Risky relationships: why women are more likely to die of a broken heart

In her new book, heart surgeon Dr Nikki Stamp explores how modern medicine is only beginning to understand the connection between body and emotion

Takotsubo cardiomyopathy commonly known as broken heart syndrome is rare but real. As a heart and lung surgeon, Dr Nikki Stamp has seen a few cases herself, and the phenomenon provides a compelling opening chapter to her first book, Can You Die of a Broken Heart? The title reminds us of when Debbie Reynolds died of a broken heart the day after her daughter, Carrie Fisher, passed away in 2016, but this book rises far above the online pseudoscience accompanying those reports. It is possible to be so affected by grief or shock that a predisposed heart simply cannot cope, and Stamp uses this as an opener to explore the myriad ways modern medicine is only recently understanding (and admitting) to the connection between body and emotion.

Weve sort of come full circle in terms of emotion and health, Stamp says. When early physicians were discovering organs and the body, they actually thought the heart was the centre of emotion, because it was warm and hot and thats where the idea of being hot-blooded came from. And then we got kind of cold and clinical; that your emotions come from the brain, that your emotional state has nothing to do with your physical state, and now weve come full circle and were starting to encompass a more holistic view of health.

Relationships are a great example. There is a trend to suggest that the risk of dying is higher after the loss of someone important and close to you, Stamp says. Conversely, she says, both romantic and platonic relationships are hugely beneficial. Theres a lot of positive physiology and positive actions that happen in the body when youre in a relationship. When you have social connection and emotional connection, it seems that our brains recognise that as something that means youre healthy.

Australian heart and lung surgeon Dr Nikki Stamp. Her book Can You Die of a Broken Heart? argues research into womens heart health has suffered from entrenched gender bias. Photograph: Chris Chen

Good hormones such as serotonin and oxytocin flood the body, preventing inflammation and assisting with blood flow.

The book doesnt sugarcoat the risks of relationships though, and the section about divorce is sobering. One study Stamp notes in the book showed that pain centres in the brain lit up when people were shown photos of their ex-partners, and of course pain and stress have negative effects on the heart.

Its interesting because weve come to a point in culture and in society where were socially more accepting of divorce, yet it still has this profound effect on our health, Stamp says. Divorce puts women under significantly more physiological strain than men, research reveals. When men remarry, their risk of heart attack drops again, but Stamp writes that, for women, divorce means a rewriting of their health prospectus forever: The risks posed by divorce to a womans heart health is on a similar level to that of high blood pressure or smoking. Men married to women, on the other hand, are significantly less likely to have heart attacks in the first place and those who do recover from them much faster than single men or women married to men.

The gendered issues inherent in heart health dont end there either. In fact, Stamp says one of the reasons she started writing Can You Die of a Broken Heart? was because of how scary and frustrating it was that women dont identify with heart disease despite it being the No 1 cause of death in Australian women. The book explains: If youre a woman under 50 years of age and you have a heart attack, then you are twice as likely to die than a man in the same boat.Why? A contributing factor is the dearth of resources put into womens heart health because most of the research has been done by men, on men.

Stamp who is often mistaken for a nurse and referred to by her first name where her male colleagues are addressed with titles explains that gendered issues in the industry affect medicine itself. Women in academic medicine or even in higher levels of medical research in general are quite underrepresented. And whether we like it or not, we all have a bias towards looking at things that are more pertinent to ourselves, she says. So, with all of that, were only just now learning about both the biological and social differences between mens and womens hearts. And because of that, the knowledge isnt there among healthcare practitioners, and so we dont know what to look out for and we dismiss symptoms. Women dont want to seem silly and then they go to their healthcare expert, a doctor or nurse, and they dismiss it as well because the symptoms are strange or because women are more likely to be perceived as being anxious. Its just this storm of complications that mean that womens hearts are so much more at risk.

Photograph: Murdoch Books

The most affecting thing about the book is Stamps infectious admiration for the organ. She describes how breathtaking it was the first time she saw a heart beating inside a chest as though it were love at first sight. Her book is peppered with compelling anecdotes from her professional adventures (when one patient threw a table at her, she responded, No judgment there: grief is a nasty piece of work). A lot of health books seem quite prescriptive and almost paternalistic. I didnt want to write something like that, Stamp says. In the introduction we learn that the very human side of what it is to care for another person is what got her into medicine, and it shows. One patients heart surgery was put on hold so she could marry the love of her life right there in the ward. Two days after her wedding she was wheeled down the same corridor to the operating theatre.

Stamp admits that knowing the effect of heartbreak on her heart hasnt made her superhuman. At times when I was researching this book and learning about the effects of heartbreak it just sort of made me cross at the people who had broken my heart all over again, she says, laughing, But I think I muddle through. One of the sad inevitabilities of life is that heartbreak is going to happen to all of us at some point in time and I just hope that if and when it happens again that I do remember some of this stuff and that I might muddle my way through it just a little bit better.

Can You Die of a Broken Heart? by Dr Nikki Stamp is out now through Murdoch Books

Read more: https://www.theguardian.com/lifeandstyle/2018/feb/24/risky-relationships-why-women-are-more-likely-to-die-of-a-broken-heart

Afternoon heart surgery has lower risk of complications, study suggests

Heart attacks and heart failure less common in patients having heart operations in the afternoon as opposed to the morning, say researchers

Patients undergoing open heart surgery in the afternoon have a lower risk of potentially fatal complications than those undergoing operations in the morning, new research suggests.

The study found that events including heart attacks and heart failure were less common among those who had undergone a valve replacement operation in the afternoon.

The finding appears to be linked to the ability of the heart tissue to recover after being starved of blood supply during surgery an effect the researchers say is influenced by the cells biological or circadian clock.

While the study suggests patients might fare better if they undergo afternoon surgery, Professor David Montaigne, first author of the research from the University of Lille in France, said it also highlighted another approach to reduce complications.

We have to find a drug that can alter the circadian clock to induce a jet lag, he said, noting that it could also help to improve patient outcomes for heart attacks and organ transplantation.

Writing the in Lancet, Montaigne and colleagues report how they looked at the outcomes of 596 patients, half of whom had valve surgery in the morning, and half in the afternoon. While 18% of morning surgery patients experienced a major cardiac event such as a heart attack or heart failure in the following 500 days, only 9% of those who had afternoon surgery experienced such events.

The team then randomly assigned 88 valve surgery patients to either morning or afternoon operations and monitored levels of a protein in their blood linked to heart tissue damage.

The results reveal that afternoon surgery patients had lower levels of the protein after their operation, suggesting about 20% less damage to the heart than those who underwent morning surgery.

Delving deeper, the team took biopsies from 14 morning surgery patients and 16 afternoon surgery patients, finding that tissue from the latter recovered better after being deprived of oxygen.

Further analysis found 287 genes within the cells that showed different levels of activity depending on whether the cells were from morning or afternoon patients genes which have, in many cases, previously been linked to the circadian clock.

With a time-of-day effect also found in the recovery of mouse heart tissue, the team explored the impact of tinkering with the activity linked to one of the body clock genes, both using drugs and by looking at mice without the gene. Both approaches improved the recovery of the heart tissue at the time of day when it was typically worse.

Dr John ONeill, an expert in circadian rhythms from the MRC Laboratory of Molecular Biology, said the research backed up previous work in mice and fruitflies that had explored the genes involved in the body clock work which scooped a trio of scientists the Nobel prize for medicine earlier this month.

The biological clock, the circadian rhythm, is in every single cell of the body, therefore it affects the biological activity of each cell type, commensurate with the function of those cells, he said, adding that in healthy humans the heart is known to follow a daily pattern of activity and is not at its optimum performance in the morning.

But, he noted, since systems including that of inflammation are also influenced by circadian rhythms, they too might play a role in the different outcomes for morning and afternoon surgeries.

Whats more, said ONeill, the study did not consider whether the surgeons performed the operation better in the afternoon, adding that more work was need to explore whether the findings would hold for patients at other hospitals, or for other types of surgery.

It is not the case that every single medical intervention is necessarily going to be best dealt with in the afternoon, he said, adding that the research did not mean that patients should try to jet lag themselves before surgery.

Professor Bryan Williams, chair of medicine at University College London, described the new research as fascinating and elegant, adding that the study builds on the fact that cardiovascular events, such as heart attacks, are more common in the morning. What this research suggests is that an intrinsic body clock within cells of the heart may render these cells more susceptible to injury during cardiac surgery in the morning versus the afternoon, he said.

But Williams agreed that it was too soon to consider rescheduling heart surgeries to the afternoon, and that large-scale, robust clinical trials would be needed to probe the effect further. This would be needed to change practice because the logistical implications of doing so would be huge and require definitive proof that there is a real benefit, he said.

Read more: https://www.theguardian.com/science/2017/oct/26/afternoon-heart-surgery-has-lower-risk-of-complications-study-suggests

Blood-thinning drugs ‘can reduce risk of dementia by up to 48%’

Research strongly suggests that patients taking anticoagulants for irregular heartbeat could be protected against dementia and stroke

Blood-thinning drugs could protect against dementia and stroke in people with an irregular heartbeat, research suggests.

A study found that patients being treated for atrial fibrillation (AF) were less likely to develop dementia if they were taking anticoagulants. Their risk was reduced by up to 48% compared with others with the same condition who were not prescribed the drugs.

Scientists analysed health record data from more than 444,000 Swedish AF patients.

While the findings could not prove cause and effect, they strongly suggested blood-thinning pills protect against dementia in patients with the condition, the team said.

Atrial fibrillation increases the risk of stroke and blood clots, which some experts think may appear in the brain and help trigger dementia.

Dr Leif Friberg from the Karolinska Institute in Stockholm, Sweden, who co-led the study, said: As a clinician I know there are AF patients who have a fatalistic view on stroke. Either it happens or it does not. Few patients are fatalistic about dementia, which gradually makes you lose your mind.

No brain can withstand a constant bombardment of microscopic clots in the long run. Patients probably want to hang on to as many of their little grey cells for as long as they can.

In order to preserve what youve got, you should take care to use anticoagulants if you are diagnosed with AF, as they have been proved to protect against stroke and, which this study indicates, also appear to protect against dementia.

The researchers identified everyone in Sweden who had been given a diagnosis of AF between 2006 and 2014. Monitoring each persons progress provided 1.5m years of follow-up during which 26,210 patients were diagnosed with dementia.

Prescribed blood thinners include the drugs warfarin, apixaban, dabigatran, edoxaban and rivaroxaban. Their protective effect was greater the earlier treatment started after a diagnosis of AF, the scientists found.

Friberg said patients should begin taking the drugs as soon as possible and continue using them.

He added: Doctors should not tell their patients to stop using oral anticoagulants without a really good reason. To patients, I would say dont stop unless your doctor says so.

The study, published in the European Heart Journal, found no difference in dementia prevention between the older blood-thinning drug warfarin and newer anticoagulants.

Prof Jeremy Pearson, associate medical director at the British Heart Foundation, said: Strokes caused by a clot blocking the blood vessels in the brain are a major cause of dementia, and atrial fibrillation is an important risk factor as it increases the chances of these clots forming.

By treating AF patients with blood-thinning drugs, you reduce the risk of both stroke and dementia.

Dr Carol Routledge, head of science at Alzheimers Research UK, said: The findings highlight a need to investigate this link further, but the nature of the study prevents us from firmly concluding that anticoagulants reduce the risk of dementia.

It will be important to see the results of other ongoing studies in this area, as well as teasing apart the exact relationship between anticoagulants and the risk of different types of dementia.

Read more: https://www.theguardian.com/science/2017/oct/25/blood-thinning-pills-irregular-heartbeat-patients-dementia-stroke

No, a standing desk isn’t as unhealthy as smoking

Does a new study really claim that standing at work is as unhealthy as a cigarette a day? Closer inspection suggests probably not

A headline in the Independent today has proclaimed that standing at work is as unhealthy as a cigarette a day, citing a new study published in the American Journal of Epidemiology. Illustrated with a picture of a woman bent over her standing desk clutching at her back, were instructed to sit back down.

But a closer look at the research in question reveals very little to do with standing desks. In fact, the study did not look at standing desks at all. The research was conducted on a sample of 7,320 residents of Ontario, Canada, followed up for over a decade. And its findings are striking people whose job requires them to stand for long periods of time were twice as likely to contract heart disease compared to those who do jobs that predominantly involve being seated.

So should we all lower our standing desks and recover our office chairs from wherever weve stashed them? I am not going to rush to do so (at this point I should fess up and say I have used a standing desk for the past three years and I love it).

Firstly, did the researchers ask people whether they stood or sat at work? No, they did not. People were categorised by the job they did. This immediately means that if youre an office worker with a standing desk, youll be categorised as a sitter, because thats predominantly what office workers do. The supplementary table of the paper lists a number of common jobs and how they were categorised for the study. Seated jobs included truck drivers, administrative officers, secretaries, professional occupations in business services and accounting clerks. Standing jobs on the other hand included retail salespersons, cooks, food and beverage servers and machine or tool operators.

Now here we get on to the classic problem with observational epidemiology. People who work different types of jobs are going to be different in loads of ways other than their jobs, all of which might also impact on risk of heart disease. This is called confounding. The authors of the study take a number of these in to account, for example pre-existing health conditions, whether the person smokes, whether they were obese, and various others. But its very hard to be sure that youve taken all of the potential confounding factors like these in to account. There could very easily be other differences rather than just whether a person is more likely to be standing or sitting. For example how much they exercise could have a big impact. Perhaps, as one person on Twitter suggested to me, after a day on your feet youre less inclined to go for a run of an evening.

Also, as can be seen from the list of jobs theyve included in each group, there might be socio-economic differences between people who do jobs that require standing at work and those who are more likely to sit and these might be related to how good your diet is, how much disposable income you have, all things that sadly are associated with ill health. Even if you attempt to take these factors in to account in a statistical model, if youre relying on self-reported or large scale data its almost impossible to be sure youve really accounted for all the variability.

So while this study is really interesting, and might indicate that jobs where youre more likely to stand are linked to an increased risk of heart disease, personally I think theres a little more going on than simply that we should all sit down at work if we want to protect our hearts. Not to mention that this study has absolutely nothing to do with standing desks, and didnt actually ask the individuals included whether they did stand or sit at work, but inferred it from the type of job they did. Im not lowering my standing desk just yet.

Read more: https://www.theguardian.com/science/sifting-the-evidence/2017/sep/21/no-a-standing-desk-isnt-as-unhealthy-as-smoking

New heart treatment is biggest breakthrough since statins, scientists say

US researchers find heart attack survivors given anti-inflammatory injections have fewer future episodes and lower cancer risk

Anti-inflammatory injections could lower the risk of heart attacks and may slow the progression of cancer, a study has found, in what researchers say is the biggest breakthrough since the discovery of statins.

Heart attack survivors given injections of a targeted anti-inflammatory drug called canakinumab had fewer attacks in the future, scientists found. Cancer deaths were also halved in those treated with the drug, which is normally used only for rare inflammatory conditions.

Statins are the mainstay drugs for heart attack prevention and work primarily by lowering cholesterol levels. But a quarter of people who have one heart attack will suffer another within five years despite taking statins regularly. It is believed this is because of unchecked inflammation within the hearts arteries.

The research team, led from Brigham and Womens hospital in Boston, tested whether targeting the inflammation with a potent anti-inflammatory agent would provide an extra benefit over statin treatment.

The researchers enrolled more than 10,000 patients who had had a heart attack and had a positive blood test for inflammation into the trial, known as the Cantos study. All patients received high doses of statins as well as either canakinumab or a placebo, both administered by injection every three months. The trial lasted for four years.

For patients who received the canakinumab injections the team reported a 15% reduction in the risk of a cardiovascular event, including fatal and non-fatal heart attacks and strokes. Also, the need for expensive interventional procedures, such as bypass surgery and inserting stents, was cut by more than 30%. There was no overall difference in death rates between patients on canakinumab and those given placebo injections, and the drug did not change cholesterol levels.

Dr Paul Ridker, who led the research team, said the study ushers in a new era of therapeutics.

For the first time, weve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk, he said.

This has far-reaching implications. It tells us that by leveraging an entirely new way to treat patients targeting inflammation we may be able to significantly improve outcomes for certain very high-risk populations.

The hospital said the reductions in risk were above and beyond those seen in patients who only took statins.

Ridker said the study showed that the use of anti-inflammatories was the next big breakthrough following the linkage of lifestyle issues and then statins.

In my lifetime, Ive gotten to see three broad eras of preventative cardiology, he said. In the first, we recognised the importance of diet, exercise and smoking cessation. In the second, we saw the tremendous value of lipid-lowering drugs such as statins. Now, were cracking the door open on the third era. This is very exciting.

But there were some downsides to the treatment. The researchers reported an increase in the chances of dying from a severe infection of about one for every 1,000 people treated, although this was offset by an unexpected halving of cancer deaths across all cancer types. In particular, the odds of succumbing to lung cancer were cut by over 75%, for reasons the team do not yet understand. The researchers are planning further trials to investigate canakinumabs potentially protective effect against cancer.

Prof Martin Bennett, a cardiologist from Cambridge who was not involved in the study, said the trial results were an important advance in understanding why heart attacks happen. But, he said, he had concerns about the side effects, the high cost of the drug and the fact that death rates were not better in those given the drug.

Treatment of UK patients is unlikely to change very much as a result of this trial, but the results do support investigation of other drugs that inhibit inflammation for cardiovascular disease, and the use of this drug in cancer, he said.

Prof Jeremy Pearson, associate medical director at the British Heart Foundation, was optimistic about the trial opening the door to new types of treatment for heart attacks.

Nearly 200,000 people are hospitalised due to heart attacks every year in the UK, Pearson said. Cholesterol-lowering drugs like statins are given to these people to reduce their risk of another heart attack and this undoubtedly saves lives. But we know that lowering cholesterol alone is not always enough.

These exciting and long-awaited trial results finally confirm that ongoing inflammation contributes to risk of heart disease, and [lowering it] could help save lives.

Read more: https://www.theguardian.com/science/2017/aug/27/anti-inflammatory-drugs-may-lower-heart-attack-risk-study-finds

6 million middle-aged people take no exercise

Public Health Englands research suggests large numbers of adults do not walk for 10 minutes at a time once a month

About 6 million middle-aged people in England are endangering their health by not taking so much as a brisk walk once a month, government advisers have said.

Clinicians said such a lack of exercise increases an individuals risk of prematurely developing serious health conditions including type 2 diabetes, heart disease, dementia and cancer.

Public Health England (PHE) said 41% of the 15.3 million English adults aged 40 to 60 walk less than 10 minutes continuously each month at a brisk pace of at least 3mph.

PHE has launched a health campaign targeting the sedentary middle-aged by encouraging them to walk to the shop instead of using a car and to take up walking on lunch breaks to add many healthy years to their lives.

Health leaders believe that 10 minutes walking a day is likely to be seen as achievable by people who are chronically inactive and that the health benefits include increased fitness, improved mood, a healthier body weight and a 15% reduction in the risk of dying prematurely.

PHE said walking required no skill, facilities or equipment and was more accessible and acceptable than other forms of physical activity for most people. Guidance issued by the UKs four chief medical officers in 2011 instructed the British population on how much exercise they should be participating in each week.

They said that adults should do at least two and a half hours of moderately intensive activity a week.

The PHE report said a quarter of the English population are inactive, doing less than 30 minutes of exercise a week. For some of these individuals 150 minutes may seem an unrealistic aim, according to the PHE report.

PHEs One You campaign is urging those people to take up the challenge of walking briskly for 10 minutes a day. As part of the drive it has released the Active 10 app which will help users achieve the goal and GPs will be recommending it to their patients to help build up their activity levels.

Dr Jenny Harries, the deputy medical director of PHE, said: I know first hand that juggling the priorities of everyday life often means exercise takes a back seat.
Walking to the shops instead of driving or going for a brisk 10-minute walk on your lunch break each day can add many healthy years to your life. The Active 10 app is a free and easy way to help anyone build more brisk walking into their daily routine.

Prof Sir Muir Gray, a clinical adviser for the Active 10 app and the One You campaign, added: We all know physical activity is good for your health but for the first time were seeing the effects that easily achievable changes can make. By walking just 10 continuous minutes at a brisk pace every day, an individual can reduce their risk of early death by 15%.

They can also prevent or delay the onset of disability and further reduce their risk of serious health conditions, such as type 2 diabetes, heart disease, dementia and some cancers.

Read more: https://www.theguardian.com/lifeandstyle/2017/aug/24/around-6-million-middle-aged-english-people-take-no-exercise

Robot hearts: medicines new frontier

The long read: From bovine valves to electrical motors and 3-D printed hearts, cardiologists are forging ahead with technologies once dismissed as crazy ideas

On a cold, bright January morning I walked south across Westminster Bridge to St Thomas Hospital, an institution with a proud tradition of innovation: I was there to observe a procedure generally regarded as the greatest advance in cardiac surgery since the turn of the millennium and one that can be performed without a surgeon.

The patient was a man in his 80s with aortic stenosis, a narrowed valve which was restricting outflow from the left ventricle into the aorta. His heart struggled to pump sufficient blood through the reduced aperture, and the muscle of the affected ventricle had thickened as the organ tried to compensate. If left unchecked, this would eventually lead to heart failure. For a healthier patient the solution would be simple: an operation to remove the diseased valve and replace it with a prosthesis. But the mans age and a long list of other medical conditions made open-heart surgery out of the question. Happily, for the last few years, another option has been available for such high-risk patients: transcatheter aortic valve implantation, known as TAVI for short.

This is a non-invasive procedure, and takes place not in an operating theatre but in the catheterisation laboratory, known as the cath lab. When I got there, wearing a heavy lead gown to protect me from X-rays, the patient was already lying on the table. He would remain awake throughout the procedure, receiving only a sedative and a powerful analgesic. I was shown the valve to be implanted, three leaflets fashioned from bovine pericardium (a tough membrane from around the heart of a cow), fixed inside a collapsible metal stent. After being soaked in saline it was crimped on to a balloon catheter and squeezed, from the size and shape of a lipstick, into a long, thin object like a pencil.

The consultant cardiologist, Bernard Prendergast, had already threaded a guidewire through an incision in the patients groin, entering the femoral artery and then the aorta, until the tip of the wire had arrived at the diseased aortic valve. The catheter, with its precious cargo, was then placed over the guidewire and pushed gently up the aorta. When it reached the upper part of the vessel we could track its progress on one of the large X-ray screens above the table. We watched intently as the metal stent described a slow curve around the aortic arch before coming to rest just above the heart.

There was a pause as the team checked everything was ready, while on the screen the silhouette of the furled valve oscillated gently as it was buffeted by pulses of high-pressure arterial blood. When Prendergast was satisfied that the catheter was precisely aligned with the aortic valve, he pressed a button to inflate the tiny balloon. As it expanded it forced the metal stent outwards and back to its normal diameter, and on the X-ray monitor it suddenly snapped into position, firmly anchored at the top of the ventricle. For a second or two the patient became agitated as the balloon obstructed the aorta and stopped the flow of blood to his brain; but as soon as it was deflated he became calm again.

Prendergast and his colleagues peered at the monitors to check the positioning of the device. In a conventional operation the diseased valve would be excised before the prosthesis was sewn in; during a TAVI procedure the old valve is left untouched and the new one simply placed inside it. This makes correct placement vital, since unless the device fits snugly there may be a leak around its edge. The X-ray picture showed that the new valve was securely anchored and moving in unison with the heart. Satisfied that everything had gone according to plan, Prendergast removed the catheter and announced the good news in a voice that was probably audible on the other side of the river. Just minutes after being given a new heart valve, the patient raised an arm from under the drapes and shook the cardiologists hand warmly. The entire procedure had taken less than an hour.

According to many experts, this is what the future will look like. Though available for little more than a decade, TAVI is already having a dramatic impact on surgical practice: in Germany the majority of aortic valve replacements, more than 10,000 a year, are now performed using the catheter rather than the scalpel.

In the UK, the figure is much lower, since the procedure is still significantly more expensive than surgery this is largely down to the cost of the valve itself, which can be as much as 20,000 for a single device. But as the manufacturers recoup their initial outlay on research and development, it is likely to become more affordable and its advantages are numerous. Early results suggest that it is every bit as effective as open-heart surgery, without many of surgerys undesirable aspects: the large chest incision, the heart-lung machine, the long period of post-operative recovery.

The essential idea of TAVI was first suggested more than half a century ago. In 1965, Hywel Davies, a cardiologist at Guys Hospital in London, was mulling over the problem of aortic regurgitation, in which blood flows backwards from the aorta into the heart. He was looking for a short-term therapy for patients too sick for immediate surgery something that would allow them to recover for a few days or weeks, until they were strong enough to undergo an operation. He hit upon the idea of a temporary device that could be inserted through a blood vessel, and designed a simple artificial valve resembling a conical parachute. Because it was made from fabric, it could be collapsed and mounted on to a catheter. It was inserted with the top of the parachute uppermost, so that any backwards flow would be caught by its inside surface like air hitting the underside of a real parachute canopy. As the fabric filled with blood it would balloon outwards, sealing the vessel and stopping most of the anomalous blood flow.

This was a truly imaginative suggestion, made at a time when catheter therapies had barely been conceived of, let alone tested. But, in tests on dogs, Davies found that his prototype tended to provoke blood clots and he was never able to use it on a patient.

Doctors perform minimally invasive heart surgery on a patient. Photograph: Steve Russell/Toronto Star via Getty Images

Another two decades passed before anybody considered anything similar. That moment came in 1988, when a trainee cardiologist from Denmark, Henning Rud Andersen, was at a conference in Arizona, attending a lecture about coronary artery stenting. It was the first he had heard of the technique, which at the time had been used in only a few dozen patients, and as he sat in the auditorium he had a thought, which at first he dismissed as ridiculous: why not make a bigger stent, put a valve in the middle of it, and implant it into the heart via a catheter? On reflection, he realised that this was not such an absurd idea, and when he returned home to Denmark he visited a local butcher to buy a supply of pig hearts. Working in a pokey room in the basement of his hospital with basic tools obtained from a local DIY warehouse, Andersen constructed his first experimental prototypes. He began by cutting out the aortic valves from the pig hearts, mounted each inside a home-made metal lattice then compressed the whole contraption around a balloon.

Within a few months Andersen was ready to test the device in animals, and on 1 May 1989 he implanted the first in a pig. It thrived with its prosthesis, and Andersen assumed that his colleagues would be excited by his works obvious clinical potential. But nobody was prepared to take the concept seriously folding up a valve and then unfurling it inside the heart seemed wilfully eccentric and it took him several years to find a journal willing to publish his research.

When his paper was finally published in 1992, none of the major biotechnology firms showed any interest in developing the device. Andersens crazy idea worked, but still it sank without trace.

Andersen sold his patent and moved on to other things. But at the turn of the century there was a sudden explosion of interest in the idea of valve implantation via catheter. In 2000, a heart specialist in London, Philipp Bonhoeffer, replaced the diseased pulmonary valve of a 12-year-old boy, using a valve taken from a cows jugular vein, which had been mounted in a stent and put in position using a balloon catheter.

In France, another cardiologist was already working on doing the same for the aortic valve. Alain Cribier had been developing novel catheter therapies for years; it was his company that bought Andersens patent in 1995, and Cribier had persisted with the idea even after one potential investor told him that TAVI was the most stupid project ever heard of.

Eventually, Cribier managed to raise the necessary funds for development and long-term testing, and by 2000 had a working prototype. Rather than use an entire valve cut from a dead heart, as Andersen had, Cribier built one from bovine pericardium, mounted in a collapsible stainless-steel stent. Prototypes were implanted in sheep to test their durability: after two-and-a-half years, during which they opened and closed more than 100m times, the valves still worked perfectly.

Cribier was ready to test the device in humans, but his first patient could not be eligible for conventional surgical valve replacement, which is safe and highly effective: to test an unproven new procedure on such a patient would be to expose them to unnecessary risk.

In early 2002, he was introduced to a 57-year-old man who was, in surgical terms, a hopeless case. He had catastrophic aortic stenosis which had so weakened his heart that with each stroke it could pump less than a quarter of the normal volume of blood; in addition, the blood vessels of his extremities were ravaged by atherosclerosis, and he had chronic pancreatitis and lung cancer. Several surgeons had declined to operate on him, and his referral to Cribiers clinic in Rouen was a final roll of the dice. An initial attempt to open the stenotic valve using a simple balloon catheter failed, and a week after this treatment Cribier recorded in his notes that his patient was near death, with his heart barely functioning. The mans family agreed that an experimental treatment was preferable to none at all, and on 16 April he became the first person to receive a new aortic valve without open-heart surgery.

Over the next couple of days the patients condition improved dramatically: he was able to get out of bed, and the signs of heart failure began to retreat. But shortly afterwards complications arose, most seriously a deterioration in the condition of the blood vessels in his right leg, which had to be amputated 10 weeks later. Infection set in, and four months after the operation, he died.

He had not lived long nobody expected him to but the episode had proved the feasibility of the approach, with clear short-term benefit to the patient. When Cribier presented a video of the operation to colleagues they sat in stupefied silence, realising that they were watching something that would change the nature of heart surgery.

When surgeons and cardiologists overcame their initial scepticism about TAVI they quickly realised that it opened up a vista of exciting new surgical possibilities. As well as replacing diseased valves it is now also possible to repair them, using clever imitations of the techniques used by surgeons. The technology is still in its infancy, but many experts believe that this will eventually become the default option for valvular disease, making surgery increasingly rare.

While TAVI is impressive, there is one even more spectacular example of the capabilities of the catheter. Paediatric cardiologists at a few specialist centres have recently started using it to break the last taboo of heart surgery operating on an unborn child. Nowhere is the progress of cardiac surgery more stunning than in the field of congenital heart disease. Malformations of the heart are the most common form of birth defect, with as many as 5% of all babies born with some sort of cardiac anomaly though most of these will cause no serious, lasting problems. The heart is especially prone to abnormal development in the womb, with a myriad of possible ways in which its structures can be distorted or transposed. Over several decades, specialists have managed to find ways of taming most; but one that remains a significant challenge to even the best surgeon is hypoplastic left heart syndrome (HLHS), in which the entire left side of the heart fails to develop properly. The ventricle and aorta are much smaller than they should be, and the mitral valve is either absent or undersized. Until the early 1980s this was a defect that killed babies within days of birth, but a sequence of complex palliative operations now makes it possible for many to live into adulthood.

Because their left ventricle is incapable of propelling oxygenated blood into the body, babies born with HLHS can only survive if there is some communication between the pulmonary and systemic circulations, allowing the right ventricle to pump blood both to the lungs and to the rest of the body. Some children with HLHS also have an atrial septal defect (ASD), a persistent hole in the tissue between the atria of the heart which improves their chances of survival by increasing the amount of oxygenated blood that reaches the sole functioning pumping chamber. When surgeons realised that this defect conferred a survival benefit in babies with HLHS, they began to create one artificially in those with an intact septum, usually a few hours after birth. But it was already too late: elevated blood pressure was causing permanent damage to the delicate vessels of the lungs while these babies still in the womb.

A prototype of a fully implantable artificial heart, as presented by the French heart specialist Alain Carpentier. Photograph: Jacques Brinon/AP

The logical albeit risky response was to intervene even earlier. In 2000, a team at Boston Childrens Hospital adopted a new procedure to create an ASD during the final trimester of pregnancy: they would deliberately create one heart defect in order to treat another. A needle was passed through the wall of the uterus and into the babys heart, and a balloon catheter used to create a hole between the left and right atria. This reduced the pressures in the pulmonary circulation and hence limited the damage to the lungs; but the tissues of a growing foetus have a remarkable ability to repair themselves, and the artificially created hole would often heal within a few weeks. Cardiologists needed to find a way of keeping it open until birth, when surgeons would be able to perform a more comprehensive repair.

In September 2005 a couple from Virginia, Angela and Jay VanDerwerken, visited their local hospital for a routine antenatal scan. They were devastated to learn that their unborn child had HLHS, and the prognosis was poor. The ultrasound pictures revealed an intact septum, making it likely that even before birth her lungs would be damaged beyond repair. They were told that they could either terminate the pregnancy or accept that their daughter would have to undergo open-heart surgery within hours of her birth, with only a 20% chance that she would survive.

Devastated, the VanDerwerkens returned home, where Angela researched the condition online. Although few hospitals offered any treatment for HLHS, she found several references to the Boston foetal cardiac intervention programme, the team of doctors that had pioneered the use of the balloon catheter during pregnancy.

They arranged an appointment with Wayne Tworetzky, the director of foetal cardiology at Boston Childrens Hospital, who performed a scan and confirmed that their unborn childs condition was treatable. A greying, softly spoken South African, Tworetzky explained that his team had recently developed a new procedure, but that it had never been tested on a patient. It would mean not just making a hole in the septum, but also inserting a device to prevent it from closing. The VanDerwerkens had few qualms about accepting the opportunity: the alternatives gave their daughter a negligible chance of life.

The procedure took place at Brigham and Womens Hospital in Boston on 7 November 2005, 30 weeks into the pregnancy, in a crowded operating theatre. Sixteen doctors, with a range of specialisms, took part: cardiologists, surgeons, and four anaesthetists two to look after the mother, two for her unborn child. Mother and child needed to be completely immobilised during a delicate procedure lasting several hours, so both were given a general anaesthetic. The team watched on the screen of an ultrasound scanner as a thin needle was guided through the wall of the uterus, then the foetuss chest and finally into her heart an object the size of a grape.

A guidewire was placed in the cardiac chambers, then a tiny balloon catheter was inserted and used to create an opening in the atrial septum. This had all been done before; but now the cardiologists added a refinement. The balloon was withdrawn, then returned to the heart, this time loaded with a 2.5 millimetre stent that was set in the opening between the left and right atria. There was a charged silence as the balloon was inflated to expand the stent; then, as the team saw on the monitor that blood was flowing freely through the aperture, the room erupted in cheers.

Grace VanDerwerken was born in early January after a normal labour, and shortly afterwards underwent open-heart surgery. After a fortnight she was allowed home, her healthy pink complexion proving that the interventions had succeeded in producing a functional circulation.

But just when she seemed to be out of danger, Grace died suddenly at the age of 36 days not as a consequence of the surgery, but from a rare arrhythmia, a complication of HLHS that occurs in just 5%. This was the cruellest luck, when she had seemingly overcome the grim odds against her. Her death was a tragic loss, but her parents courage had brought about a new era in foetal surgery.

Much of the most exciting contemporary research focuses on the greatest, most fundamental cardiac question of all: what can the surgeon do about the failing heart? Half a century after Christiaan Barnard performed the first human heart transplant, transplantation remains the gold standard of care for patients in irreversible heart failure once drugs have ceased to be effective. It is an excellent operation, too, with patients surviving an average of 15 years. But it will never be the panacea that many predicted, because there just arent enough donor hearts to go round.

With too few organs available, surgeons have had to think laterally. As a result, a new generation of artificial hearts is now in development. Several companies are now working on artificial hearts with tiny rotary electrical motors. In addition to being much smaller and more efficient than pneumatic pumps, these devices are far more durable, since the rotors that impel the blood are suspended magnetically and are not subject to the wear and tear caused by friction. Animal trials have shown promising results, but, as yet, none of these have been implanted in a patient.

Another type of total artificial heart, as such devices are known, has, however, recently been tested in humans. Alain Carpentier, an eminent French surgeon still active in his ninth decade, has collaborated with engineers from the French aeronautical firm Airbus to design a pulsatile, hydraulically powered device whose unique feature is the use of bioprosthetic materials both organic and synthetic matter. Unlike earlier artificial hearts, its design mimics the shape of the natural organ; the internal surfaces are lined with preserved bovine pericardial tissue, a biological surface far kinder to the red blood cells than the polymers previously used. Carpentiers artificial heart was first implanted in December 2013. Although the first four patients have since died two following component failures the results were encouraging, and a larger clinical trial is now under way.

Christiaan Barnard having dinner in Monte Carlo with Princess Grace of Monaco. Photograph: AP

One drawback to the artificial heart still leads many surgeons to dismiss the entire concept out of hand: the price tag. These high-precision devices cost in excess of 100,000 each, and no healthcare service in the world, publicly or privately funded, could afford to provide them to everybody in need of one. And there is one still more tantalising notion: that we will one day be able to engineer spare parts for the heart, or even an entire organ, in the laboratory.

In the 1980s, surgeons began to fabricate artificial skin for burns patients, seeding sheets of collagen or polymer with specialised cells in the hope that they would multiply and form a skin-like protective layer. But researchers had loftier ambitions, and a new field tissue engineering began to emerge.

High on the list of priorities for tissue engineers was the creation of artificial blood vessels, which would have applications across the full range of surgical specialisms. In 1999 surgeons in Tokyo performed a remarkable operation in which they gave a four-year-old girl a new artery grown from cells taken from elsewhere in her body. She had been born with a rare congenital defect which had completely obliterated the right branch of her pulmonary artery, the vessel conveying blood to the right lung. A short section of vein was excised from her leg, and cells from its inside wall were removed in the laboratory. They were then left to multiply in a bioreactor, a vessel that bathed them in a warm nutrient broth, simulating conditions inside the body.

After eight weeks, they had increased in number to more than 12m, and were used to seed the inside of a polymer tube which functioned as a scaffold for the new vessel. The tissue was allowed to continue growing for 10 days, and then the graft was transplanted. Two months later the polymer scaffold around the tissue, designed to break down inside the body, had completely dissolved, leaving only new tissue that would it was hoped grow with the patient.

At the turn of the millennium, a new world of possibility opened up when researchers gained a powerful new tool: stem cell technology. Stem cells are not specialised to one function but have the potential to develop into many different tissue types. One type of stem cell is found in growing embryos, and another in parts of the adult body, including the bone marrow (where they generate the cells of the blood and immune system) and skin. In 1998 James Thomson, a biologist at the University of Wisconsin, succeeded in isolating stem cells from human embryos and growing them in the laboratory.

But an arguably even more important breakthrough came nine years later, when Shinya Yamanaka, a researcher at Kyoto University, showed that it was possible to genetically reprogram skin cells and convert them into stem cells. The implications were enormous. In theory, it would now be possible to harvest mature, specialised cells from a patient, reprogram them as stem cells, then choose which type of tissue they would become.

Sanjay Sinha, a cardiologist at the University of Cambridge, is attempting to grow a patch of artificial myocardium (heart muscle tissue) in the laboratory for later implantation in the operating theatre. His technique starts with undifferentiated stem cells, which are then encouraged to develop into several types of specialised cell. These are then seeded on to a scaffold made from collagen, a tough protein found in connective tissue. The presence of several different cell types means that when they have had time to proliferate, the new tissue will develop its own blood supply.

Clinical trials are still some years away, but Sinha hopes that one day it will be possible to repair a damaged heart by sewing one of these patches over areas of muscle scarred by a heart attack.

Using advanced tissue-engineering techniques, researchers have already succeeded in creating replacement valves from the patients own tissue. This can be done by harvesting cells from elsewhere in the body (usually the blood vessels) and breeding them in a bioreactor, before seeding them on to a biodegradable polymer scaffold designed in the shape of a valve. Once the cells are in place they are allowed to proliferate before implantation, after which the scaffold melts away, leaving nothing but new tissue. The one major disadvantage of this approach is that each valve has to be tailor-made for a specific patient, a process that takes weeks. In the last couple of years, a group in Berlin has refined the process by tissue-engineering a valve and then stripping it of cellular material, leaving behind just the extracellular matrix the structure that holds the cells in position.

The end result is therefore not quite a valve, but a skeleton on which the body lays down new tissue. Valves manufactured in this way can be implanted, via catheter, in anybody; moreover, unlike conventional prosthetic devices, if the recipient is a child the new valve should grow with them.

If it is possible to tissue-engineer a valve, then why not an entire heart? For many researchers this has come to be the ultimate prize, and the idea is not necessarily as fanciful as it first appears.

In 2008, a team led by Doris Taylor, a scientist at the University of Minnesota, announced the creation of the worlds first bioartificial heart composed of both living and manufactured parts. They began by pumping detergents through hearts excised from rats. This removed all the cellular tissue from them, leaving a ghostly heart-shaped skeleton of extracellular matrix and connective fibre, which was used as a scaffold onto which cardiac or blood-vessel cells were seeded. The organ was then cultured in a bioreactor to encourage cell multiplication, with blood constantly perfused through the coronary arteries. After four days, it was possible to see the new tissue contracting, and after a week the heart was even capable of pumping blood though only 2% of its normal volume.

This was a brilliant achievement, but scaling the procedure up to generate a human-sized heart is made far more difficult by the much greater number of cells required. Surgeons in Heidelberg have since applied similar techniques to generate a human-sized cardiac scaffold covered in living tissue. The original heart came from a pig, and after it had been decellularised it was populated with human vascular cells and cardiac cells harvested from a newborn rat. After 10 days the walls of the organ had become lined with new myocardium which even showed signs of electrical activity. As a proof of concept, the experiment was a success, though after three weeks of culture the organ could neither contract nor pump blood.

A surgeon using a catheter during an operation. Photograph: Kent Nishimura/Denver Post via Getty Images

Growing tissues and organs in a bioreactor is a laborious business, but recent improvements in 3D printing offer the tantalising possibility of manufacturing a new heart rapidly and to order. 3D printers work by breaking down a three-dimensional object into a series of thin, two-dimensional slices, which are laid down one on top of another. The technology has already been employed to manufacture complex engineering components out of metal or plastic, but it is now being used to generate tissues in the laboratory. To make an aortic valve, researchers at Cornell University took a pigs valve and X-rayed it in a high-resolution CT scanner. This gave them a precise map of its internal structure which could be used as a template. Using the data from the scan, the printer extruded thin jets of a hydrogel, a water-absorbent polymer that mimics natural tissue, gradually building up a duplicate of the pig valve layer by layer. This scaffold could then be seeded with living cells and incubated in the normal way.

Pushing the technology further, Adam Feinberg, a materials scientist at Carnegie Mellon University in Pittsburgh, recently succeeded in fabricating the first anatomically accurate 3D-printed heart. This facsimile was made of hydrogel and contained no tissue, but it did show a remarkable fidelity to the original organ. Since then, Feinberg has used natural proteins such as fibrin and collagen to 3D-print hearts. For many researchers in this field, a fully tissue-engineered heart is the ultimate prize.

We are left with several competing visions of the future. Within a few decades it is possible that we will be breeding transgenic pigs in vast sterile farms and harvesting their hearts to implant in sick patients. Or that new organs will be 3D-printed to order in factories, before being dispatched in drones to wherever they are needed. Or maybe an unexpected breakthrough in energy technology will make it possible to develop a fully implantable, permanent mechanical heart.

Whatever the future holds, it is worth reflecting on how much has been achieved in so little time. Speaking in 1902, six years after Ludwig Rehn became the first person to perform cardiac surgery, Harry Sherman remarked that the road to the heart is only two or three centimetres in a direct line, but it has taken surgery nearly 2,400 years to travel it. Overcoming centuries of cultural and medical prejudice required a degree of courage and vision still difficult to appreciate today. Even after that first step had been taken, another 50 years elapsed before surgeons began to make any real progress. Then, in a dizzying period of three decades, they learned how to open the heart, repair and even replace it. In most fields, an era of such fundamental discoveries happens only once if at all and it is unlikely that cardiac surgeons will ever again captivate the world as Christiaan Barnard and his colleagues did in 1967. But the history of heart surgery is littered with breakthroughs nobody saw coming, and as long as there are surgeons of talent and imagination, and a determination to do better for their patients, there is every chance that they will continue to surprise us.

Main photograph: Getty Images

This is an adapted extract from The Matter of the Heart by Thomas Morris, published by the Bodley Head

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Read more: https://www.theguardian.com/science/2017/may/23/robot-hearts-medicines-new-frontier

No such thing as ‘fat but fit’, major study finds

Metabolically healthy obese are 50% more likely to suffer heart disease than those of normal weight, finds University of Birmingham study

People who are obese run an increased risk of heart failure and stroke even if they appear healthy, without the obvious warning signs such as high blood pressure or diabetes, according to a major new study.

The findings, presented at the European Congress on Obesity in Porto, Portugal, may be the final death knell for the claim that it is possible to be obese but still metabolically healthy or fat but fit say scientists.

Several studies in the past have suggested that the idea of metabolically healthy obese individuals is an illusion, but they have been smaller than this one. The new study, from the University of Birmingham, involved 3.5 million people, approximately 61,000 of whom developed coronary heart disease.

The issue has been controversial. Obesity is usually measured by body mass index (BMI) a ratio of weight against height. It is generally agreed to be imperfect because athletes and very fit people with dense muscle can have the same BMI as somebody who is obese.

The scientists examined electronic health records from 1995 to 2015 in the Health Improvement Network a large UK general practice database. They found records for 3.5 million people who were free of coronary heart disease at the starting point of the study and divided them into groups according to their BMI and whether they had diabetes, high blood pressure [hypertension], and abnormal blood fats [hyperlipidemia], which are all classed as metabolic abnormalities. Anyone who had none of those was classed as metabolically healthy obese.

The study found that those obese individuals who appeared healthy in fact had a 50% higher risk of coronary heart disease than people who were of normal weight. They had a 7% increased risk of cerebrovascular disease problems affecting the blood supply to the brain which can cause a stroke, and double the risk of heart failure.

Dr Rishi Caleyachetty, who led the study, said it was true that weightlifters could be healthy and yet have a BMI that suggested they were obese. I understand that argument. BMI is crude but it is the only measure we have in the clinic to get a proxy for body fat. It is not realistic [to use anything else] in a GP setting or in the normal hospital clinic. We have to rely on BMI measurements, however crude they may be, he said.

While BMI results for particular individuals could be misleading, the study showed that on a population level, the idea that large numbers of people can be obese and yet metabolically healthy and at no risk of heart disease was wrong.

Caleyachetty said: The priority of health professionals should be to promote and facilitate weight loss among obese persons, regardless of the presence or absence of metabolic abnormalities.

At the population level, so-called metabolically healthy obesity is not a harmless condition and perhaps it is better not to use this term to describe an obese person, regardless of how many metabolic complications they have.

Last August a study from Sweden, which followed 1.3 million men over 30 years, found that those who were the fittest when they were 18 years old were 51% less likely to die prematurely than those who were the least fit. But if the men were obese, that cancelled out the advantage they had from their fitness in their youth.

Professor Peter Nordstrom, who led the study published in the International Journal of Epidemiology, said at the time: These results suggest low BMI early in life is more important than high physical fitness with regard to reducing the risk of early death.

Professor Timothy Gill from the Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders at the University of Sydney, Australia, said that there would always be some people who remain healthy in spite of obesity, just as there are some lifetime smokers who do not get lung cancer.

I think you can argue that there are still likely to be some people who are not going to suffer the ill-health consequences as much as other people just because of the distribution of risk, he said.

The World Obesity Federation has this month officially recognised obesity as a disease because of the wide variety of health problems associated with it.

Susannah Brown, senior scientist at World Cancer Research Fund, said the studys finding, emphasise the urgent need to take the obesity epidemic seriously.

As well as increasing your risk of cardiovascular disease, being overweight or obese can increase your risk of 11 common cancers, including prostate and liver. If everyone were a healthy weight, around 25,000 cases of cancer could be prevented in the UK each year.

Read more: https://www.theguardian.com/society/2017/may/17/obesity-health-no-such-thing-as-fat-but-fit-major-study

White Coats Making Blood Pressure Rise?

High blood pressure can lead to heart attack, stroke or kidney failure if left untreated. But for some people, a higher-than-normal reading may be triggered just by visiting a doctor.

“White Coat Hypertension has been defined as the person who comes into the physician’s office and the blood pressure is elevated, but when they go back home or outside the physician’s office it’s within the normal range,” explains Dr. Gary Goforth, a family physician with Lee Memorial Health System.

Although it may not truly reflect a patient’s condition, white coat hypertension or syndrome is very real, elevating blood pressure even 15-20 points whenever a susceptible patient walks through the door.

“Some people say it’s the doctors white coat that makes people nervous and their blood pressure goes up – so we have our nurses take it but it still goes up for them too.”

Blood pressure can rise and fall throughout the day for a variety of reasons. But if it’s jittery nerves that are behind the boost, experts suggest you take several readings at home if possible – because there’s strength in numbers.

“You need to get multiple readings on different days. If they have a device that they can measure it accurately I’ll just have them check it at home and have them bring those numbers,” says Dr. Goforth.

Once dismissed as ‘not serious’ research finds that 50% people who suffer from white coat hypertension go on to get the real thing. So before you discount it, try to listening to your heart. And use the opportunity to make healthy changes

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Lee Memorial Health System in Fort Myers, FL is the largest network of medical care facilities in Southwest Florida and is highly respected for its expertise, innovation and quality of care. For nearly a century, we’ve been providing our community with everything from primary care treatment to highly specialized care services and robotic assisted surgeries.

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British Heart Foundation – I hate heart disease

This advert shows how devastating heart disease can be and that it can affect anyone – but we're fighting back through research.

Each scene in the advert features somebody who has been affected by heart disease, including Claire, whose unborn baby has congenital heart disease, footballer Fabrice Muamba, who survived a cardiac arrest and Emma, who died when she was just 13 years old.

Watch Claire's story here .

Watch Emma's story here .

All the researchers featured are BHF funded researchers who are currently working on life-saving research projects.

Our research is powered by your support. Join the fight for every heartbeat – donate today at