Custom implants on demand? Bandages for the heart? 3D printing method makes it possible

In the quest to develop life-like materials to replace and repair human body parts, scientists face a formidable challenge: Real tissues are often both strong and stretchable and vary in shape and size.

A CU Boulder-led team, in collaboration with researchers at the University of Pennsylvania, has taken a critical step toward cracking that code. They've developed a new way to 3D print material that is at once elastic enough to withstand a heart's persistent beating, tough enough to endure the crushing load placed on joints, and easily shapable to fit a patient's unique defects.

Better yet, it sticks easily to wet tissue.

Their breakthrough, described in the Aug. 2 edition of the journal Science, helps pave the way toward a new generation of biomaterials, from internal bandages that deliver drugs directly to the heart to cartilage patches and needle-free sutures.

"Cardiac and cartilage tissues are similar in that they have very limited capacity to repair themselves. When they're damaged, there is no turning back," said senior author Jason Burdick, a professor of chemical and biological engineering at CU Boulder's BioFrontiers Institute. "By developing new, more resilient materials to enhance that repair process, we can have a big impact on patients."

Worm 'blobs' as inspiration

Historically, biomedical devices have been created via molding or casting, techniques which work well for mass production of identical implants but aren't practical when it comes to personalizing those implants for specific patients. In recent years, 3D printing has opened a world of new possibilities for medical applications by allowing researchers to make materials in many shapes and structures.

Unlike typical printers, which simply place ink on paper, 3D printers deposit layer after layer of plastics, metals or even living cells to create multidimensional objects.

One specific material, known as a hydrogel (the stuff that contact lenses are made of), has been a favorite prospect for fabricating artificial tissues, organs and implants.

But getting these from the lab to the clinic has been tough because traditional 3D-printed hydrogels tend to either break when stretched, crack under pressure or are too stiff to mold around tissues.

"Imagine if you had a rigid plastic adhered to your heart. It wouldn't deform as your heart beats," said Burdick. "It would just fracture."

To achieve both strength and elasticity within 3D printed hydrogels, Burdick and his colleagues took a cue from worms, which repeatedly tangle and untangle themselves around one another in three-dimensional "worm blobs" that have both solid and liquid-like properties. Previous research has shown that incorporating similarly intertwined chains of molecules, known as "entanglements," can make them tougher.

Their new printing method, known as CLEAR (for Continuous-curing after Light Exposure Aided by Redox initiation), follows a series of steps to entangle long molecules inside 3D-printed materials much like those intertwined worms.

When the team stretched and weight-loaded those materials in the lab (one researcher even ran over a sample with her bike) they found them to be exponentially tougher than materials printed with a standard method of 3D printing known as Digital Light Processing (DLP). Better yet: They also conformed and stuck to animal tissues and organs.

"We can now 3D print adhesive materials that are strong enough to mechanically support tissue," said co-first author Matt Davidson, a research associate in the Burdick Lab. "We have never been able to do that before."

Revolutionizing care

Burdick imagines a day when such 3D-printed materials could be used to repair defects in hearts, deliver tissue-regenerating drugs directly to organs or cartilage, restrain bulging discs or even stitch people up in the operating room without inflicting tissue damage like a needle and suture can.

His lab has filed for a provisional patent and plans to launch more studies soon to better understand how tissues react to the presence of such materials.

But the team stresses that their new method could have impacts far beyond medicine -- in research and manufacturing too. For instance, their method eliminates the need for additional energy to cure, or harden, parts, making the 3D printing process more environmentally friendly.

Read more at Science Daily

Any activity is better for your heart than sitting -- even sleeping

The study, supported by the British Heart Foundation (BHF) and published in the European Heart Journal, is the first to assess how different movement patterns throughout the 24-hour day are linked to heart health. It is the first evidence to emerge from the international Prospective Physical Activity, Sitting and Sleep (ProPASS) consortium.

Cardiovascular disease, which refers to all diseases of the heart and circulation, is the number one cause of mortality globally. In 2021, it was responsible for one in three deaths (20.5m), with coronary heart disease alone the single biggest killer. Since 1997, the number of people living with cardiovascular disease across the world has doubled and is projected to rise further.

In this study, researchers at UCL analysed data from six studies, encompassing 15,246 people from five countries, to see how movement behaviour across the day is associated with heart health, as measured by six common indicators*. Each participant used a wearable device on their thigh to measure their activity throughout the 24-hour day and had their heart health measured.

The researchers identified a hierarchy of behaviours that make up a typical 24-hour day, with time spent doing moderate-vigorous activity providing the most benefit to heart health, followed by light activity, standing and sleeping compared with the adverse impact of sedentary behaviour.

The team modelled what would happen if an individual changed various amounts of one behaviour for another each day for a week, in order to estimate the effect on heart health for each scenario. When replacing sedentary behaviour, as little as five minutes of moderate-vigorous activity had a noticeable effect on heart health.

For a 54-year-old woman with an average BMI of 26.5, for example, a 30-minute change translated into a 0.64 decrease in BMI, which is a difference of 2.4%. Replacing 30 minutes of daily sitting or lying time with moderate or vigorous exercise could also translate into a 2.5 cm (2.7%) decrease in waist circumference or a 1.33 mmol/mol (3.6%) decrease in glycated haemoglobin.

Dr Jo Blodgett, first author of the study from UCL Surgery & Interventional Science and the Institute of Sport, Exercise & Health, said: "The big takeaway from our research is that while small changes to how you move can have a positive effect on heart health, intensity of movement matters. The most beneficial change we observed was replacing sitting with moderate to vigorous activity -- which could be a run, a brisk walk, or stair climbing -- basically any activity that raises your heart rate and makes you breathe faster, even for a minute or two."

The researchers pointed out that although time spent doing vigorous activity was the quickest way to improve heart health, there are ways to benefit for people of all abilities -- it's just that the lower the intensity of the activity, the longer the time is required to start having a tangible benefit. Using a standing desk for a few hours a day instead of a sitting desk, for example, is a change over a relatively large amount of time but is also one that could be integrated into a working routine fairly easily as it does not require any time commitment.

Those who are least active were also found to gain the greatest benefit from changing from sedentary behaviours to more active ones.

Professor Emmanuel Stamatakis, joint senior author of the study from the Charles Perkins Centre and Faculty of Medicine and Health at the University of Sydney, said: "A key novelty of the ProPASS consortium is the use of wearable devices that better differentiate between types of physical activity and posture, allowing us to estimate the health effects of even subtle variations with greater precision."

Though the findings cannot infer causality between movement behaviours and cardiovascular outcomes, they contribute to a growing body of evidence linking moderate to vigorous physical activity over 24 hours with improved body fat metrics. Further long-term studies will be crucial to better understanding the associations between movement and cardiovascular outcomes.

Professor Mark Hamer, joint senior author of the study from UCL Surgery & Interventional Science and the Institute of Sport, Exercise & Health, said: "Though it may come as no surprise that becoming more active is beneficial for heart health, what's new in this study is considering a range of behaviours across the whole 24-hour day. This approach will allow us to ultimately provide personalised recommendations to get people more active in ways that are appropriate for them."

James Leiper, Associate Medical Director at the British Heart Foundation, said: "We already know that exercise can have real benefits for your cardiovascular health and this encouraging research shows that small adjustments to your daily routine could lower your chances of having a heart attack or stroke. This study shows that replacing even a few minutes of sitting with a few minutes of moderate activity can improve your BMI, cholesterol, waist size, and have many more physical benefits.

"Getting active isn't always easy, and it's important to make changes that you can stick to in the long-term and that you enjoy -- anything that gets your heart rate up can help. Incorporating 'activity snacks' such as walking while taking phone calls, or setting an alarm to get up and do some star jumps every hour is a great way to start building activity into your day, to get you in the habit of living a healthy, active lifestyle."

Read more at Science Daily

The more you walk, the lower your risk of early death, even if you walk fewer than 5,000 steps

The number of steps you should walk every day to start seeing benefits to your health is lower than previously thought, according to the largest analysis to investigate this.

The study, published in the European Journal of Preventive Cardiology [1] today (Wednesday), found that walking at least 3967 steps a day started to reduce the risk of dying from any cause, and 2337 steps a day reduced the risk of dying from diseases of the heart and blood vessels (cardiovascular disease).

However, the new analysis of 226,889 people from 17 different studies around the world has shown that the more you walk, the greater the health benefits. The risk of dying from any cause or from cardiovascular disease decreases significantly with every 500 to 1000 extra steps you walk. An increase of 1000 steps a day was associated with a 15% reduction in the risk of dying from any cause, and an increase of 500 steps a day was associated with a 7% reduction in dying from cardiovascular disease.

The researchers, led by Maciej Banach, Professor of Cardiology at the Medical University of Lodz, Poland, and Adjunct Professor at the Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, found that even if people walked as many as 20,000 steps a day, the health benefits continued to increase. They have not found an upper limit yet.

"Our study confirms that the more you walk, the better," says Prof. Banach. "We found that this applied to both men and women, irrespective of age, and irrespective of whether you live in a temperate, sub-tropical or sub-polar region of the world, or a region with a mixture of climates. In addition, our analysis indicates that as little as 4,000 steps a day are needed to significantly reduce deaths from any cause, and even fewer to reduce deaths from cardiovascular disease."

There is strong evidence that a sedentary lifestyle may contribute to an increase in cardiovascular disease and a shorter life. Studies have shown that insufficient physical activity affects more than a quarter of the world's population. More women than men (32% versus 23%), and people in higher income countries compared to low-income countries (37% versus 16%) do not undertake a sufficient amount of physical activity. According to World Health Organization data, insufficient physical activity is the fourth most frequent cause of death in the world, with 3.2 million deaths a year related to physical inactivity. The COVID-19 pandemic also resulted in a reduction in physical activity, and activity levels have not recovered two years on from it.

Dr Ibadete Bytyçi from the University Clinical Centre of Kosovo, Pristina, Kosovo, senior author of the paper, says: "Until now, it's not been clear what is the optimal number of steps, both in terms of the cut-off points over which we can start to see health benefits, and the upper limit, if any, and the role this plays in people's health. However, I should emphasise that there were limited data available on step counts up to 20,000 a day, and so these results need to be confirmed in larger groups of people."

This meta-analysis is the first not only to assess the effect of walking up to 20,000 steps a day, but also to look at whether there are any differences depending on age, sex or where in the world people live.

The studies analysed by the researchers followed up participants for a median (average) of seven years. The mean (average) age was 64, and 49% of participants were female.

In people aged 60 years or older, the size of the reduction in risk of death was smaller than that seen in people aged younger than 60 years. In the older adults, there was a 42% reduction in risk seen in those who walked between 6,000 and 10,000 steps a day, while there was a 49% reduction in risk in younger adults who walked between 7,000 and 13,000 steps a day.

Prof. Banach says: "In a world where we have more and more advanced drugs to target specific conditions such as cardiovascular disease, I believe we should always emphasise that lifestyle changes, including diet and exercise, which was a main hero of our analysis, might be at least as, or even more effective in reducing cardiovascular risk and prolonging lives. We still need good studies to investigate whether these benefits may exist for intensive types of exertion, such as marathon running and iron man challenges, and in different populations of different ages, and with different associated health problems. However, it seems that, as with pharmacological treatments, we should always think about personalising lifestyle changes."

Strengths of the meta-analysis include its size and that it was not restricted to looking at studies limited to a maximum of 16,000 steps a day. Limitations include that it was an observational study and so cannot prove that increased step counts cause the reduction in the risk of death, only that it is associated with it. The impact of step counts was not tested on people with different diseases; all the participants were generally healthy when they entered the studies analysed. The researchers were not able to account for differences in race and socioeconomic status, and the methods for counting steps were not identical in all the studies included in this meta-analysis.

Read more at Science Daily

Detailed map of the heart provides new insights into cardiac health and disease

In a new study, published today (12 July) in Nature, researchers have produced the most detailed and comprehensive human Heart Cell Atlas to date, including the specialised tissue of the cardiac conduction system -- where the heartbeat originates.

The multi-centre team is led by the Wellcome Sanger Institute and the National Heart and Lung Institute at Imperial College London, and has also presented a new drug-repurposing computational tool called Drug2cell, which can provide insights into the effects of drugs on heart rate.

This study is part of the international Human Cell Atlas* (HCA) initiative, which is mapping every cell type in the human body, to transform our understanding of health and disease, and will form the foundation for a fully integrated HCA Human Heart Cell Atlas.

Charting eight regions of the human heart, the work describes 75 different cell states including the cells of the cardiac conduction system -- the group of cells responsible for the heartbeat -- not understood at such a detailed level in humans before. The human cardiac conduction system, the heart's 'wiring', sends electrical impulses from the top to the bottom of the heart and coordinates the heartbeat.

By using spatial transcriptomics, which gives a "map" of where cells sit within a tissue, researchers were also able to understand how these cells communicate with each other for the first time. This map acts as a molecular guidebook, showing what healthy cells look like, and providing a crucial reference to understand what goes wrong in disease. The findings will help understand diseases such as those affecting the heart rhythm.

The assembly of a Human Heart Cell Atlas is key given that cardiovascular diseases are the leading cause of death globally. Around 20,000 electronic pacemakers are implanted each year in the UK for these disorders. These can be ineffective and are prone to complications and side-effects. Understanding the biology of the cells of the conduction system and how they differ from muscle cells paves the way to therapies to boost cardiac health and develop targeted treatments for arrhythmias.

The team also presents a new computational tool called Drug2cell. The tool can predict drug targets as well as drug side effects. It leverages single-cell profiles and the 19 million drug-target interactions in the EMBL-EBI ChEMBL database.

Unexpectedly, this tool identified that pacemaker cells express the target of certain medications, such as GLP1 drugs, which are used for diabetes and weight loss and are known to increase the heart rate as a side-effect, the mechanism of which was unclear. This study suggests that the increase in heart rate might be partly due to a direct action of these drugs on pacemaker cells, a finding the team also showed in an experimental stem cell model of pacemaker cells.

Dr James Cranley, joint first author, a cardiologist specialising in heart rhythm disorders and PhD student at the Wellcome Sanger Institute, said: "The cardiac conduction system is critical for the regular and coordinated beating of our hearts, yet the cells which make it up are poorly understood. This study sheds new light by defining the profiles of these cells, as well as the multicellular niches they inhabit. This deeper understanding opens the door to better, targeted anti-arrhythmic therapies in the future."

Dr Kazumasa Kanemaru, joint first author and Postdoctoral Fellow in the Gene Expression Genomics team at the Wellcome Sanger Institute, said: "The mechanism of activating and suppressing pacemaker cell genes is not clear, especially in humans. This is important for improving cell therapy to facilitate the production of pacemaker cells or to prevent the excessive spontaneous firing of cells. By understanding these cells at an individual genetic level, we can potentially develop new ways to improve heart treatments."

The study unearthed an unexpected discovery: a close relationship between conduction system cells and glial cells. Glial cells are part of the nervous system and are traditionally found in the brain. They have been explored very little in the heart. This research suggests that glial cells are in physical contact with conduction system cells and may play an important supporting role: communicating with the pacemaker cells, guiding nerve endings to them, and supporting their release of glutamate, a neurotransmitter.

Another key finding of the study is an immune structure on the heart's outer surface. This contains plasma cells, which release antibodies into the space around the heart to prevent infection from the nearby lungs. The researchers also identified a cellular niche enriching for a hormone that could be interpreted as an early warning sign of heart failure.

Dr Michela Noseda, senior Lecturer in Cardiac Molecular Pathology at the National Heart and Lung Institute, Imperial College London, a Coordinator of the Human Cell Atlas Heart BioNetwork and a lead author, said: "We often don't fully know what impact a new treatment will have on the heart and its electrical impulses -- this can mean a drug is withdrawn or fails to make it to the market. Our team developed the Drug2cell platform to improve how we evaluate new treatments and how they can affect our hearts, and potentially other tissues too. This could provide us with an invaluable tool to identify new drugs which target specific cells, as well as help to predict any potential side-effects early on in drug development."

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, which part-funded the research with the German Centre for Cardiovascular Research (DZHK), said: "Using cutting-edge technologies, this research provides further intricate detail about the cells that make up specialised regions of the human heart and how those cells communicate with each other. The new findings on the heart's electrical conduction system and its regulation are likely to open up new approaches to preventing and treating rhythm disturbances that can impair the heart's function and may even become life-threatening."

"International collaboration is key to scientific progress. This impactful study and other discoveries from the broader Human Cell Atlas initiative are excellent examples of what can be achieved when the international research community works together across borders. Our combined efforts can ultimately produce better outcomes for patients worldwide."

Read more at Science Daily

A miniature heart in a petri dish: Organoid emulates development of the human heart

A team at the Technical University of Munich (TUM) has induced stem cells to emulate the development of the human heart. The result is a sort of "mini-heart" known as an organoid. It will permit the study of the earliest development phase of our heart and facilitate research on diseases.

The human heart starts forming approximately three weeks after conception. This places the early phase of heart development in a time when women are often still unaware of their pregnancy. That is one reason why we still have little knowledge of many details of how the heart is formed. Findings from animal studies are not fully transferable to humans. An organoid developed at TUM could prove helpful to researchers.

A ball of 35,000 cells

The team working with Alessandra Moretti, Professor of Regenerative Medicine in Cardiovascular Disease, has developed a method for making a sort of "mini-heart" using pluripotent stem cells. Around 35,000 cells are spun into a sphere in a centrifuge. Over a period of several weeks, different signaling molecules are added to the cell culture under a fixed protocol. "In this way, we mimic the signaling pathways in the body that control the developmental program for the heart," explains Alessandra Moretti. The group has now published its work in the journal Nature Biotechnology.

First-ever "epicardioids"

The resulting organoids are about half a millimeter in diameter. Although they do not pump blood, they can be stimulated electrically and are capable of contracting like human heart chambers. Prof. Moretti and her team are the first researchers in the world to successfully create an organoid containing both heart muscle cells (cardiomyocytes) and cells of the outer layer of the heart wall (epicardium). In the young history of heart organoids -- the first were described in 2021 -- researchers had previously created only organoids with cardiomyocytes and cells from the inner layer of the heart wall (endocardium).

"To understand how the heart is formed, epicardium cells are decisive," says Dr. Anna Meier, first author of the study. "Other cell types in the heart, for example in connecting tissues and blood vessels, are formed from these cells. The epicardium also plays a very important role in forming the heart chambers." The team has appropriately named the new organoids "epicardioids."

New cell type discovered

Along with the method for producing the organoids, the team has reported its first new discoveries. Through the analysis of individual cells they have determined that precursor cells of a type only recently discovered in mice are formed around the seventh day of the development of the organoid. The epicardium is formed from these cells. "We assume that these cells also exist in the human body -- if only for a few days," says Prof. Moretti.

These insights may also offer clues as to why the fetal heart can repair itself, a capability almost entirely absent in the heart of an adult human. This knowledge could help to find new treatment methods for heart attacks and other conditions.

Producing "personalized organoids"

The team also showed that the organoids can be used to investigate the illnesses of individual patients. Using pluripotent stem cells from a patient suffering from Noonan syndrome, the researchers produced organoids that emulated characteristics of the condition in a Petri dish. Over the coming months the team plans to use comparable personalized organoids to investigate other congenital heart defects.

With the possibility of emulating heart conditions in organoids, drugs could be tested directly on them in the future. "It is conceivable that such tests could reduce the need for animal experiments when developing drugs," says Alessandra Moretti.

Read more at Science Daily

Heart-healthy lifestyle linked to a longer life, free of chronic health conditions

Two new studies by related research groups have found that adults who live a heart-healthy lifestyle, as measured by the American Heart Association's Life's Essential 8 (LE8) cardiovascular health scoring, tend to live longer lives free of chronic disease. The preliminary studies will be presented at the American Heart Association's Epidemiology, Prevention, Lifestyle & Cardiometabolic Health Scientific Sessions 2023, held in Boston, February 28-March 3, 2023. The meeting offers the latest science on population-based health and wellness and implications for lifestyle and cardiometabolic health.

In June 2022, the American Heart Association updated the metrics for optimal cardiovascular health to include sleep -- Life's Essential 8. The tool measures 4 indicators related to cardiovascular and metabolic health status (blood pressure, cholesterol, blood sugar and body mass index); and 4 behavioral/lifestyle factors (smoking status, physical activity, sleep and diet).

"These two abstracts really give us some nice new insight into how we can understand at different stages across the life course just how important focusing on your cardiovascular health is going to be, particularly using the new American Heart Association Life's Essential 8 metrics," said Donald M. Lloyd-Jones, M.D., Sc.M., FAHA. Lloyd-Jones led the advisory writing group for Life's Essential 8 and is immediate past president of the American Heart Association President and chair of the department of preventive medicine, the Eileen M. Foell Professor of Heart Research and professor of preventive medicine, medicine and pediatrics at Northwestern University's Feinberg School of Medicine in Chicago. "The cardiovascular health construct studied in these two abstracts really does nail what patients are trying to do, which is find the fountain of youth. Yes, live longer, but more importantly, live healthier longer, and extend that healthspan so that you can really enjoy quality in your remaining life years."

Life's Essential 8 And Life Expectancy Free of Cardiovascular Disease, Diabetes, Cancer, And Dementia in Adults

The first study investigated whether levels of cardiovascular health estimated by the Association's Life's Essential 8 metrics were associated with life expectancy free of major chronic disease, including cardiovascular disease, Type 2 diabetes, cancer and dementia.

"Our study looked at the association of Life's Essential 8 and life expectancy free of major chronic disease in adults in the United Kingdom," said lead author Xuan Wang, M.D., Ph.D., a postdoctoral fellow and biostatistician in the department of epidemiology at Tulane University's School of Public Health and Tropical Medicine in New Orleans.

Wang and colleagues analyzed health information for 136,599 adults in the U.K. who did not have cardiovascular disease, Type 2 diabetes, cancer or dementia when they enrolled in the study and as measured by the Life's Essential 8 tool.

"We categorized Life's Essential 8 scores according to the American Heart Association's recommendations, with scores of less than 50 out of 100 being poor cardiovascular health, 50 to less than 80 being intermediate, and 80 and above being ideal," Wang said. Life's Essential 8 scores of 80 and above are defined as "high cardiovascular health" by the Association.

When the researchers compared life expectancy and disease-free years among the groups, they found:

•     Adults who scored as having ideal cardiovascular health lived substantially longer than those scored in the poor heart health category. Men and women with ideal cardiovascular health at age 50 had an average 5.2 years and 6.3 years more of total life expectancy, respectively, when compared to the men and women who scored as having poor cardiovascular health.
•     Adults with ideal cardiovascular health scores lived longer without chronic disease. Disease-free life expectancy accounted for nearly 76% of total life expectancy for men and more than 83% for women who had ideal cardiovascular health -- in contrast, disease-free life expectancy was only 64.9% of men and 69.4% of women with poor cardiovascular health.

"Moreover, we found disparities in disease-free life expectancy due to low socioeconomic status may be offset considerably by maintaining an ideal cardiovascular health score in all adults," Wang said. "Our findings may stimulate interest in individual self-assessment and motivate people to improve their cardiovascular health. These findings support improving population health by promoting adherence to ideal cardiovascular health, which may also narrow health disparities related to socioeconomic status."

The study's limitations were that the researchers only included CVD, diabetes, cancer and dementia in their definition of "disease-free life expectancy;" information on e-cigarettes was not available in the U.K. Biobank, which may lead to a slight overestimation of the LE8 score in this study; and participants in the U.K. Biobank are overwhelmingly white race, therefore, further studies are needed to confirm if these results are consistent among people from diverse racial and ethnic backgrounds who may experience negative social determinants of health throughout their lifetime.

"What's really important is that people maintaining high cardiovascular health into midlife are avoiding those chronic diseases of aging, things like cancer and dementia that we also worry about, not just cardiovascular disease," Lloyd-Jones said. "They're delayed until much later in the lifespan, so people can enjoy the life in their years as well as the years in their life."

Co-authors with Wang are Hao Ma, M.D., Ph.D.; Xiang Li, M.D., Ph.D.; Yoriko Heianza, R.D., Ph.D.; JoAnn E. Manson, M.D., M.P.H., Dr.P.H..; Oscar H. Franco, M.D., Ph.D.; and Lu Qi, M.D., Ph.D. Authors' disclosures are listed in the abstract.

The study was funded by the National Heart, Lung, and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases, which are divisions of the National Institutes of Health; the Fogarty International Center; and Tulane Research Centers of Excellence Awards.

Life's Essential 8 And Life Expectancy Among Adults in the United States

The second study focused on whether the association of Life's Essential 8 with total life expectancy differed by sex or race in U.S. adults.

The researchers analyzed health information, including Life's Essential 8 scores, for more than 23,000 U.S. adults who took part in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018.

The analysis found:

•     Life expectancy for adults at age 50 was an average of an additional 33.4 years for those with ideal cardiovascular health, or scores of 80 or greater; in comparison, additional life expectancy was 25.3 years for adults with poor cardiovascular health, LE8 scores of less than 50.
•     Adults with ideal cardiovascular health gained an estimated 8.1 years (7.5 additional years for men and 8.9 for women) of life expectancy at age 50, compared with those in the poor cardiovascular health category.

"We found that more than 40% of the increased life expectancy at age 50 from adhering to ideal cardiovascular health may be explained by the reduced incidence of cardiovascular disease death," said lead author Hao Ma, M.D., Ph.D., a postdoctoral fellow and biostatistician in epidemiology at Tulane University and co-author on Wang's study.

According to Ma, this indicates that maintaining one's cardiovascular health may improve one's lifespan. However, more research needs to be done on the impact of cardiovascular health on lifespan among people from diverse racial and ethnic groups, he said.

The study had several limitations such as the researchers did not consider potential changes of cardiovascular health during the follow-up because information on the cardiovascular health metrics was only available at baseline. Additionally, the researchers' analyses of different racial/ethnic groups only included non-Hispanic white, non-Hispanic Black and people of Mexican heritage due to the limited sample size for additional racial/ethnic groups.

"What struck me about this abstract particularly was that there's a really big jump going from individuals who have poor cardiovascular health to just intermediate levels of cardiovascular health," Lloyd-Jones said. "Overall, we see this seven-and-a-half-year difference going from poor to high cardiovascular health. That's a really big difference in life expectancy, and I think what it tells us is that we need to try to move people and get them to improve their cardiovascular health in mid-life, because that's really going to have a major influence on their total life expectancy."

Read more at Science Daily

Custom, 3D-printed heart replicas look and pump just like the real thing

No two hearts beat alike. The size and shape of the the heart can vary from one person to the next. These differences can be particularly pronounced for people living with heart disease, as their hearts and major vessels work harder to overcome any compromised function.

MIT engineers are hoping to help doctors tailor treatments to patients' specific heart form and function, with a custom robotic heart. The team has developed a procedure to 3D print a soft and flexible replica of a patient's heart. They can then control the replica's action to mimic that patient's blood-pumping ability.

The procedure involves first converting medical images of a patient's heart into a three-dimensional computer model, which the researchers can then 3D print using a polymer-based ink. The result is a soft, flexible shell in the exact shape of the patient's own heart. The team can also use this approach to print a patient's aorta -- the major artery that carries blood out of the heart to the rest of the body.

To mimic the heart's pumping action, the team has fabricated sleeves similar to blood pressure cuffs that wrap around a printed heart and aorta. The underside of each sleeve resembles precisely patterned bubble wrap. When the sleeve is connected to a pneumatic system, researchers can tune the outflowing air to rhythmically inflate the sleeve's bubbles and contract the heart, mimicking its pumping action.

The researchers can also inflate a separate sleeve surrounding a printed aorta to constrict the vessel. This constriction, they say, can be tuned to mimic aortic stenosis -- a condition in which the aortic valve narrows, causing the heart to work harder to force blood through the body.

Doctors commonly treat aortic stenosis by surgically implanting a synthetic valve designed to widen the aorta's natural valve. In the future, the team says that doctors could potentially use their new procedure to first print a patient's heart and aorta, then implant a variety of valves into the printed model to see which design results in the best function and fit for that particular patient. The heart replicas could also be used by research labs and the medical device industry as realistic platforms for testing therapies for various types of heart disease.

"All hearts are different," says Luca Rosalia, a graduate student in the MIT-Harvard Program in Health Sciences and Technology. "There are massive variations, especially when patients are sick. The advantage of our system is that we can recreate not just the form of a patient's heart, but also its function in both physiology and disease."

Rosalia and his colleagues report their results in a study appearing today in Science Robotics. MIT co-authors include Caglar Ozturk, Debkalpa Goswami, Jean Bonnemain, Sophie Wang, and Ellen Roche, along with Benjamin Bonner of Massachusetts General Hospital, James Weaver of Harvard University, and Christopher Nguyen, Rishi Puri, and Samir Kapadia at the Cleveland Clinic in Ohio.

Print and pump

In January 2020, team members, led by mechanical engineering professor Ellen Roche, developed a "biorobotic hybrid heart" -- a general replica of a heart, made from synthetic muscle containing small, inflatable cylinders, which they could control to mimic the contractions of a real beating heart.

Shortly after those efforts, the Covid-19 pandemic forced Roche's lab, along with most others on campus, to temporarily close. Undeterred, Rosalia continued tweaking the heart-pumping design at home.

"I recreated the whole system in my dorm room that March," Rosalia recalls.

Months later, the lab reopened, and the team continued where it left off, working to improve the control of the heart-pumping sleeve, which they tested in animal and computational models. They then expanded their approach to develop sleeves and heart replicas that are specific to individual patients. For this, they turned to 3D printing.

"There is a lot of interest in the medical field in using 3D printing technology to accurately recreate patient anatomy for use in preprocedural planning and training," notes Wang, who is a vascular surgery resident at Beth Israel Deaconess Medical Center in Boston.

An inclusive design

In the new study, the team took advantage of 3D printing to produce custom replicas of actual patients' hearts. They used a polymer-based ink that, once printed and cured, can squeeze and stretch, similarly to a real beating heart.

As their source material, the researchers used medical scans of 15 patients diagnosed with aortic stenosis. The team converted each patient's images into a three-dimensional computer model of the patient's left ventricle (the main pumping chamber of the heart) and aorta. They fed this model into a 3D printer to generate a soft, anatomically accurate shell of both the ventricle and vessel.

The team also fabricated sleeves to wrap around the printed forms. They tailored each sleeve's pockets such that, when wrapped around their respective forms and connected to a small air pumping system, the sleeves could be tuned separately to realistically contract and constrict the printed models.

The researchers showed that for each model heart, they could accurately recreate the same heart-pumping pressures and flows that were previously measured in each respective patient.

"Being able to match the patients' flows and pressures was very encouraging," Roche says. "We're not only printing the heart's anatomy, but also replicating its mechanics and physiology. That's the part that we get excited about."

Going a step further, the team aimed to replicate some of the interventions that a handful of the patients underwent, to see whether the printed heart and vessel responded in the same way. Some patients had received valve implants designed to widen the aorta. Roche and her colleagues implanted similar valves in the printed aortas modeled after each patient. When they activated the printed heart to pump, they observed that the implanted valve produced similarly improved flows as in actual patients following their surgical implants.

Finally, the team used an actuated printed heart to compare implants of different sizes, to see which would result in the best fit and flow -- something they envision clinicians could potentially do for their patients in the future.

"Patients would get their imaging done, which they do anyway, and we would use that to make this system, ideally within the day," says co-author Nyugen. "Once it's up and running, clinicians could test different valve types and sizes and see which works best, then use that to implant."

Ultimately, Roche says the patient-specific replicas could help develop and identify ideal treatments for individuals with unique and challenging cardiac geometries.

Read more at Science Daily

Heart of our evolution discovered: 380-million-year-old heart

Researchers have discovered a 380-million-year-old heart -- the oldest ever found -- alongside a separate fossilised stomach, intestine and liver in an ancient jawed fish, shedding new light on the evolution of our own bodies.

The new research, published today in Science, found that the position of the organs in the body of arthrodires -- an extinct class of armoured fishes that flourished through the Devonian period from 419.2 million years ago to 358.9 million years ago -- is similar to modern shark anatomy, offering vital new evolutionary clues.

Lead researcher John Curtin Distinguished Professor Kate Trinajstic, from Curtin's School of Molecular and Life Sciences and the Western Australian Museum, said the discovery was remarkable given that soft tissues of ancient species were rarely preserved and it was even rarer to find 3D preservation.

"As a palaeontologist who has studied fossils for more than 20 years, I was truly amazed to find a 3D and beautifully preserved heart in a 380-million-year-old ancestor," Professor Trinajstic said.

"Evolution is often thought of as a series of small steps, but these ancient fossils suggest there was a larger leap between jawless and jawed vertebrates. These fish literally have their hearts in their mouths and under their gills -- just like sharks today."

This research presents -- for the first time -- the 3D model of a complex s-shaped heart in an arthrodire that is made up of two chambers with the smaller chamber sitting on top.

Professor Trinajstic said these features were advanced in such early vertebrates, offering a unique window into how the head and neck region began to change to accommodate jaws, a critical stage in the evolution of our own bodies.

"For the first time, we can see all the organs together in a primitive jawed fish, and we were especially surprised to learn that they were not so different from us," Professor Trinajstic said.

"However, there was one critical difference -- the liver was large and enabled the fish to remain buoyant, just like sharks today. Some of today's bony fish such as lungfish and birchers have lungs that evolved from swim bladders but it was significant that we found no evidence of lungs in any of the extinct armoured fishes we examined, which suggests that they evolved independently in the bony fishes at a later date."

The Gogo Formation, in the Kimberley region of Western Australia where the fossils were collected, was originally a large reef.

Enlisting the help of scientists at the Australian Nuclear Science and Technology Organisation in Sydney and the European Synchrotron Radiation Facility in France, researchers used neutron beams and synchrotron x-rays to scan the specimens, still embedded in the limestone concretions, and constructed three-dimensional images of the soft tissues inside them based on the different densities of minerals deposited by the bacteria and the surrounding rock matrix.

This new discovery of mineralised organs, in addition to previous finds of muscles and embryos, makes the Gogo arthrodires the most fully understood of all jawed stem vertebrates and clarifies an evolutionary transition on the line to living jawed vertebrates, which includes the mammals and humans.

Co-author Professor John Long, from Flinders University, said: "These new discoveries of soft organs in these ancient fishes are truly the stuff of palaeontologists' dreams, for without doubt these fossils are the best preserved in the world for this age. They show the value of the Gogo fossils for understanding the big steps in our distant evolution. Gogo has given us world firsts, from the origins of sex to the oldest vertebrate heart, and is now one of the most significant fossil sites in the world. It's time the site was seriously considered for world heritage status."

Co-author Professor Per Ahlberg, from Uppsala University, said: "What's really exceptional about the Gogo fishes is that their soft tissues are preserved in three dimensions. Most cases of soft-tissue preservation are found in flattened fossils, where the soft anatomy is little more than a stain on the rock. We are also very fortunate in that modern scanning techniques allow us to study these fragile soft tissues without destroying them. A couple of decades ago, the project would have been impossible."

Read more at Science Daily

Alcohol may be more risky to the heart than previously thought

Levels of alcohol consumption currently considered safe by some countries are linked with development of heart failure, according to research presented at Heart Failure 2022, a scientific congress of the European Society of Cardiology (ESC).1

"This study adds to the body of evidence that a more cautious approach to alcohol consumption is needed," said study author Dr. Bethany Wong of St. Vincent's University Hospital, Dublin, Ireland. "To minimise the risk of alcohol causing harm to the heart, if you don't drink, don't start. If you do drink, limit your weekly consumption to less than one bottle of wine or less than three-and-a-half 500 ml cans of 4.5% beer."

According to the World Health Organization, the European Union is the heaviest-drinking region in the world.2 While it is well recognised that long-term heavy alcohol use can cause a type of heart failure called alcoholic cardiomyopathy,3 evidence from Asian populations suggests that lower amounts may also be detrimental.4,5 "As there are genetic and environmental differences between Asian and European populations this study investigated if there was a similar relationship between alcohol and cardiac changes in Europeans at risk of heart failure or with pre-heart failure," said Dr. Wong. "The mainstay of treatment for this group is management of risk factors such as alcohol, so knowledge about safe levels is crucial."

This was a secondary analysis of the STOP-HF trial.6 The study included 744 adults over 40 years of age either at risk of developing heart failure due to risk factors (e.g. high blood pressure, diabetes, obesity) or with pre-heart failure (risk factors and heart abnormalities but no symptoms).7 The average age was 66.5 years and 53% were women. The study excluded former drinkers and heart failure patients with symptoms (e.g. shortness of breath, tiredness, reduced ability to exercise, swollen ankles). Heart function was measured with echocardiography at baseline and follow up.

The study used the Irish definition of one standard drink (i.e. one unit), which is 10 grams of alcohol.8 Participants were categorised according to their weekly alcohol intake: none; low (less than seven units; up to one 750 ml bottle of 12.5% wine or three-and-a-half 500 ml cans of 4.5% beer); moderate (7-14 units; up to two bottles of 12.5% wine or seven 500 mL cans of 4.5% beer); high (above 14 units; more than two bottles of 12.5% wine or seven 500 ml cans of 4.5% beer).

The researchers analysed the association between alcohol use and heart health over a median of 5.4 years. The results were reported separately for the at-risk and pre-heart failure groups. In the at-risk group, worsening heart health was defined as progression to pre-heart failure or to symptomatic heart failure. For the pre-heart failure group, worsening heart health was defined as deterioration in the squeezing or relaxation functions of the heart or progression to symptomatic heart failure. The analyses were adjusted for factors that can affect heart structure including age, gender, obesity, high blood pressure, diabetes, and vascular disease.

A total of 201 (27%) patients reported no alcohol usage, while 356 (48%) were low users and 187 (25%) had moderate or high intake. Compared to the low intake group, those with moderate or high use were younger, more likely to be male, and had a higher body mass index.

In the pre-heart failure group, compared with no alcohol use, moderate or high intake was associated with a 4.5-fold increased risk of worsening heart health. The relationship was also observed when moderate and high levels were analysed separately. In the at-risk group, there was no association between moderate or high alcohol use with progression to pre-heart failure or to symptomatic heart failure. No protective associations were found for low alcohol intake.

Read more at Science Daily

New miniature heart could help speed heart disease cures

There's no safe way to get a close-up view of the human heart as it goes about its work: you can't just pop it out, take a look, then slot it back in. Scientists have tried different ways to get around this fundamental problem: they've hooked up cadaver hearts to machines to make them pump again, attached lab-grown heart tissues to springs to watch them expand and contract. Each approach has its flaws: reanimated hearts can only beat for a few hours; springs can't replicate the forces at work on the real muscle. But getting a better understanding of this vital organ is urgent: in America, someone dies of heart disease every 36 seconds, according to the Centers for Disease Control and Prevention.

Now, an interdisciplinary team of engineers, biologists, and geneticists has developed a new way of studying the heart: they've built a miniature replica of a heart chamber from a combination of nanoengineered parts and human heart tissue. There are no springs or external power sources -- like the real thing, it just beats by itself, driven by the live heart tissue grown from stem cells. The device could give researchers a more accurate view of how the organ works, allowing them to track how the heart grows in the embryo, study the impact of disease, and test the potential effectiveness and side effects of new treatments -- all at zero risk to patients and without leaving a lab.

The Boston University-led team behind the gadget -- nicknamed miniPUMP, and officially known as the cardiac miniaturized Precision-enabled Unidirectional Microfluidic Pump -- says the technology could also pave the way for building lab-based versions of other organs, from lungs to kidneys. Their findings have been published in Science Advances.

"We can study disease progression in a way that hasn't been possible before," says Alice White, a BU College of Engineering professor and chair of mechanical engineering. "We chose to work on heart tissue because of its particularly complicated mechanics, but we showed that, when you take nanotechnology and marry it with tissue engineering, there's potential for replicating this for multiple organs."

According to the researchers, the device could eventually speed up the drug development process, making it faster and cheaper. Instead of spending millions -- and possibly decades -- moving a medicinal drug through the development pipeline only to see it fall at the final hurdle when tested in people, researchers could use the miniPUMP at the outset to better predict success or failure.

The project is part of CELL-MET, a multi-institutional National Science Foundation Engineering Research Center in Cellular Metamaterials that's led by BU. The center's goal is to regenerate diseased human heart tissue, building a community of scientists and industry experts to test new drugs and create artificial implantable patches for hearts damaged by heart attacks or disease.

"Heart disease is the number one cause of death in the United States, touching all of us," says White, who was chief scientist at Alcatel-Lucent Bell Labs before joining BU in 2013. "Today, there is no cure for a heart attack. The vision of CELL-MET is to change this."

Personalized Medicine

There's a lot that can go wrong with your heart. When it's firing properly on all four cylinders, the heart's two top and two bottom chambers keep your blood flowing so that oxygen-rich blood circulates and feeds your body. But when disease strikes, the arteries that carry blood away from your heart can narrow or become blocked, valves can leak or malfunction, the heart muscle can thin or thicken, or electrical signals can short, causing too many -- or too few -- beats. Unchecked, heart disease can lead to discomfort -- like breathlessness, fatigue, swelling, and chest pain -- and, for many, death.

"The heart experiences complex forces as it pumps blood through our bodies," says Christopher Chen, BU's William F. Warren Distinguished Professor of Biomedical Engineering. "And while we know that heart muscle changes for the worse in response to abnormal forces -- for example, due to high blood pressure or valve disease -- it has been difficult to mimic and study these disease processes. This is why we wanted to build a miniaturized heart chamber."

At just 3 square centimeters, the miniPUMP isn't much bigger than a postage stamp. Built to act like a human heart ventricle -- or muscular lower chamber -- its custom-made components are fitted onto a thin piece of 3D-printed plastic. There are miniature acrylic valves, opening and closing to control the flow of liquid -- water, in this case, rather than blood -- and small tubes, funneling that fluid just like arteries and veins. And beating away in one corner, the muscle cells that make heart tissue contract, cardiomyocytes, made using stem cell technology.

"They're generated using induced pluripotent stem cells," says Christos Michas (ENG'21), a postdoctoral researcher who designed and led the development of the miniPUMP as part of his PhD thesis.

To make the cardiomyocyte, researchers take a cell from an adult -- it could be a skin cell, blood cell, or just about any other cell -- reprogram it into an embryonic-like stem cell, then transform that into the heart cell. In addition to giving the device literal heart, Michas says the cardiomyocytes also give the system enormous potential in helping pioneer personalized medicines. Researchers could place a diseased tissue in the device, for instance, then test a drug on that tissue and watch to see how its pumping ability is impacted.

"With this system, if I take cells from you, I can see how the drug would react in you, because these are your cells," says Michas. "This system replicates better some of the function of the heart, but at the same time, gives us the flexibility of having different humans that it replicates. It's a more predictive model to see what would happen in humans -- without actually getting into humans."

According to Michas, that could allow scientists to assess a new heart disease drug's chances of success long before heading into clinical trials. Many drug candidates fail because of their adverse side effects.

"At the very beginning, when we're still playing with cells, we can introduce these devices and have more accurate predictions of what will happen in clinical trials," says Michas. "It will also mean that the drugs might have fewer side effects."

Thinner than a Human Hair

One of the key parts of the miniPUMP is an acrylic scaffold that supports, and moves with, the heart tissue as it contracts. A series of superfine concentric spirals -- thinner than a human hair -- connected by horizontal rings, the scaffold looks like an artsy piston. It's an essential piece of the puzzle, giving structure to the heart cells -- which would just be a formless blob without it -- but not exerting any active force on them.

"We don't think previous methods of studying heart tissue capture the way the muscle would respond in your body," says Chen, who's also director of BU's Biological Design Center and an associate faculty member at Harvard University's Wyss Institute for Biologically Inspired Engineering. "This gives us the first opportunity to build something that mechanically is more similar to what we think the heart is actually experiencing -- it's a big step forward."

To print each of the tiny components, the team used a process called two-photon direct laser writing -- a more precise version of 3D printing. When light is beamed into a liquid resin, the areas it touches turn solid; because the light can be aimed with such accuracy -- focused to a tiny spot -- many of the components in the miniPUMP are measured in microns, smaller than a dust particle.

The decision to make the pump so small, rather than life-size or larger, was deliberate and is crucial to its functioning.

"The structural elements are so fine that things that would ordinarily be stiff are flexible," says White. "By analogy, think about optical fiber: a glass window is very stiff, but you can wrap a glass optical fiber around your finger. Acrylic can be very stiff, but at the scale involved in the miniPUMP, the acrylic scaffold is able to be compressed by the beating cardiomyocytes."

Chen says that the pump's scale shows "that with finer printing architectures, you might be able to create more complex organizations of cells than we thought was possible before." At the moment, when researchers try to create cells, he says, whether heart cells or liver cells, they're all disorganized -- "to get structure, you have to cross your fingers and hope the cells create something." That means the tissue scaffolding pioneered in the miniPUMP has big potential implications beyond the heart, laying the foundation for other organs-on-a-chip, from kidneys to lungs.

Refining the Technology

According to White, the breakthrough is possible because of the range of experts on CELL-MET's research team, which included not just mechanical, biomedical, and materials engineers like her, Chen, and Arvind Agarwal of Florida International University, but also geneticist Jonathan G. Seidman of Harvard Medical School and cardiovascular medicine specialist Christine E. Seidman of Harvard Medical School and Brigham and Women's Hospital. It's a breadth of experience that's benefited not just the project, but Michas. An electrical and computer engineering student as an undergraduate, he says he'd "never seen cells in my life before starting this project." Now, he's preparing to start a new position with Seattle-based biotech Curi Bio, a company that combines stem cell technology, tissue biosystems, and artificial intelligence to power the development of drugs and therapeutics.

"Christos is someone who understands the biology," says White, "can do the cell differentiation and tissue manipulation, but also understands nanotechnology and what's required, in an engineering way, to fabricate the structure."

Read more at Science Daily

Good news for coffee lovers: Daily coffee may benefit the heart

Drinking coffee -- particularly two to three cups a day -- is not only associated with a lower risk of heart disease and dangerous heart rhythms but also with living longer, according to studies being presented at the American College of Cardiology's 71st Annual Scientific Session. These trends held true for both people with and without cardiovascular disease. Researchers said the analyses -- the largest to look at coffee's potential role in heart disease and death -- provide reassurance that coffee isn't tied to new or worsening heart disease and may actually be heart protective.

"Because coffee can quicken heart rate, some people worry that drinking it could trigger or worsen certain heart issues. This is where general medical advice to stop drinking coffee may come from. But our data suggest that daily coffee intake shouldn't be discouraged, but rather included as a part of a healthy diet for people with and without heart disease," said Peter M. Kistler, MD, professor and head of arrhythmia research at the Alfred Hospital and Baker Heart Institute in Melbourne, Australia, and the study's senior author. "We found coffee drinking had either a neutral effect -- meaning that it did no harm -- or was associated with benefits to heart health."

Kistler and his team used data from the UK BioBank, a large-scale prospective database with health information from over half a million people who were followed for at least 10 years. Researchers looked at varying levels of coffee consumption ranging from up to a cup to more than six cups a day and the relationship with heart rhythm problems (arrhythmias); cardiovascular disease, including coronary artery disease, heart failure and stroke; and total and heart-related deaths among people both with and without cardiovascular disease. Patients were grouped by how much coffee they reported drinking each day: 0, <1, 1, 2-3, 4-5, >5 cups/day. Coffee drinking was assessed from questionnaires completed upon entry into the registry. Overall, they either found no effect or, in many cases, significant reductions in cardiovascular risk after controlling for exercise, alcohol, smoking, diabetes and high blood pressure that could also play a role in heart health and longevity.

For the first study, researchers examined data from 382,535 individuals without known heart disease to see whether coffee drinking played a role in the development of heart disease or stroke during the 10 years of follow up. Participants' average age was 57 years and half were women. In general, having two to three cups of coffee a day was associated with the greatest benefit, translating to a 10%-15% lower risk of developing coronary heart disease, heart failure, a heart rhythm problem, or dying for any reason. The risk of stroke or heart-related death was lowest among people who drank one cup of coffee a day. Researchers did observe a U-shaped relationship with coffee intake and new heart rhythm problems. The maximum benefit was seen among people drinking two to three cups of coffee a day with less benefit seen among those drinking more or less.

The second study included 34,279 individuals who had some form of cardiovascular disease at baseline. Coffee intake at two to three cups a day was associated with lower odds of dying compared with having no coffee. Importantly, consuming any amount of coffee was not associated with a higher risk of heart rhythm problems, including atrial fibrillation (AFib) or atrial flutter, which Kistler said is often what clinicians are concerned about. Of the 24,111 people included in the analysis who had an arrhythmia at baseline, drinking coffee was associated with a lower risk of death. For example, people with AFib who drank one cup of coffee a day were nearly 20% less likely to die than non-coffee drinkers.

"Clinicians generally have some apprehension about people with known cardiovascular disease or arrhythmias continuing to drink coffee, so they often err on the side of caution and advise them to stop drinking it altogether due to fears that it may trigger dangerous heart rhythms," Kistler said. "But our study shows that regular coffee intake is safe and could be part of a healthy diet for people with heart disease."

Although two to three cups of coffee a day seemed to be the most favorable overall, Kistler said that people shouldn't increase their coffee intake, particularly if it makes them feel anxious or uncomfortable.

"There is a whole range of mechanisms through which coffee may reduce mortality and have these favorable effects on cardiovascular disease," he said. "Coffee drinkers should feel reassured that they can continue to enjoy coffee even if they have heart disease. Coffee is the most common cognitive enhancer -- it wakes you up, makes you mentally sharper and it's a very important component of many people's daily lives."

So how might coffee beans benefit the heart? People often equate coffee with caffeine, but coffee beans actually have over 100 biologically active compounds. These substances can help reduce oxidative stress and inflammation, improve insulin sensitivity, boost metabolism, inhibit the gut's absorption of fat and block receptors known to be involved with abnormal heart rhythms, Kistler said.

In a third study, researchers looked at whether there were any differences in the relationship between coffee and cardiovascular disease depending on whether someone drank instant or ground coffee or caffeinated or decaf. They found, once again, two to three cups a day to be associated with the lowest risk of arrhythmias, blockages in the heart's arteries, stroke or heart failure regardless of whether they had ground or instant coffee. Lower rates of death were seen across all coffee types. Decaf coffee did not have favorable effects against incident arrhythmia but did reduce cardiovascular disease, with the exception of heart failure. Kistler said the findings suggest caffeinated coffee is preferable across the board, and there are no cardiovascular benefits to choosing decaf over caffeinated coffees.

There are several important limitations to these studies. Researchers were unable to control for dietary factors that may play a role in cardiovascular disease, nor were they able to adjust for any creamers, milk or sugar consumed. Participants were predominantly white, so additional studies are needed to determine whether these findings extend to other populations. Finally, coffee intake was based on self-report via a questionnaire fielded at study entry. This should be considered when interpreting the study findings, though Kistler noted that research suggests people's dietary habits don't change much in adulthood or over time. Kistler said the results should be validated in randomized trials.

Read more at Science Daily

Poor sleep can triple risk for heart disease

Individual aspects of poor sleep can be detrimental to heart health. But if you combine them, the risk of heart disease can increase by as much as 141 percent. That's the finding of a new study published in the journal Scientific Reports.

The University of South Florida-led study reviewed sleep data of 6,820 U.S. adults with an average age of 53 who self-reported their sleep characteristics and heart disease history. Among the participants, 633 also wore a research device (actigraphy) around their wrist that captured sleep activity.

Researchers focused on multiple aspects of sleep health, such as regularity, satisfaction, alertness during waking hours, timing of sleep, sleep efficiency and sleep duration and linked them to physician-diagnosed heart disease. They found that each additional increase in self-reported sleep health problems was associated with a 54 percent increased risk of heart disease. The estimated risk of heart disease associated with an increase in sleep health problems was much higher for those who provided sleep data by both self-report and the research device. They had a 141 percent increase -- a figure that could be perceived to be more accurate.

"These findings show the importance of assessing 'co-existing sleep health problems' within an individual to capture the risk of heart disease. This is one of the first studies showing that, among well-functioning adults in midlife, having more sleep health problems may increase the risk of heart disease," said lead author Soomi Lee, assistant professor of aging studies and director of the STEALTH lab at USF. "The higher estimated risk in those who provided both self-report and actigraphy sleep data suggests that measuring sleep health accurately and comprehensively is important to increase the prediction of heart disease."

The research team asked participants about their health, including if their physician confirmed a heart condition such as arrythmia, heart murmur or an enlarged heart. High blood pressure was not considered a diagnosis as it's labeled a risk factor for heart disease rather than a heart disease condition. They also controlled for family history of heart disease and sociodemographic factors, such as race, sex, smoking, depression and physical activity.

Researchers found that while women reported having more sleep health problems, men were more likely to suffer heart disease -- yet gender did not impact the overall correlation between the two factors. They also found that Black participants had more sleep health problems and a higher prevalence of heart disease than white participants, but the strong association between sleep health and heart disease did not differ by race in general.

Lee says while sleep health is important for all ages, the team focused on middle adulthood as it spans for a longer period of time and consists of diverse and more stressful life experiences due to work and family roles. This is also when precursors for heart disease and age-related sleep issues begin to arise.

Read more at Science Daily

Tweaked genes borrowed from bacteria excite heart cells in live mice

Biomedical engineers at Duke University have demonstrated a gene therapy that helps heart muscle cells electrically activate in live mice. The first demonstration of its kind, the approach features engineered bacterial genes that code for sodium ion channels and could lead to therapies to treat a wide variety of electrical heart diseases and disorders.

The results appeared online February 2 in the journal Nature Communications.

"We were able to improve how well heart muscle cells can initiate and spread electrical activity, which is hard to accomplish with drugs or other tools," said Nenad Bursac, professor of biomedical engineering at Duke. "The method we used to deliver genes in heart muscle cells of mice has been previously shown to persist for a long time, which means it could effectively help hearts that struggle to beat as regularly as they should."

Sodium-ion channels are proteins in the outer membranes of electrically excitable cells, such as heart or brain cells, that transmit electrical charges into the cell. In the heart, these channels tell muscle cells when to contract and pass the instruction along so that the organ pumps blood as a cohesive unit. Damaged heart cells, however, whether from disease or trauma, often lose all or part of their ability to transmit these signals and join the effort.

One approach researchers can take to restoring this functionality is gene therapy. By delivering the genes responsible for creating sodium channel proteins, the technique can produce more ion channels in the diseased cells to help boost their activity.

In mammals, sodium channel genes are unfortunately too large to fit within the viruses currently used in modern gene therapies in humans. To skirt this issue, Bursac and his laboratory instead turned to smaller genes that code for similar sodium ion channels in bacteria. While these bacterial genes are different than their human counterparts, evolution has conserved many similarities in the channel design since multi-cellular organisms diverged from bacteria hundreds of millions of years ago.

Several years ago, Hung Nguyen, a former doctoral student in Bursac's laboratory who now works for Fujifilm Diosynth Biotechnologies, mutated these bacterial genes so that the channels they encode could become active in human cells. In the new work, current doctoral student Tianyu Wu further optimized the content of the genes and combined them with a "promoter" that exclusively restricts channel production to heart muscle cells. The researchers then tested their approach by delivering a virus loaded with the bacterial gene into veins of a mouse to spread throughout the body.

"We worked to find where the sodium ion channels were actually formed, and, as we hoped, we found that they only went into the working muscle cells of the heart within the atria and ventricles," Wu said. "We also found that they did not end up in the heart cells that originate the heartbeat, which we also wanted to avoid."

This gene therapy approach only delivers extra genes within a cell; it does not attempt to cut out, replace or rewrite the existing DNA in any way. Scientists believe these types of delivered genes make proteins while floating freely within the cell, making use of the existing biochemical machinery. Previous research with this viral gene delivery approach suggests the transplanted genes should remain active for many years.

As a proof of concept, tests on cells in a laboratory setting suggest that the treatment improves electrical excitability enough to prevent human abnormalities like arrhythmias. Within live mice, the results demonstrate that the sodium ion channels are active in the hearts, showing trends toward improved excitability. However, further tests are needed to measure how much of an improvement is made on the whole-heart level, and whether it is enough to rescue electrical function in damaged or diseased heart tissue to be used as a viable treatment.

Moving forward, the researchers have already identified different bacterial sodium channel genes that work better in preliminary benchtop studies. The team is also working with the laboratories of Craig Henriquez, professor of biomedical engineering at Duke, and Andrew Landstrom, director of the Duke Pediatric Research Scholars Program, to test the ability of these genes to restore heart functionality in mouse models that mimic human heart diseases.

Read more at Science Daily

Using the eye as a window into heart disease

Scientists have developed an artificial intelligence (AI) system that can analyse eye scans taken during a routine visit to an optician or eye clinic and identify patients at a high risk of a heart attack.

Doctors have recognised that changes to the tiny blood vessels in the retina are indicators of broader vascular disease, including problems with the heart.

In the research, led by the University of Leeds, deep learning techniques were used to train the AI system to automatically read retinal scans and identify those people who, over the following year, were likely to have a heart attack.

Deep learning is a complex series of algorithms that enable computers to identify patterns in data and to make predictions.

Writing in the journal Nature Machine Intelligence, the researchers report that the AI system had an accuracy of between 70% and 80% and could be used as a second referral mechanism for in-depth cardiovascular investigation.

The use of deep learning in the analysis of retinal scans could revolutionise the way patients are regularly screened for signs of heart disease.

Professor Alex Frangi, who holds the Diamond Jubilee Chair in Computational Medicine at the University of Leeds and is a Turing Fellow at the Alan Turing Institute, supervised the research. He said: "Cardiovascular diseases, including heart attacks, are the leading cause of early death worldwide and the second-largest killer in the UK. This causes chronic ill-health and misery worldwide.

"This technique opens-up the possibility of revolutionising the screening of cardiac disease. Retinal scans are comparatively cheap and routinely used in many optician practices. As a result of automated screening, patients who are at high risk of becoming ill could be referred to specialist cardiac services.

"The scans could also be used to track the early signs of heart disease."

The study involved a worldwide collaboration of scientists, engineers and clinicians from the University of Leeds; Leeds Teaching Hospitals' NHS Trust; the University of York; the Cixi Institute of Biomedical Imaging in Ningbo, part of the Chinese Academy of Sciences; the University of Cote d'Azur, France; the National Centre for Biotechnology Information and the National Eye Institute, both part of the National Institutes for Health in the US; and KU Leuven in Belgium.

The UK Biobank provided data for the study.

Chris Gale, Professor of Cardiovascular Medicine at the University of Leeds and a Consultant Cardiologist at Leeds Teaching Hospitals NHS Trust, was one of the authors of the research paper.

He said: "The AI system has the potential to identify individuals attending routine eye screening who are at higher future risk of cardiovascular disease, whereby preventative treatments could be started earlier to prevent premature cardiovascular disease."

Deep learning

During the deep learning process, the AI system analysed the retinal scans and cardiac scans from more than 5,000 people. The AI system identified associations between pathology in the retina and changes in the patient's heart.

Once the image patterns were learned, the AI system could estimate the size and pumping efficiency of the left ventricle, one of the heart's four chambers, from retinal scans alone. An enlarged ventricle is linked with an increased risk of heart disease.

With information on the estimated size of the left ventricle and its pumping efficiency combined with basic demographic data about the patient, their age and sex, the AI system could make a prediction about their risk of a heart attack over the subsequent 12 months.

Currently, details about the size and pumping efficiency of a patient's left ventricle can only be determined if they have diagnostic tests such as echocardiography or magnetic resonance imaging of the heart. Those diagnostic tests can be expensive and are often only available in a hospital setting, making them inaccessible for people in countries with less well-resourced healthcare systems -- or unnecessarily increasing healthcare costs and waiting times in developed countries.

Read more at Science Daily

My heart will go on: Patient-derived heart cells mimic disease in vitro

How can you mend a broken heart? According to researchers from Japan, in some cases gene replacement therapy just might do the trick.

In a study published in January in Stem Cell Reports, researchers from Osaka University report that heart cells from a patient with an inherited heart disease called arrhythmogenic cardiomyopathy do not contract correctly when grown in the laboratory, and that replacing the mutated gene responsible for this effect fixes this defect.

Arrhythmogenic cardiomyopathy occurs due to mutations in genes involved in desmosomes, which form 'welds' between cells that help them communicate and move in a coordinated way. One of these genes, PKP2, encodes a protein known as plakophilin-2 that is crucial to maintaining heart cell structure.

"Previous studies carried out in cardiomyocytes have shown that mutations in PKP2 play a pathological role in arrhythmogenic cardiomyopathy," says lead author of the study Hiroyuki Inoue. "However, the cells used in those experiments were derived from healthy individuals and were not assessed for contractile function."

To investigate how cells derived from patients behave in the laboratory, the researchers first took a blood sample from a young patient with arrhythmogenic cardiomyopathy, induced some of the blood cells to become stem cells, and then differentiated these stem cells into heart cells. They then modified this original batch of heart cells into three different cell lines with precisely adjusted PKP2 expression based on how many mutated or intact copies of the gene were present.

"The cells with two mutated copies of PKP2 clearly exhibited reduced contractility and impaired desmosome assembly due to plakophilin-2 deficiency," explains Shuichiro Higo, senior author. "These effects were also observed in cells with only one mutated copy of PKP2, although they were less severe."

Replacing the mutated PKP2 with an intact copy of the gene repaired the defects in both cell contraction and desmosome assembly, which the researchers were able to observe using a time-lapse approach and fluorescently labeled desmosomes.

"These findings suggest that our cardiomyocyte cell lines recapitulate the pathology of arrhythmogenic cardiomyopathy and provide a rapid and convenient platform for developing gene-based therapies for this disease," says Higo.

Read more at Science Daily

Successful transplant of porcine heart into adult human with end-stage heart disease

In a first-of-its-kind surgery, a 57-year-old patient with terminal heart disease received a successful transplant of a genetically-modified pig heart and is still doing well three days later. It was the only currently available option for the patient. The historic surgery was conducted by University of Maryland School of Medicine (UMSOM) faculty at the University of Maryland Medical Center (UMMC), together known as the University of Maryland Medicine.

This organ transplant demonstrated for the first time that a genetically-modified animal heart can function like a human heart without immediate rejection by the body. The patient, David Bennett, a Maryland resident, is being carefully monitored over the next days and weeks to determine whether the transplant provides lifesaving benefits. He had been deemed ineligible for a conventional heart transplant at UMMC as well as at several other leading transplant centers that reviewed his medical records.

"It was either die or do this transplant. I want to live. I know it's a shot in the dark, but it's my last choice," said Mr. Bennett, the patient, a day before the surgery was conducted. He had been hospitalized and bedridden for the past few months. "I look forward to getting out of bed after I recover."

The U.S. Food and Drug Administration granted emergency authorization for the surgery on New Year's Eve through its expanded access (compassionate use) provision. It is used when an experimental medical product, in this case the genetically-modified pig's heart, is the only option available for a patient faced with a serious or life-threatening medical condition. The authorization to proceed was granted in the hope of saving the patient's life.

"This was a breakthrough surgery and brings us one step closer to solving the organ shortage crisis. There are simply not enough donor human hearts available to meet the long list of potential recipients," said Bartley P. Griffith, MD, who surgically transplanted the pig heart into the patient. Dr. Griffith is the Thomas E. and Alice Marie Hales Distinguished Professor in Transplant Surgery at UMSOM. "We are proceeding cautiously, but we are also optimistic that this first-in-the-world surgery will provide an important new option for patients in the future."

Considered one of the world's foremost experts on transplanting animal organs, known as xenotransplantation, Muhammad M. Mohiuddin, MD, Professor of Surgery at UMSOM, joined the UMSOM faculty five years ago and established the Cardiac Xenotransplantation Program with Dr. Griffith. Dr. Mohiuddin serves as the program's Scientific/Program Director and Dr. Griffith as its Clinical Director.

"This is the culmination of years of highly complicated research to hone this technique in animals with survival times that have reached beyond nine months. The FDA used our data and data on the experimental pig to authorize the transplant in an end-stage heart disease patient who had no other treatment options," said Dr. Mohiuddin. "The successful procedure provided valuable information to help the medical community improve this potentially life-saving method in future patients."

About 110,000 Americans are currently waiting for an organ transplant, and more than 6,000 patients die each year before getting one, according to the federal government's organdonor.gov. Xenotransplantation could potentially save thousands of lives but does carry a unique set of risks, including the possibility of triggering a dangerous immune response. These responses can trigger an immediate rejection of the organ with a potentially deadly outcome to the patient.

Xenotransplants were first tried in the 1980s, but were largely abandoned after the famous case of Stephanie Fae Beauclair (known as Baby Fae) at Loma Linda University in California. The infant, born with a fatal heart condition, received a baboon heart transplant and died within a month of the procedure due to the immune system's rejection of the foreign heart. However, for many years, pig heart valves have been used successfully for replacing valves in humans.

Before consenting to receive the transplant, Mr. Bennett, the patient, was fully informed of the procedure's risks, and that the procedure was experimental with unknown risks and benefits. He had been admitted to the hospital more than six weeks earlier with life-threatening arrythmia and was connected to a heart-lung bypass machine, called extracorporeal membrane oxygenation (ECMO), to remain alive. In addition to not qualifying to be on the transplant list, he was also deemed ineligible for an artificial heart pump due to his arrhythmia.

Revivicor, a regenerative medicine company based in Blacksburg, VA, provided the genetically-modified pig to the xenotransplantation laboratory at UMSOM. On the morning of the transplant surgery, the surgical team, led by Dr. Griffith and Dr. Mohiuddin, removed the pig's heart and placed it in the XVIVO Heart Box, perfusion device, a machine that keeps the heart preserved until surgery.

The physician-scientists also used a new drug along with conventional anti-rejection drugs, which are designed to suppress the immune system and prevent the body from rejecting the foreign organ. The new drug used is an experimental compound made by Kiniksa Pharmaceuticals.

"This unprecedented and historic procedure highlights the importance of translational research which lays the groundwork for patients to benefit in the future. It is the culmination of our longstanding commitment to discovery and innovation in our xenotransplantation program," said E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine. "Our transplant surgeon-scientists are among the most talented in the country, and are helping to bring the promise of xenotransplantation to fruition. We hope it will one day become a standard of care for patients in need of organ transplants. As has happened throughout our history, the University of Maryland School of Medicine continues to address the most complex medical and scientific problems."

Bruce Jarrell, MD, President of the University of Maryland, Baltimore, who himself is a transplant surgeon, recalled: "Dr. Griffith and I began as organ transplant surgeons when it was in its infancy. Back then, it was the dream of every transplant surgeon, myself included, to achieve xenotransplantation and it is now personally gratifying to me to see this long-sought goal clearly in view. It is a spectacular achievement."

"This is truly a historic, monumental step forward. While we have long been at the forefront of research driving progress toward the promise of xenotransplantation as a viable solution to the organ crisis, many believed this breakthrough would be well into the future," said Bert W. O'Malley, MD, President and CEO, University of Maryland Medical Center. "I couldn't be more proud to say the future is now. Our skilled team of UMMC and UMSOM physician-scientists will continue to advance and adapt medical discovery for patient care that could offer a lifeline for more patients in dire need."

Mohan Suntha, MD, MBA, President and CEO, University of Maryland Medical System, added: "The University of Maryland Medical System is committed to working with our University of Maryland School of Medicine partners to explore, research, and in many cases implement the innovations in patient care that make it possible to improve quality of life and save lives. We appreciate the tremendous courage of this live recipient, who has made an extraordinary decision to participate in this groundbreaking procedure to not only potentially extend his own life, but also for the future benefit of others."

Organs from genetically modified pigs have been the focus of much of the research in xenotransplantation, in part because of physiologic similarities between pigs, human, and nonhuman primates. UMSOM received $15.7 million sponsored research grant to evaluate Revivicor genetically-modified pig UHearts™ in baboon studies.

Three genes -- responsible for rapid antibody-mediated rejection of pig organs by humans -- were "knocked out" in the donor pig. Six human genes responsible for immune acceptance of the pig heart were inserted into the genome. Lastly, one additional gene in the pig was knocked out to prevent excessive growth of the pig heart tissue, which totaled 10 unique gene edits made in the donor pig.

"We are thrilled to support the world-class team of transplant surgeons led by Dr. Griffith and Dr. Mohiuddin at the University of Maryland School of Medicine," said David Ayares, PhD, Chief Scientific Officer of Revivicor, Inc. "This transplant is groundbreaking, and is another step in the investigation of xeno organs for human use."

Dr. Mohiuddin, Dr. Griffith, and their research team spent the past five years perfecting the surgical technique for transplantation of pig hearts into non-human primates. Dr. Mohiuddin's xenotransplant research experience spans over 30 years during which time he demonstrated in peer-reviewed research that genetically-modified pig's hearts can function when placed in the abdomen for as long as three years. Success was dependent on the right combination of genetic modifications to the experimental donor pig UHeart™ and anti-rejection drugs, including some experimental compounds.

"As a cardiothoracic surgeon who does lung transplants, this is an amazing moment in the history of our field. Decades of research here at Maryland and elsewhere have gone into this achievement. This has the potential to revolutionize the field of transplantation by eventually eliminating the organ shortage crisis," said Christine Lau, MD, MBA the Dr. Robert W. Buxton Professor and Chair of the Department of Surgery at UMSOM and Surgeon-in-Chief at UMMC. "This is a continuation of steps to making xenotransplantation a life-saving reality for patients in need."

Read more at Science Daily

Aspirin is linked with increased risk of heart failure in some

Aspirin use is associated with a 26% raised risk of heart failure in people with at least one predisposing factor for the condition. That's the finding of a study published today in ESC Heart Failure, a journal of the European Society of Cardiology (ESC).1 Predisposing factors included smoking, obesity, high blood pressure, high cholesterol, diabetes, and cardiovascular disease.

"This is the first study to report that among individuals with a least one risk factor for heart failure, those taking aspirin were more likely to subsequently develop the condition than those not using the medication," said study author Dr. Blerim Mujaj of the University of Freiburg, Germany. "While the findings require confirmation, they do indicate that the potential link between aspirin and heart failure needs to be clarified."

The influence of aspirin on heart failure is controversial. This study aimed to evaluate its relationship with heart failure incidence in people with and without heart disease and assess whether using the drug is related to a new heart failure diagnosis in those at risk.

The analysis included 30,827 individuals at risk for developing heart failure who were enrolled from Western Europe and the US into the HOMAGE study. "At risk" was defined as one or more of the following: smoking, obesity, high blood pressure, high cholesterol, diabetes and cardiovascular disease. Participants were aged 40 years and above and free of heart failure at baseline. Aspirin use was recorded at enrolment and participants were classified as users or non-users. Participants were followed-up for the first incidence of fatal or non-fatal heart failure requiring hospitalisation.

The average age of participants was 67 years and 34% were women. At baseline, a total of 7,698 participants (25%) were taking aspirin. During the 5.3-year follow-up, 1,330 participants developed heart failure.

The investigators assessed the association between aspirin use and incident heart failure after adjusting for sex, age, body mass index, smoking, alcohol use, blood pressure, heart rate, blood cholesterol, creatinine, hypertension, diabetes, cardiovascular disease, and treatment with renin-angiotensin-aldosterone-system inhibitors, calcium channel blockers, diuretics, beta-blockers and lipid-lowering drugs. Taking aspirin was independently associated with a 26% raised risk of a new heart failure diagnosis.

To check the consistency of the results, the researchers repeated the analysis after matching aspirin users and non-users for heart failure risk factors. In this matched analysis, aspirin was associated with a 26% raised risk of a new heart failure diagnosis. To check the results further, the analysis was repeated after excluding patients with a history of cardiovascular disease. In 22,690 participants (74%) free of cardiovascular disease, aspirin use was associated with a 27% increased risk of incident heart failure.

Dr. Mujaj said: "This was the first large study to investigate the relationship between aspirin use and incident heart failure in individuals with and without heart disease and at least one risk factor. Aspirin is commonly used -- in our study one in four participants were taking the medication. In this population, aspirin use was associated with incident heart failure, independent of other risk factors."

Read more at Science Daily

Only alcohol -- not caffeine, diet or lack of sleep -- might trigger heart rhythm condition

New research from UC San Francisco that tested possible triggers of a common heart condition, including caffeine, sleep deprivation and sleeping on the left side, found that only alcohol use was consistently associated with more episodes of the heart arrhythmia.

The authors conclude that people might be able to reduce their risk of atrial fibrillation (AF) by avoiding certain triggers.

The study is published in JAMA Cardiology and was presented November 14, 2021, at the annual Scientific Sessions of the American Heart Association.

Researchers were surprised to find that although most of the things that participants thought would be related to their AF were not, those in the intervention group still experienced less arrhythmia than the people in a comparison group that was not self-monitoring.

"This suggests that those personalized assessments revealed actionable results," said lead author Gregory Marcus, MD, professor of medicine in the Division of Cardiology at UCSF. "Although caffeine was the most commonly selected trigger for testing, we found no evidence of a near-term relationship between caffeine consumption and atrial fibrillation. In contrast, alcohol consumption most consistently exhibited heightened risks of atrial fibrillation."

Atrial fibrillation contributes to more than 150,000 deaths in the United States each year, reports the federal Centers for Disease Control and Prevention, with the death rate on the rise for more than 20 years.

To learn more about what patients felt was especially important to study about the disease, researchers held a brainstorming session in 2014. Patients said researching individual triggers for AF was their top priority, giving rise to the I-STOP-AFib study, which enabled individuals to test any presumed AF trigger. About 450 people participated, more than half of whom (58 percent) were men, and the overwhelming majority of whom were white (92 percent).

Participants in the randomized clinical trial utilized a mobile electrocardiogram recording device along with a phone app to log potential triggers like drinking alcohol and caffeine, sleeping on the left side or not getting enough sleep, eating a large meal, a cold drink, or sticking to a particular diet, engaging in exercise, or anything else they thought was relevant to their AF. Although participants were most likely to select caffeine as a trigger, there was no association with AF. Recent research from UCSF has similarly failed to demonstrate a relationship between caffeine and arrhythmias -- on the contrary, investigators found it may have a protective effect.

The new study demonstrated that consumption of alcohol was the only trigger that consistently resulted in significantly more self-reported AF episodes.

The individualized testing method, known as n-of-1, did not validate participant-selected triggers for AF. But trial participants did report fewer AF episodes than those in the control group, and the data suggest that behaviors like avoiding alcohol could lessen the chances of having an AF episode.

Read more at Science Daily