High levels of LDL cholesterol provoke and exacerbate what doctors call atherosclerotic cardiovascular disease, an umbrella term for atherosclerotic changes that can develop in blood vessels throughout the body; this includes CAD, which specifically affects the coronary arteries. 

Other factors that can provoke atherosclerosis include uncontrolled type 2 diabetes, hypertension (high blood pressure) and tobacco use.

What are the symptoms of coronary artery disease?

Symptoms of coronary artery disease generally don't appear until the narrowing and hardening of coronary arteries begins to obstruct the flow of blood to the myocardium (the muscular layer of the heart). 

When this obstruction does occur, it can produce angina — chest pain or chest heaviness that arises when the heart doesn't get enough oxygen — as well as pain in other places, such as the neck, shoulder or arm. Angina can be stable at first, meaning that it generally occurs only with exertion, related to physical activity or emotional stress and the strength of each heart contraction. However, this can progress to unstable angina, which is a type of acute coronary syndrome (ACS), a range of conditions associated with sudden, reduced blood flow to a part of the heart. 

Known colloquially as a "heart attack," ACS is a spectrum running from its least severe subtype, unstable angina; to an intermediate subtype, non-ST elevation myocardial infarction (NSTEMI); to its most severe subtype, ST elevation myocardial infarction (STEMI).

According to the Mayo Clinic, symptoms of ACS resulting from coronary artery disease may include:

• Dyspnea (difficulty breathing or shortness of breath)
• Chest pain or chest heaviness
• Pain in other places, such as the neck, shoulder or arm 
• Fatigue 
• Palpitations
• Dizziness or fainting
• Nausea
• Sudden sweating

How is coronary artery disease diagnosed?

To diagnose coronary artery disease, doctors will look at a patient's medical history and any symptoms that could indicate heart problems. They may also perform a physical examination.

Often, they will request an electrocardiography (ECG) test. ECG is a technique that detects changes in voltage over time across the heart, at different angles. When CAD causes enough blockage of blood flow to cause ischemia (insufficient blood supply) in particular parts of the heart, ECG can show abnormalities in the heart's activity.

Doctors also will request blood tests. Important blood values include the concentration of LDL cholesterol in a person's blood and the concentration of triglycerides (fat molecules). 

Patients may be referred to a cardiologist for further tests, such as additional ECG testing, ultrasound imaging of the heart (echocardiography), or evaluation with a wearable heart monitor, a version of ECG that you wear for a few days or weeks that transmits data to the cardiologist.

Complications of coronary artery disease

Coronary artery disease can lead to a condition called myocardial ischemia in which an artery cannot deliver adequate quantities of blood and oxygen to the myocardium. This can happen due to an artery gradually becoming blocked with plaque, resulting in the lumen of the artery (the hollow middle through which blood passes) narrowing and the wall of the artery hardening. 

In addition, an atherosclerotic artery that has not been blocked enough to cause ischemia can suddenly become blocked by a piece of plaque breaking off, getting stuck and growing larger by stimulating the clotting process. Generally, this would lead to ACS.

Even without a plaque rupture, however, the gradual increase in blockage driven by atherosclerosis disrupts a person's ability to perform physical activities, such as walking up stairs or around the block.

When doctors suspect that a patient's CAD may be causing life-threatening problems with the heart, such as ACS, myocarditis (inflammation of the heart's muscular tissue) or pericarditis (inflammation of the sac surrounding the heart), blood is tested to see if levels of certain enzymes are elevated, including a group of enzymes called troponins. Troponins are measured because they leak out of heart muscle tissue when it is damaged. 

In cases of ACS, doctors can use troponin measurements and ECG to distinguish between broad subtypes of ACS, which has important implications for treatment and further testing. In cases when either heart failure or myocarditis is suspected, they'll also check blood for levels of brain natriuretic peptide (BNP), a hormone that enters the blood when the heart is stressed.

Treatment for coronary artery disease

Treatment for CAD usually involves a combination of medication and lifestyle changes. 

Medications can include cholesterol-lowering drugs, aspirin (to make it harder for platelets to stick to one another and to walls of blood vessels to form clots), medications to slow the heart while increasing the power of each contraction, or medications to widen blood vessels and/or to decrease blood pressure.

Lifestyle changes can also help to reduce a patient's risk of CAD and related health problems. According to the Cleveland Clinic, these include stopping smoking, limiting alcohol use, maintaining a healthy weight, limiting foods high in saturated fat, sodium and sugar, and getting enough sleep.

This article is for informational purposes only and is not meant to offer medical advice.

SpaceX's Dragon cargo ship is scheduled to launch Tuesday (March 14) evening, carrying nearly 6,300 pounds (2,860 kilograms) of cargo to the International Space Station (ISS). But among the spacewalk equipment, vehicle hardware and fresh fruit for the crew, there will be several small devices that contain something a little more unusual: beating human heart tissue. 

The tissue will be used in two experiments — Cardinal Heart 2.0 and Engineered Heart Tissues-2 — which will test whether existing drugs can help prevent or reverse spaceflight's negative effects on the heart.

Research indicates that spaceflight can shrink the heart, because in microgravity, the heart muscles don't need to work as hard to pump blood through the upper parts of the body. In addition, the heart may change shape under the influence of microgravity, as blood shifts upward, out of the legs and abdomen and into the head and torso, causing the heart to swell, according to NASA. 

Studies suggest that the heart also undergoes cellular changes associated with aging during spaceflight. Therefore, this research is not only critical to future space exploration but could also lead to improved treatments for age-related heart dysfunction and disease on Earth, Devin Mair, a doctoral candidate at Johns Hopkins University who's involved in Engineered Heart Tissues-2, said during a NASA news conference Tuesday.  

Related: Tiny 'hearts' self-assemble in lab dishes and even beat like the real thing 

The experiments are part of the Tissue Chips in Space initiative, a joint project of the National Institutes of Health and the International Space Station National Laboratory aimed at understanding the effects of spaceflight and microgravity on the human body, according to NASA. 

The Engineered Heart Tissues-2 experiment involves two devices that carry cardiomyocytes — the heart muscle cells that contract — in small, fluid-filled chambers. The muscle cells were grown from stem cells and coaxed into 3D shapes in the lab. They were then strung between two posts within each chamber, similar to how tennis nets are suspended between a pair of posts. One post contains a magnet that moves each time the muscle cells contract. A sensor tracks the magnet's movement, allowing the researchers to monitor muscle contractions in real time. 

Mair and his colleagues previously sent heart tissue to space in March 2020, and in that experiment, they observed signs that cells' mitochondria were malfunctioning, he said at the NASA news conference. Mitochondria provide power to cells and thus fuel the pumping of the heart, and their dysfunction has been tied to a variety of heart problems, including irregular heartbeat and heart failure. In an experiment launched on this trip to the ISS, the team will continue to study mitochondrial dysfunction, as well as test several existing drugs to see if they prevent or reverse the problems, Mair said.  

"These drugs specifically target mitochondrial dysfunction and upstream mechanisms that lead to this dysfunction," Mair told Live Science in an email.

Similarly, the Cardinal Heart 2.0 experiment will use tiny, 3D clumps of heart tissue, known as heart organoids, to test whether already-approved drugs can protect heart cells from the stress of microgravity. The organoids will be treated prior to Dragon's launch, with the goal of preventing the negative effects of microgravity from setting in, Dilip Thomas, a postdoctoral researcher at the Stanford Cardiovascular Institute who's involved in Cardinal Heart 2.0, said at the news conference. These drugs include a statin and an anti-hypertensive drug used for heart failure, Thomas told Live Science in an email.

The organoids, grown from stem cells, are tiny models of full-size hearts that mimic key features of the organ's structure and function. They contain cardiomyocytes, as well as cells that provide physical scaffolding for heart muscles (cardiac fibroblasts), and ones that line blood vessels (endothelial cells). 

The Dragon spacecraft is set to launch at 8:30 p.m. EDT Tuesday (0030 GMT Wednesday) from NASA's Kennedy Space Center in Florida. Here's how to watch it live.

A popular zero-calorie sweetener is being linked to an increased risk of heart attack and stroke, a new study finds.

Known as erythritol, the sugar substitute occurs naturally at low levels in some plants, like grapes and mushrooms, but is also produced industrially and added to food at higher concentrations. In particular, it's often used to sweeten low-calorie, low-carb and "keto" products, which are typically high-fat and low-carb.

For the study, which was published Feb. 27 in Nature Medicine, researchers from the Cleveland Clinic in Ohio evaluated more than 4,000 Americans and Europeans who were undergoing cardiac evaluation and found that those with the highest blood concentration of the artificial sweetener were at an increased risk of experiencing a heart attack or stroke in the following three years, according to The New York Times. Notably, the majority of the participants already had some form of cardiovascular disease or exhibited risk factors for developing cardiac issues in the future, such as diabetes or high blood pressure.

"People are trying to do something healthy for themselves but inadvertently may be doing harm," study co-author Dr. Stanley Hazen, a cardiologist at the Cleveland Clinic, told The New York Times.

Related: 9 heart disease risk factors, according to experts

In laboratory experiments, erythritol boosted the activity of platelets, a type of blood cell that sticks together to form clots, causing clots to form at a faster rate. Similarly, in mice injected with erythritol, clots formed more quickly after injury than they did in mice injected with saline, the team reported. They also took blood samples from humans who'd had an erythritol-sweetened drink and found that their blood levels of the sweetener peaked within hours and remained high for two days — high enough that it could potentially affect their blood clotting, the authors wrote. 

Increased clotting has the potential to cause a heart attack or stroke because blood flow becomes constricted as clots form, according to the study. 

"Every way we looked at it, it kept showing the same signal," Hazen told The New York Times.

However, it's worth noting that there were some limitations to the study, particularly that many participants were more than 60 years old and already had heart disease, meaning they were already at some risk of heart attacks and stroke. While the study showed some connection between clot formation and erythritol, it did not show the compound actually caused strokes and heart attacks in humans.

"[This study is] extremely important, and it will likely trigger immediate changes in what we consume," Greg Neely, a professor of functional genomics at the University of Sydney who was not involved in the study, told The Washington Post. "We don't fully understand what the health consequences of industrialized food have been, and just because something is sold as 'natural' doesn't mean it is safe or good for us to consume at an industrial scale." 

The study authors concluded that "studies assessing the long-term safety of erythritol are warranted."

Heart disease is the leading cause of death in the United States, accounting for 1 in 5 deaths, according to the Centers for Disease Control and Prevention (CDC). It encompasses a range of conditions, including blood vessel diseases such as coronary artery disease, problems with heart rhythm, and congenital heart defects, according to the Mayo Clinic.  Many heart disease risk factors interact with one another: Stress, for example, increases blood pressure, but so do obesity and smoking, which all increase the strain on the heart. 

From high cholesterol to a sedentary lifestyle, here are nine things that increase the risk of heart disease.

1. Smoking

Smoking is a significant risk factor and causes 1 in 4 deaths from cardiovascular disease, according to the CDC. Even people who smoke less than five cigarettes a day may begin to show signs of heart disease, according to the CDC. Non-smokers can also be at risk if they are frequently around people who smoke, with more than 33,000 Americans dying each year from heart disease caused by exposure to secondhand smoke, the CDC said.

Smoking contributes to a condition called atherosclerosis, or the buildup of plaques, fat and other substances within the arterial walls, according to the Mayo Clinic. Chemicals in cigarettes can also contribute to arterial inflammation, which further restricts blood flow, according to the CDC.  

2. Overweight or obesity

Those who are overweight or obese are more likely to suffer from heart disease, even in the absence of other risk factors such as diabetes or hypertension. But a 2021 review in the journal Circulation found that obesity also increases the risk of developing type 2 diabetes and hypertension (high blood pressure), which are separate risk factors in their own right. It's not completely clear why having a high body mass index (BMI) may increase heart disease risk, but obesity can cause inflammation within the body, which is known to increase cardiovascular risk.

3. A sedentary lifestyle

A sedentary lifestyle (where a person spends too much time engaging in behaviors that expend little energy) can be a risk factor for the development of heart disease, according to the British Heart Foundation (BHF). Regular physical activity can reduce the risk of developing some heart and circulatory diseases by as much as 35%, according to the BHF, by helping to control blood pressure, exercising the heart and helping to manage blood glucose levels. 

4. Diabetes

Both type 1 and type 2 diabetes increase the risk of heart disease. Diabetes leads to high levels of glucose in the blood, and over long time periods, such high blood sugar can damage the nerves that control the heart, as well as blood vessels, according to the CDC. Diabetes also increases the risk of high cholesterol and blood pressure, both of which raise heart disease risk, according to the CDC. 

5. High cholesterol

"One of the most common types of heart disease is coronary artery disease," said Dr. Daniel Sado, a consultant cardiologist for London Bridge Hospital, part of HCA Healthcare UK, and lead for the cardiac magnetic resonance imaging (MRI) program at King's College Hospital in the U.K.

"It results in your coronary arteries, which supply the heart muscle with blood, [becoming blocked] with fatty deposits known as atheroma," Sado told Live Science in an email. "This can mean that your heart muscle gets less blood than it needs to function properly."

Formation of these atheromas is driven by so-called "bad" cholesterol, or low-density lipoproteins (LDL). LDL can build up in the arteries, putting more pressure on the heart by restricting blood flow, according to the CDC. 

"High cholesterol" is classified as total blood cholesterol equal to or greater than 200 milligrams per deciliter. However, this is the sum of HDL and LDL cholesterol — readings are also given separately. If a person’s cholesterol is high because of a high HDL number, their health may not necessarily be in danger, according to WebMD. High LDL, on the other hand, may be cause for concern. 

6. Genetics

A person’s genes can be a risk factor for cardiomyopathy, a general term for diseases that affect the heart muscle. "There are many different types of cardiomyopathy," Sado said. "Many are genetic in cause. Sometimes the heart muscle is too thick, sometimes it does not contract well or sometimes it becomes stiff and hence finds it difficult to relax when filled with blood." 

These diseases can present in many different ways, Sado said. 

While cardiomyopathy can’t be cured, there are treatments that can help manage symptoms and reduce the risk of heart failure. According to the BHF, these include reducing alcohol intake, swapping saturated fats for unsaturated fats, getting regular exercise and lowering stress.  

Sometimes, the first sign that someone has a genetic cardiomyopathy is sudden death. "This has been seen in high profile athletes and is why many elite sports organizations perform regular heart screens on their members," he said.

7. Sex

One of the most common types of heart disease is coronary artery disease, which causes the deaths of 1 in 8 men and 1 in 14 women in the U.S., Sado said.

According to John Hopkins Medicine, women and men share many heart disease risk factors, but some that relate specifically to women, or can affect women disproportionately, include high testosterone levels prior to menopause, increasing hypertension during menopause, and stress and depression.

Erectile dysfunction (ED) can be an early indicator of whether a man will develop cardiovascular disease, according to a 2013 article in the Arab Journal of Urology. Younger men with ED but no cardiac symptoms at a significantly increased risk, the review noted. 

Men also display signs of heart disease on average 10 years earlier than women, according to a 2010 review in the Netherlands Heart Journal.

8. Age

Another risk factor for heart disease that is out of a person's control is age.

"Men typically develop heart disease in their 50s and women in their 60s," said Dr. John Whyte, the chief medical officer at WebMD. 

According to the CDC, 2 in 10 people who die of coronary heart disease are less than 65 years old. 

9.Stress

Stress may predispose people to face heart problems at a younger age. This may be because stress can cause high blood pressure. In addition, a 2017 paper in The Lancet suggested that when people are stressed, their brain signals to the bone marrow to produce more white blood cells, which in turn leads to overall inflammation of the arteries, restricting blood flow. 

This article is for informational purposes only and is not meant to offer medical advice.  

Cold weather is a challenge in itself, with travel disruptions, snow and ice making even the simplest tasks take twice as long. But winter also poses a risk to physical health for those who are at a higher risk of heart attack, angina or high blood pressure, because of the ways the body responds to the cold. 

A 2021 study in the journal Medicine found that overall, U.S. cardiac arrests peak during December and January, although the exact statistics is difficult to determine. Live Science spoke to experts to find out why. 

How does cold weather affect the heart?

So how does cold weather, and the body’s response to it, affect the heart?

Dr. Oliver Guttmann, a consultant cardiologist at The Wellington Hospital, part of HCA Healthcare U.K., told Live Science that cold weather decreases body heat, meaning the heart needs to work harder to keep the body warm. This can increase the chance of a cardiac event in people already at a heightened risk, such as people who smoke and the elderly, he said.

Cold weather also causes blood vessels to narrow around extremities such as fingers and toes, a process known as vasoconstriction, Guttmann said. The result is that the body’s core remains warm and the organs continue working. “With less blood going to extremities like your fingers and toes, there is more pressure to pump blood around the rest of the body,” he said. “[However] this means that your heart has to work harder, increasing both heart rate and blood pressure.”  

The additional pressure put on the heart due to vasoconstriction can cause fatty plaques that have built up inside arteries to rupture, Guttman said, which can block the blood supply to the heart. 

In addition, colder weather changes the viscosity of blood, Guttman said. “When we are cold our blood thickens, which can also increase the chance of developing blood clots and consequently, having a heart attack,” he said.

Blood coagulability is also increased, said Dr. Deborah Lee, a medical writer for Dr Fox Online Pharmacy in the U.K. Blood coagulability is the speed at which blood forms a clot and later a scab to prevent blood loss. “Cold temperatures have been found to cause an increase in blood fibrinogen levels – this is the major protein involved in blood clot formation,” she told Live Science. Blood clots increase the risk of heart attack.

Another possible cause for the seasonal increase in heart attacks is vitamin D deficiency, which is more prevalent over the winter months due to a lack of sunlight. Vitamin D deficiency has been linked to several cardiovascular risk factors. However, more research is needed to understand the underlying mechanisms, according to a 2018 article in the journal Clinical Hypertension. 

A 2013 review in Current Treatments in Cardiovascular Medicine indicates that vitamin D may have a protective effect against cardiovascular disease, although the authors also said that more research is needed.

Risk factors

It’s difficult to quantify exactly how much the risk of cardiovascular disease increases in winter, according to a 2003 review in the journal BMC Cardiovascular Disorders, because cardiovascular and respiratory diseases are often related disorders, but either could be listed as a cause of death. Depending on what is listed, there can be a wide variation in statistics, from a 5% to 30% risk of death from cardiovascular disease across different studies carried out in different countries.

The wide range of increased risk in winter may also be because cold weather is experienced differently in different countries. For instance, the BMC Cardiovascular Disorders review found that winter mortality from cardiovascular disease is lower in Scandinavian countries compared with the U.K., which may be due to socioeconomic factors and healthcare systems. It could also be because Scandinavian countries are better set up to deal with cold weather.

A 2017 study in the journal BMJ Open looked at deaths and daily temperatures in Finland , and found that cardiac death increased by approximately 19% on "unusually cold days."

In the BMC Cardiovascular Disorders review, older patients admitted to hospital in November, December, January and February were 30% to 50% more likely to die from cardiovascular disease than those admitted in May. However, for the younger age group, there was no difference in death rates whichever month of the year they were admitted. Therefore, age may also be a risk factor.

Blood sugar, or glucose, is the main source of fuel for our bodies. It powers up our internal organs, muscles and nervous system. Keeping your blood sugar in check is essential to our physical health, wellbeing and energy levels. But what is considered a normal blood glucose level? And what happens when it rises above the normal threshold?  

Our blood sugar levels are directly related to the food we eat. We obtain glucose mostly from carbohydrate-rich foods like bread, pasta, potatoes or fruit, but many different food groups play a role in regulating glucose metabolism. How we absorb, use and store this important sugar is dependent on multiple complex processes that take place in our digestive systems. 

There is no single universal value that would describe a healthy blood sugar level. What constitutes normal blood glucose varies for an individual depending on a range of factors, including age, any underlying medical conditions, and the medications they take. It will also be heavily linked to when you consumed your last meal. Hence when we refer to 'normal blood sugar levels', we refer to a range of values that are considered healthy.

Here, we will discuss everything you need to know about a healthy blood sugar range.

Normal blood sugar before and after meals

Normal blood sugar levels vary from person to person. That's why when we talk about 'normal' blood glucose levels, we refer to a range of values that are considered healthy for most individuals. According to the World Health Organization (WHO), a normal range for fasting blood sugar (the amount of glucose in your blood at least eight hours after a meal) is between 70 and 100 milligrams per deciliter (mg/DL).

For most people, eating a meal or drinking a sugary drink will lead to a temporary increase in the blood glucose levels. As stated by the American Diabetes Association (ADA), the blood sugar two hours after eating should not exceed 140 milligrams per deciliter. However, people with certain metabolic conditions, such as prediabetes or diabetes, typically have lower blood sugar than those guidelines suggest. Researchers from the Journal of Diabetes Science and Technology continuously measured people's blood glucose and found that most individuals averaged around 82 mg/DL during the night and around 93 mg/DL during the day, and spiked to a maximum of 132 mg/DL an hour after a meal. 

Fluctuations in blood glucose levels, both before and after meals, are perfectly normal and reflect how your body absorbs, uses and stores this important sugar at a given point in time. When your food reaches your stomach, your digestive enzymes will break down complex carbohydrate molecules into smaller particles - sugars such as glucose. Glucose is then absorbed by the small intestine and eventually passed into the bloodstream, where it's distributed across the body. In order for the glucose to be shepherded into the cells and utilised, the pancreas needs to release the hormone insulin. 

Our bodies are designed to keep glucose levels constant in the blood. After all the energy needed is delivered to the body's cells, any leftover glucose needs to be stored away. It can't be stored in its original form, it needs to be transformed into a compound called glycogen. Glycogen then is built into the liver and the muscles as a backup source of energy if blood glucose levels fall below optimum levels.

When there isn't enough glucose stored to maintain normal blood-sugar levels, the body can also produce its own glucose from non-carbohydrate sources (such as amino acids and glycerol). This process is known as gluconeogenesis and occurs most often during intense exercise or starvation. It's also common when following low-carb diets, such as keto or Atkins. 

While it may seem complicated (and it is), there's a good reason for our bodies to keep up this never-ending dance with glucose: too much or too little glucose in the blood can lead to serious health problems. 

When there is too much glucose over an extended time (hyperglycemia), it can lead to severe nerve damage, impaired immunity, and heart and kidney disease. 

On the other hand, not enough glucose in the blood over several minutes to hours (hypoglycemia) can negatively affect the functioning of the nervous system. Common symptoms of hypoglycemia include fatigue, fainting, irritability and, in some cases, seizures, coma and death. 

• Related: How do we know when blood oxygen is too low?

Blood sugar targets in people with diabetes

In people with diabetes, blood sugar levels are too high, either because the individual isn't making any insulin (type 1 diabetes), or isn't able to make or use insulin efficiently (type 2 diabetes). As a result, glucose levels then remain elevated in the blood and fuel can't enter cells.

Blood sugar targets for diabetes patients are based on how long the person has had diabetes for, their age, and other underlying medical conditions and lifestyle factors. 

But generally, according to the ADA, for most non-pregnant adults with diabetes the fasting blood sugar target range should be in the range of between 80 and 130 mg/DL. Meanwhile, the ADA suggests the after-meal goal about two hours after eating for the same subset of patients should be less than 180 mg/DL. 

Overall, eating plenty of fruit and vegetables, maintaining a healthy weight, and getting regular physical activity alongside medication can all help stabilize and maintain normal blood sugar levels in people with type 2 diabetes.

For pregnant women who have pre-existing diabetes or develop diabetes during pregnancy, ADA guidelines are generally lower. Fasting glucose targets for this population should be less than 95 mg/DL, while they suggest that the after-meal goal about two hours after eating should be below 120 mg/DL.

• Related: Type 3 diabetes: Symptoms, causes and treatments
• Related: Vegan diet for diabetes: Tips, benefits and safety

What is a normal A1C?

A person's A1C is a measure of their average blood glucose levels over the previous 2 or 3 months, and it is measured through a blood test. A normal result for someone without diabetes or prediabetes would be below 5.7%; an A1C between 5.7% and 6.4% indicates prediabetes; and if your A1C is above 6.4% you would be diagnosed as having diabetes, according to the CDC.

Specifically, the A1C test is a measure of the percent of your red blood cells that have sugar-coated hemoglobin attached to them. The glucose that enters your bloodstream (from carbohydrates that you eat) gets stuck to hemoglobin molecules on red blood cells. And the more glucose in your bloodstream (higher blood sugar levels), the more of your blood's hemoglobin will be "sugar-coated," and the higher your A1C will be, according to the CDC. As such, for people with diabetes (type 1 or 2), the number can give you and your doctors a sense of how well your sugars are being controlled. 

The ADA recommends that most adults with diabetes should keep their A1C below 7% to reduce the risk of diabetes-related complications; the goal is the generally the same for many children with diabetes Targets for the elderly with diabetes are slightly less stringent — for the otherwise healthy with few coexisting chronic illnesses and intact cognitive function, the ADA recommends less than 7.5%, while those who don't meet these requirements have a more lenient goal of below 8.0% to 8.5%. 

According to the Mayo Clinic, higher A1C numbers are linked to a greater risk for diabetes complications, while lower A1Cs have been correlated with a reduced risk of these complications, such as heart disease, kidney disease and vision problems. 

This article is for informational purposes only, and is not meant to offer medical advice.  

This article was updated on Aug. 24, 2022 by Live Science Health Writer Anna Gora.

Additional resources

• Learn more about how high blood sugar levels put you on the road to developing diabetes and heart disease in this explainer by Harvard Health. 
• Read about the risk of high sugar levels and diabetes in pregnant women in this explainer by the Cleveland Clinic. 
• Discover the dangers of low blood sugar, with or without diabetes, in this explainer by the Mayo Clinic.

Bibliography

"The Big Picture: Checking Your Blood Sugar," American Diabetes Association. https://www.diabetes.org/healthy-living/medication-treatments/blood-glucose-testing-and-control/checking-your-blood-sugar

"Mean fasting blood glucose." World Health Organization. https://www.who.int/data/gho/indicator-metadata-registry/imr-details/2380 

"Continuous Glucose Profiles in Healthy Subjects under Everyday Life Conditions and after Different Meals" 2017, Journal of Diabetes Science and Technology https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769652/ 

"Management of Diabetes in Pregnancy: Standards of Medical Care in Diabetes—2021." ADA. https://diabetesjournals.org/care/article/44/Supplement_1/S200/30761/14-Management-of-Diabetes-in-Pregnancy-Standards  

"Diabetes tests." CDC. https://www.cdc.gov/diabetes/basics/getting-tested.html 

"Understanding A1C." ADA. https://www.diabetes.org/a1c

"Older Adults: Standards of Medical Care in Diabetes—2021." ADA. https://diabetesjournals.org/care/article/44/Supplement_1/S168/30583/12-Older-Adults-Standards-of-Medical-Care-in

"A1C test." Mayo Clinic. https://www.mayoclinic.org/tests-procedures/a1c-test/about/pac-20384643

Originally published on Live Science.

Can walking lower blood pressure? We’ve long known walking has many health and wellbeing benefits, including strengthening our bones and muscles and helping us to maintain a healthy weight and lose body fat. It turns out the walking perks don’t stop there. 

Regular physical activity is associated with lower blood pressure and therefore reduced cardiovascular risk. Walking to control your blood pressure, whether in the great outdoors or on one of the best walking treadmills, is easily accessible to most and is no different. 

Dr. Mahmoud Al Rifai, a member of the American College of Cardiology who has been involved in multiple studies of cardiovascular risk, tells us: “We frequently advise our patients to engage in moderate-to-vigorous physical activity, and that can include walking.” And it’s not hard to see why. 

According to the Centers for Disease Control and Prevention (CDC), hypertension (the more formal term for high or raised blood pressure) affects 47% of people in the US. Furthermore the CDC estimates that only one in four adults with hypertension have their condition under control. Clearly, finding a reliable and consistent way to keep your blood pressure within healthy limits is more important than ever.

Below, you’ll find everything you need to know about walking and its potential role in lowering blood pressure, including how it helps and exactly how much walking you need to do to see positive results. 

Can walking lower blood pressure?

Studies suggest that it can. One systematic review, published in the Database of Abstracts of Reviews of Effects, examined trials conducted on walking and its impact on hypertension. The authors concluded: “There was evidence for the beneficial effects of walking on lowering either systolic or diastolic blood pressure, or both.”

• Related: How do we know when blood oxygen is too low?

Another review, published in the journal of Preventive Medicine, found evidence to suggest that individuals who take up a programme of ‘regular brisk walking’ improve several known risk factors for cardiovascular disease – including high blood pressure.

The CDC defines systolic blood pressure, the upper number in a blood pressure measurement, as ‘the pressure in your arteries when your heart beats’. The lower number in a blood pressure measurement, the diastolic blood pressure, ‘measures the pressure in your arteries when your heart rests between beats’. 

A normal blood pressure level is less than 120/80 millimeters of mercury (mmHg).

How does walking help to lower blood pressure?

According to Dr. Al Rifai, walking decreases the ‘tone of the blood vessels’. He explains: “Blood vessels are surrounded by what's called smooth muscle cells. And these are muscle cells that can contract and relax. And what determines how contracted or relaxed they are, is the amount of sympathetic tone.”

If you increase the tone, you raise blood pressure. If you decrease it, you lower blood pressure. “Walking is thought to decrease the tone of blood vessels,” Dr Al Rifai adds.

How much walking do you need to do to lower blood pressure?

According to the Physical Activity Guidelines for Americans, adults should do 150 minutes of moderate-intensity or 75 minutes of vigorous cardiovascular exercise each week. This might seem like a high number but you can hit this target by exercising for 30 minutes, four-to-five days a week.

Weight lifting, swimming and running lower blood pressure, and walking can have the same effect. In a review of 73 trials published in the Cochrane Library researchers concluded: “Our findings suggest that moderate-intensity walking, three to five times per week, of 20 to 40 minutes duration, and 150 minutes per week for approximately three months could have an effect on lowering blood pressure.”

Another study published in Hypertension Research found good evidence that walking 10,000 steps a day lowered systolic blood pressure in middle-aged male subjects . If you’re looking for an easy way to make sure you’re getting your required steps in each day, check out our guide to the best fitness trackers. 

What else can you do to lower blood pressure?

Dr Al Rifai says that the first step to lowering blood pressure is through therapeutic lifestyle interventions. He says: “Being physically active is very important.You can do physical activities, like doing yard work or going up the stairs, and dedicated exercise like jogging, swimming, weightlifting.” Just make sure you have one of the best water bottles with you so that you can stay hydrated during your workout. 

Dr. Al Rifai tells us you can also reduce blood pressure by reducing salt intake. A study published in the journal of Electrolytes and Blood Pressure found: “A reduction in dietary salt from the current [global average] intake of 9-12 g/day to the recommended level of less than 5-6 g/day will have major beneficial effects on cardiovascular health.”

Finally, you can reduce blood pressure by losing weight. Dr Al Rifai says: “Weight loss in itself can lead to dramatic reduction in blood pressure.” There is evidence to prove it:  in one study published in Hypertension, researchers found that a 1kg loss of body weight was associated with an approximate 1-mm Hg drop in blood pressure. 

Additional reading

Physical Activity Guidelines for Americans

CDC Facts About Hypertension