Tag Archives: heart

The difference between cardiac arrest and heart attack

While these two terms are used quite interchangeably, they denote different medical events. A heart attack (myocardial infarction) is a circulation problem that involves blood flow being blocked from reaching the heart. During cardiac arrest, an electrical problem causes the heart to stop beating and needs to be restarted.

Image credits Peggy and Marco Lachmann-Anke.

We’ve all heard these terms at one point or another. Because they’re both serious conditions and quite similar in symptoms, we also tend to lump them together and treat them as synonyms. That being said, however, they are not the same thing, and they are not interchangeable.

So let’s dive into the differences between them.

Heart attacks

These occur when one of the coronary arteries supplying oxygenated blood to a section of the heart gets blocked. If this blockage isn’t cleared quickly, cells in the affected area of the heart start dying due to a lack of oxygen. This effect builds up over time so the longer an individual goes without treatment, the more damage accumulates in tissues in that part of their heart.

Blockages are typically caused by build-ups of fat, either cholesterol (that’s why your doctor is so insistent you lower it), or a series of other substances.

While symptoms can definitely be immediate and intense (such as feelings of pressure, tightness, or intense pain in the chest), they can also occur over time, up to weeks in advance of an actual heart attack. There is also quite a large degree of variation in regards to the symptoms of various patients. Women can have different symptoms than men; some patients have no symptoms at all. Angina (recurrent chest pain or pressure) triggered by physical activity and relieved by stress is the most common and earliest warning sign of heart attack.

That being said, it’s important to act quickly in case you’re experiencing these symptoms or think you’re having a heart attack. Call emergency services even if you’re not sure you’re having a heart attack, as every minute matters. Emergency services personnel can begin treatment the moment when they arrive; getting to the hospital by yourself would take a lot longer. They can also provide resuscitation in case a patient’s heart has stopped completely.

Cardiac arrest

Unlike a heart attack, cardiac arrest occurs suddenly and very often without warning. It involves an abrupt loss of heart function and can be extremely dangerous.

It is caused by an electrical malfunction in the heart which produces arrhythmia (irregular heartbeat). Due to this disruption, blood flow to the brain, lungs, and other organs is disrupted — and with it, the flow of oxygen as well. The lack of oxygen supply to the brain can render a person unconscious in mere seconds and stop heart function completely. Victims of cardiac arrest can die within minutes without treatment.

Symptoms of cardiac arrest include dizziness, loss of consciousness, and shortness of breath. Cardiac arrest events can happen in individuals who may or may not have been diagnosed with heart disease. It may be reversed, however, if CPR is performed on the patient, and a defibrillator is used to restore a normal heart rhythm within a few minutes.

If someone near you is experiencing cardiac arrest, first call emergency services. Then, get an automated external defibrillator (AED) if one is available; if not, begin performing CPR on the patient. If two people are available, one should begin CPR immediately, while the other handles the call and retrieves an AED. If AED solutions are available, they must be used as quickly as possible.

It may be needed that you perform CPR on the patient for a longer period of time. If that’s the case, don’t worry. Hands-only CPR to the beat of “Stayin’ Alive” can double or even triple a victim’s chances of survival — hang in there!

Fried food can promote poor cardiovascular health, heart disease, stroke

Fried food tastes good, but it’s not very healthy for you. A new metastudy reports that consumption of such food is linked to an increased risk of major heart disease and stroke.

Most of us today make an effort to not eat only fast food and take-out, which is admirable, but that doesn’t make our diets ‘healthy’ per se. Western dietary habits are known to promote poor cardiovascular health, the authors note, but it was still unknown how much fried food specifically contributed to this. In order to get a better idea of the effect such food has on our cardiovascular health, a team of Chinese researchers has reviewed past research on this subject.

Don’t fry

The team reviewed 17 studies involving 62,445 participants and 36,727 major cardiovascular events (such as a heart attack or stroke). They also pooled in data from a further 6 which tracked their patients over a long timeframe (9.5 years on average), involving 54,873 participants and 85,906 deaths. Put together, the data was meant to help us gauge how damaging fried food is to our cardiovascular health, and how much they increase our risk of death from cardiovascular disease.

The results show that participants in the group who consumed the most fried food had a 28% higher chance of experiencing a cardiovascular (CVS) event than those who consumed the least. They also had a 22% higher risk of coronary heart disease and a 37% higher risk of heart failure.

Even when the team controlled for various factors and participant characteristics, the link between the consumption of fried food and major cardiovascular events, coronary heart disease, and heart failure remained. The risk increased with each additional 114 g weekly serving by 3%, 2%, and 12%, respectively, the authors report.

Still, the findings aren’t necessarily conclusive. Some of the studies only tracked one type of fried food, for example fried fish or potatoes, not participants’ total intake. Furthermore, every study was designed differently and all relied on information the participants were asked to remember (which is unreliable). The team explains that all these elements could mean the studies “underestimated” the association between these and cardiovascular health. They also note that such factors need to be taken into account when interpreting the results.

Exactly how fried foods can influence the development of cardiovascular disease is still unclear, but the team has some possible explanations. First off, fatty foods are very energy-dense but the vegetable oil they contain gets broken down into trans fatty acids inside our bodies, which is harmful. Frying also generates a host of byproducts involved in inflammatory processes, and fried food is often very salty (an excess of salt is also bad for you).

The paper “Fried-food consumption and risk of cardiovascular disease and all-cause mortality: a meta-analysis of observational studies” has been published in the journal BMJ.

Air pollution can contaminate your heart cells with metal nanoparticles from infancy

Researchers are uncovering further evidence of the adverse health effects of air pollution.

Smog in Warsaw, 2015.
Image via Pixabay.

Toxic metallic nanoparticles from such pollution can find their way into the mitochondria of our hearts, a new paper reports, with a negative impact on our health. Mitochondria provide the power that keeps our cells going; damaging them will thus damage our cells.

This effect was seen in the hearts of people living in polluted cities and could be an important cause of cardiac stress, the team adds.

Poor air, poor health

“It’s been known for a long time that people with high exposure to particulate air pollution experience increased levels and severity of heart disease,” says Professor Barbara Maher of Lancaster University, lead author of the paper. “We found these metal particles inside the heart of even a three-year-old.”

“It’s really urgent to reduce emissions of ultrafine particles from our vehicles and from industry before we give heart disease to the next generation, too,” she adds.

The team analyzed the hearts retrieved from two young people who had died in accidents and lived in the Mexico City area. Air pollution levels here often exceed health guidelines, the authors explain.

They found metallic nanoparticles associated with air pollution (such as iron and titanium-rich particles) inside damaged heart cells of a 26- and 3-year-old, randomly selected from 63 previously-investigated children and young adults.

Dark-field scanning/transmission electron microscopy image of heart tissue in the left ventricle, with F showing the iron-rich particles highlighted in A and D.
Image credits B.A. Maher et al., (2020), Environmental Research.

Using high-resolution transmission electron microscopy and X-ray analysis, they found that mitochondria containing iron-rich nanoparticles were damaged, showing ruptured membranes or deformities. Such particles were associated with the development of heart disease, as they cause oxidative stress which chemically damages cells, even in very young tissues.

The team found “abundant presence of rounded, electron-dense nanoparticles, mostly ~15–40 nanometers, most frequently inside mitochondria”. They note that the presence of iron inside mitochondria can alter their chemical mechanism to produce highly reactant oxygen species which attack proteins.

The particles are “indistinguishable from the iron-rich nanoparticles so abundant and pervasive in urban and roadside air pollution”, the team notes.

The results show that such nanoparticles may jump-start heart disease in early life and cardiovascular illness later on. Air pollution can thus be responsible for the international “silent epidemic” of heart disease. It could also contribute to the high death rates from COVID-19 seen in areas with poor air quality.

Another point of concern is the magnetic properties of these particles. It’s possible that, should they build-up in the heart in large amounts, these will react to the magnetic fields produced by appliances and electronics. Exposure could cause cell damage and lead to heart dysfunction. People who work jobs that expose them to magnetic fields, such as welders or certain branches of engineering, could also be at risk.

The paper “Iron-rich air pollution nanoparticles: An unrecognized environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress” has been published in the journal Environmental Research.

Coronavirus damages the lungs in severe cases, as well as the heart and kidneys

 This image shows a CT scan from a man with COVID-19. Pneumonia caused by the new severe acute respiratory coronavirus 2 can show up as distinctive hazy patches on the outer edges of the lungs, indicated by arrows. 

The new coronavirus causes COVID-19, a respiratory disease that in the most severe cases attacks the lungs, destroying cells and potentially triggering death. Every day we learn new things about the coronavirus, and most of them aren’t pretty. The latest reports suggest that it’s not just the lungs that are attacked, other organs like the kidneys and heart are also severely affected, with potentially life-threatening consequences.

When the virus infects lung cells, it starts replicating. But our immune system doesn’t just wait by idly. It knows that the body is under attack by a foreign invader and, in response, it starts mobilizing the troops — a swarm of antibodies. However, these immune cells don’t just kill infected cells, they can also attack healthy cells, triggering inflammation.

As a result, air sacs in the lungs become swollen and filled with fluid — essentially the patient now has pneumonia and experiences breathing difficulties.

These symptoms also make it challenging for the lungs to pump oxygen in the blood, which can trigger a cascade of problems. Less oxygen naturally triggers more inflammation. All types of tissue, especially organs, require oxygen to function properly. So, with limited oxygen supply, other organs start to fail.

According to Alan Kliger, a nephrologist at Yale School of Medicine, about half of the COVID-19 patients who were hospitalized had blood or protein in their urine, which is a telltale sign of kidney damage.

Speaking to the Washington Post, Kliger added that preliminary data shows that 14% to 30% of intensive-care patients in New York and Wuhan, China, lost kidney function and required dialysis. In China, autopsies on deceased COVID-19 patients found that nine out of 26 had acute kidney injuries.

“That’s a huge number of people who have this problem. That’s new to me,” Kliger said. “I think it’s very possible that the virus attaches to the kidney cells and attacks them.”

There’s also evidence that the virus also attacks the heart. Physicians in both New York and China have reported a similar incidence of myocarditis and irregular heart rhythms that can lead to cardiac arrest in COVID-19 patients. According to a review of ICU cases from China, 40% of patients suffered arrhythmias and 20% had some form of cardiac injury.

Although much rarer, there are reports of liver damage due to COVID-19. There’s one such case in Long Island and five in China, but the small sample size is not enough to draw definite conclusions.

What’s particularly worrisome is the danger of blood clots in the veins of legs and other blood vessels. A study published last week monitored 81 patients with COVID-19 pneumonia in a Wuhan hospital, finding that 20 patients had blood clots that traveled to the lungs. lungs. Blood clots in the lungs are particularly dangerous because they can potentially trigger a fatal pulmonary embolism. Eight of the patients died as a result.

In New York, doctors are already treating ICU patients with blood thinners to counter the viral-triggered blood clots.

This kind of damage might be due to a cytokine storm — the overreaction of the body’s immune system that can cause complications and multiple organ failure. Cytokines are small proteins released by many different cells in the body, including those of the immune system where they coordinate the body’s response against infection and trigger inflammation.

Researchers hope to get to the bottom of things by investigating other possible causes of organ and tissue damage. Other causes include respiratory distress, medication, high fever, and the stress of intensive care unit hospitalization.

New method helps screen COVID-19 patients at risk from drug-induced heart attack

As unlicensed medication is increasingly deployed against COVID-19 by medical staff desperate to save their patients, a new study looks into how to determine who can bear the treatment, and who can’t.

The current pandemic is pushing doctors and researchers to find safe treatments for patients with COVID-19, and several candidates are already being tested. Until certified treatment options are made available, however, doctors are throwing anything that works against the virus in a bid to give those suffering from the worst cases a shot at life.

However, a new study cautions that certain patients are at risk of dying from such treatments. Some medications can affect (prolong) the QTc of certain patients, an indicator that quantifies the length of an individual’s heartbeats. Patients are at increased risk of life-threatening ventricular rhythm abnormalities that can culminate in sudden cardiac death when their QTc gets too long.

The heart of the matter

“Correctly identifying which patients are most susceptible to this unwanted, tragic side effect and knowing how to safely use these medications is important in neutralizing this threat,” says Michael J. Ackerman, M.D., Ph.D., a Mayo Clinic genetic cardiologist and director of the Mayo Clinic Windland Smith Rice Comprehensive Sudden Cardiac Death Program.

A study published in Mayo Clinic Proceedings examines the potential dangers of using uncertified drugs to treat the outbreak and showcase the potential application of QTc monitoring to guide treatment when using such drugs.

Hydroxychloroquine is one of the compounds pushed in the fight against SARS-CoV-2 and, from the limited data we have so far, it does seem to be effective. Hydroxychloroquine was designed as a preventive and treatment compound against malaria and is also used to manage and minimize symptoms of inflammatory immune diseases, such as lupus and rheumatoid arthritis. In laboratory tests, hydroxychloroquine has prevented both the SARS-CoV and SARS-CoV-2 viruses from infecting (animal) cells, suggesting that it could work similarly in humans.

On a cellular level, some medications, including hydroxychloroquine, can block the potassium channels that underpin our heart muscles’ ability to contract — which interferes with our natural cardiac rhythm.

Image result for qt interval
The QTc, or corrected QT interval, is the length of a heartbeat at a standard heart rate of 60 bpm.
Image via Wikimedia.

The Mayo Clinic team has pieced together an emergency guide on how to use 12-lead electrocardiograms (ECG), telemetry ECG, or smartphone-enabled mobile ECG, to determine a patient’s QTc in order to minimize the change of drug-induced cardiac arrest.

“Right now, it is the Wild West out there, ranging from doing no QTc surveillance whatsoever and just accepting this potential tragic side effect as part of ‘friendly fire,’ to having ECG technicians going into the room of a patient with COVID-19 daily, exposing them to coronavirus and consuming personal protective equipment,” says Dr. Ackerman.

“Here Mayo Clinic has stepped forward to provide timely and critical guidance.”

The guides put forth by the team (essentially) explain the following:

The antimalarial drugs chloroquine and hydroxychloroquine, alongside the HIV drugs lopinavir and ritonavir, are all known to possibly induce ventricular arrhythmias and sudden cardiac death. It is important to get an ECG measurement on the patient before administering these drugs to establish a baseline. This starting point measurement could be from a standard 12-lead ECG, telemetry or a smartphone-enabled mobile ECG device. The team notes that the Food and Drug Administration (FDA) granted emergency approval of AliveCor’s Kardia 6L mobile ECG device, currently the only mobile device approved by the FDA for the purpose.

Dr. Ackerman and colleagues developed an algorithm that can rate a patient’s risk of drug-induced arrhythmias based on these measurements, which can help doctors tailor the treatment to a patient’s specific needs.

Dr. Ackerman says that patients under 40 with mild symptoms and a QTc greater than or equal to 500 milliseconds may choose to avoid treatment altogether, as the arrhythmia risk may far outweigh the risk of developing COVID-19-related acute respiratory distress syndrome. However, for patients with a QTc greater than or equal to 500 milliseconds who have progressively worsening respiratory symptoms or are at greater risk of respiratory complications due to advanced age, immunosuppression, or having another high-risk condition, the potential benefit of QTc-prolonging medicines may exceed the arrhythmia risk.

“Importantly, the vast majority of patients, about 90%, are going to be QTc cleared with a ‘green light go’ and can proceed, being at extremely low risk for this side effect,” says Dr. Ackerman.

Ultimately, the weighing of risks and benefits depends on whether hydroxychloroquine is truly an effective treatment against COVID-19, the team concludes.

New heart rate measurements suggest that blue whales are about as large as animals can get

Researchers at Stanford University have made the first recording of a wild blue whale’s heart rate to date. The data suggests that the animals’ hearts are operating close to their maximum capacity, which may act as a hard cap on their maximum possible size.

Image credits Thomas Kelley.

The team developed a sensor array which, through the use of four suction cups, can be secured near a whale’s left flipper. This device was used to record the heart rate of a wild blue whale, and offer an explanation as to why they are the largest animal we’ve ever found. The recording points to some unusual features that help whale hearts pump enough blood.

Studying animals that operate “at physiological extremes” can help us better understand biological limits on size, the team explains. Furthermore, such species may also be “particularly susceptible” to environmental changes that disrupt their food supply, since large animals need large meals. All in all, the team hopes that their research will help us design new and better conservation and management schemes for endangered species like blue whales.


“We had no idea that this would work and we were skeptical even when we saw the initial data. With a very keen eye, Paul Ponganis — our collaborator from the Scripps Institution of Oceanography [Ed. Note also a co-authror of this study] — found the first heart beats,” said Jeremy Goldbogen, assistant professor of biology in the School of Humanities Sciences at Stanford and lead author of the paper.

“There were a lot of high fives and victory laps around the lab.”

The current study draws its roots in some of Goldbogen’s and Ponganis’ previous research, in which they measured the heart rates of diving emperor penguins in McMurdo Sound, Antarctica. The duo wanted to do the same with a blue whale, but there were several issues to overcome: “finding a blue whale, getting the tag in just the right location on the whale, good contact with the whale’s skin and, of course, making sure the tag is working and recording data,” said Goldbogen.

They first tested their sensors on smaller, captive whales, to make sure the technology is sound. However, they didn’t accurately reflect the behavior of wild whales — which aren’t, for example, trained to flip belly-up for a human caretaker. Blue whales also have a wrinkly structure to the skin on their underside that expands during feeding; this could mechanically dislodge the sensor array.

“We had to put these tags out without really knowing whether or not they were going to work,” recalled David Cade, a recent graduate of the Goldbogen Lab who is a co-author of the paper and who placed the tag on the whale.

“The only way to do it was to try it. So we did our best.”

Despite all this, everything went swimmingly with the wild whales, the team reports. Cade managed to fix the tag on his first attempt near the flipper (where it could pick up on signals from the heart).

The recordings showed that when the whale dives, its heart rate slows down to an average of about 4 to 8 beats per minute, although the team did see activity drop down to just 2 beats per minute. At the lowest point of their foraging dives — when the whale needs to swim upwards and catch its prey — heart rate rose to 2.5 times above this minimum value, and then slowly decreased. The highest heart rate was recorded at the surface, between 25 to 37 beats per minute, while the whale was breathing and replenishing its oxygen stocks.

All in all, the team says the findings are very surprising. The upper limit of heart rate was faster than expected, and the lowest ones were about 30-50% slower. The lower-end heart rates seen can be explained by the whale’s elastic aortic arch, which slowly contracts and keeps blood flowing to the body between heartbeats. The highest heart rates seen are likely made possible by small features of the heart’s shape and movement which prevent pressure waves generated during contraction from disrupting blood flow, the team adds.

The blue whale’s heart likely operates near or at the limit of its capacity. The team believes that the energy needs of a larger body would simply outpace the ability of a heart to pump blood, which would explain why no animal has ever outgrown them.

Currently, the team working on improving their sensor array and plan to expand their research to other species such as fin whales, humpbacks and minke whales.

The paper “Extreme bradycardia and tachycardia in the world’s largest animal” has been published in the journal PNAS.

Electronic cigarettes aren’t good for you — in some respects, they’re worse than traditional cigarettes

E-cigarettes aren’t harmless. Although viewed as a healthier alternative, the study finds that e-cigarette smoking impacts heart health similar to the smoking of traditional cigarettes.

Image via Pixabay.

Several heart disease risk factors — cholesterol, triglycerides, and glucose levels, as well as decreased blood flow in the heart — are negatively impacted by e-cigarette smoke. The findings will be presented at the American Heart Association’s Scientific Sessions 2019, later this month.

Not harmless by far

“There is no long-term safety data on e-cigarettes. However, there are decades of data for the safety of other nicotine replacement therapies,” explains Rose Marie Robertson, M.D., FAHA, the American Heart Association’s deputy chief science and medical officer.

The American Heart Association (AHA) recommends the use of FDA-approved smoking cessation aids, which are proven safe and effective. Robertson says that people often choose e-cigarettes as an alternative to quitting (as it is perceived as being safer than traditional tobacco), or as a temporary solution while working to quit altogether. In the latter case, however, she warns that people should also plan how to subsequently stop using e-cigarettes. There is a striking lack of data on the long-term safety of such devices, and growing concerns over the physiological effects caused by the chemical cocktails therein.

One study used in this report — the Cardiovascular Injury due to Tobacco Use (CITU) Study — compared cholesterol, triglycerides, and glucose levels in healthy adult nonsmokers, e-cigarette smokers, traditional cigarette smokers, and dual smokers (who use both traditional and e-cigarettes). Participants were aged 21-45, didn’t have any preexisting cardiovascular disease, and took no relevant medication. Out of the total of 467 participants, 94 were non-smokers, 52 were dual smokers, 45 were e-cigarette smokers, and 285 were traditional cigarette smokers.

After adjusting for age, race, and sex, the team reports that total cholesterol was lower for e-cig smokers, but their low-density lipoprotein (LDL, ‘bad’ cholesterol) levels were higher, compared to nonsmokers. High-density lipoprotein (HDL, ‘good’ cholesterol) was lower in dual smokers.

“Although primary care providers and patients may think that the use of e-cigarettes by cigarette smokers makes heart health sense, our study shows e-cigarette use is also related to differences in cholesterol levels. The best option is to use FDA-approved methods to aid in smoking cessation, along with behavioral counseling,” said study author Sana Majid, M.D., a postdoctoral fellow in vascular biology at the Boston University School of Medicine.

Another study looked at heart blood flow as a measure of coronary vascular function in 19 young adult smokers (ages 24-32) immediately before and after smoking either e-cigarettes or traditional cigarettes. The study looked at this metric both at rest and after performing a handgrip exercise (meant to simulate physiological stress).

For smokers of traditional cigarettes, the team saw a “modest” increase in blood flow after cigarette inhalation, which decreased with subsequent stress. E-cig smokers, however, saw blood flow decrease both at rest and after the handgrip exercises. All in all, e-cigarette use seems to be associated with coronary vascular dysfunction to a greater degree than seen in traditional cigarettes.

“These results indicate that e-cig use is associated with persistent coronary vascular dysfunction at rest, even in the absence of physiologic stress,” said study author Florian Rader, medical director of the Human Physiology Laboratory and assistant director of the Non-Invasive Laboratory, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

“Providers counseling patients on the use of nicotine products will want to consider the possibility that e-cigs may confer as much and potentially even more harm to users and especially patients at risk for vascular disease,” added study co-author Susan Cheng, director of Public Health Research at the Cedars-Sinai Medical Center.

The studies were funded by The National Heart, Lung, and Blood Institute and the FDA Center for Tobacco Products, and The California State Tobacco-related Disease Research Program High Impact Pilot Research Award. The American Heart Association Tobacco Center for Regulatory Science provided research materials for the first study.

The findings will be presented at the American Heart Association’s Scientific Sessions 2019 conference, November 16-18 in Philadelphia, USA (sessions Mo3106, Sa3199).

Napping once or twice per week may help protect you from heart attack or strokes

A daytime nap once or twice a week can help lower the risk of having a heart attack or stroke, a new study found. So far, the findings are observational — they shouldn’t be used to infer a cause-effect relationship.

Image via Pixabay.

A paper looking at the association between napping frequency, average nap duration, and the risk of (both fatal and non-fatal) cardiovascular events found that taking as few as one or two naps a week can help reduce the risk of having a heart attack, stroke, or heart failure. However, no such link was established for greater frequency or duration of naps.

Hearty naps

“The study of napping is a challenging but also a promising field with potentially significant public health implications,” the authors explain. “While there remain more questions than answers, it is time to start unveiling the power of naps for a supercharged heart.”

Whether or not napping brings any health benefits to the table is still an ongoing debate. The authors explain that past research into the issue hasn’t taken napping frequency into account, focused purely on cardiovascular disease deaths, or compared regular nappers with those who don’t nap. All of this left us with a skewed perception of the benefits of napping.

In an effort to guide this debate, the team analyzed the association between napping frequency, average nap duration, and the risk of fatal and non-fatal cardiovascular disease ‘events,’ such as heart attack, stroke, or heart failure, among 3462 randomly selected residents of Lausanne, Switzerland. The participants were between 35 and 75 years old (when recruited for the study, between 2003 and 2006).

Each participant had a check-up sometime between 2009 and 2012 when the team recorded information on their sleep and nap patterns in the previous week. Their health was then subsequently monitored for an average of 5 years.

Over half of the participants (58%) said that they didn’t nap in the previous week, 19% said they took one to two naps, 12% reported taking between three and five, while a very-well-rested 11% said they took between six and seven naps in the previous week. The most frequent nappers (3-7 per week) tended to be older, male, smokers, and tended to weigh more and sleep for longer at night than non-nappers. They also reported more daytime sleepiness and more severe obstructive sleep apnea — a condition in which the walls of the throat relax and narrow during sleep, interrupting normal breathing.

The team recorded 155 fatal and non-fatal cardiovascular disease ‘events’ over the study period.

Occasional napping (1-2 per week) was associated with a 48% lower risk of a heart attack, stroke, or heart failure compared with those who didn’t nap at all. This association held true even after controlling for factors such as age, nighttime sleep duration, daytime sleepiness, depression, and regularity of sleep, as well as other cardiovascular disease risks, such as high blood pressure/cholesterol.

The only factors that influenced this link were older age (65+) and severe sleep apnea.

Frequent nappers initially showed a 67% heightened cardiovascular risk, but this disappeared after taking account of potentially influential factors. The team further reports finding no associations with cardiovascular disease ‘events’ for nap length (from 5 minutes to 1 hour plus).

The study relied on personally-reported information and shouldn’t be used to establish a cause-effect relationship, the team explains. However, they add that nap frequency may help to explain the differing conclusions reached by researchers about the impact of napping on heart health in previous studies. Research in this area is further hampered by the absence of a clear standard for defining and measuring naps.

“While the exact physiological pathways linking daytime napping to [cardiovascular disease] risk is not clear, [this research] contributes to the ongoing debate on the health implications of napping, and suggests that it might not only be the duration, but also the frequency that matters,” the study concludes.

The paper “Association of napping with incident cardiovascular events in a prospective cohort study” has been published in the journal Heart.

How 3-D printers are set to revolutionize heart valves

With the average age of the population on the rise, aortic heart valve replacement is being growingly requested. An expected 850,000 patients will need experience heart valve replacements in 2050. Researchers are anticipating such demand with a new alternative.

Credit: Andy G (Flickr)


A group of scientists at ETH Zurich and the South African company Strait Access Technologies are working with 3-D printers in order to manufacture custom-made artificial heart valves, made out of silicone and created in just an hour.

Working with silicone valves means tailoring it more precisely to the patient. Researchers first determine the shape and size of the heart by using computer tomography or magnetic resonance imaging. Then, they can print a valve that is a perfect match to the heart chamber.

In order to avoid any problems with the implant, researchers create a digital model and a computer simulation with a set of images. Safety is also guaranteed by the material compatibility with the human body, as blood can flow normally through the artificial valve.

The 3D-printed valves enable mechanical matching with the host biological tissue. Credit: Fergal Coulter / ETH Zurich

The new silicon valves would allow surgeons to stop using conventional implants, based on animal tissues or polymers combined with metal frames. They have a rigid shape and meant for patients the need to take life-long immunosuppressants to prevent the body from rejecting them.

“The replacement valves currently used are circular, but do not exactly match the shape of the aorta, which is different for each patient,” says Manuel Schaffner, one of the study’s lead authors and former doctoral student of André Studart, Professor for Complex Materials at ETH.

While the conventional valves take several days to be manufactured, the silicone ones can be done in about an hour thanks to the 3-D printers. Scientists need to create a negative impression of the valve, spraying the ink onto it. Then, a printer tough deposits silicone paste to print specific patterns on their surface.

Scientists expect to extend the life of the replacement valves to 10-15 years, which is how long current models last in patients before they need to be exchanged. Nevertheless, it would take at least 10 years before the new artificial valves come into clinical use, as they have to go through clinical trials first.

“It would be marvelous if we could one day produce heart valves that last an entire lifetime and possibly even grow along with the patient so that they could also be implanted in young people as well,” said Schaffner.

The study was published in the journal Matter.

Heart balloon.

Heart-repairing patches poised for human trials, researchers report

Heart ‘patches’ developed by the British Heart Foundation (BHF) have proven themselves safe in animal lab trials — and will be moving on human trials.

Heart balloon.

Image credits Peggy Lachmann-Anke , Marco Lachmann-Anke.

The patches could one day help people manage and recover from debilitating heart failure, a condition which affects an estimated 920,000 people in the UK alone, and is on the rise worldwide, say researchers from the BHF. The patches are thumb-sized bits of heart tissue measuring 3cm by 2cm and containing up to 50 million human stem cells. These cells have the ability to turn into fully-functional heart tissue, and are meant to be applied to the heart of someone after they’ve had a heart attack. Used in this fashion, they can limit, and even reverse, the loss of the heart’s pumping ability.

Heart attack, heart defense

“One day, we hope to add heart patches to the treatments that doctors can routinely offer people after a heart attack,” says Dr Richard Jabbour who carried out the research at the London BHF Centre of Regenerative Medicine.

“We could prescribe one of these patches alongside medicines for someone with heart failure, which you could take from a shelf and implant straight in to a person.”

During a heart attack, our hearts’ supply of nutrients and oxygen can become compromised, killing off parts of the heart muscle. This leaves the organ weakened and could even lead to heart failure later on. This condition involves the heart not being able to pump sufficient blood to the rest of the body, making even mundane tasks such as climbing stairs or getting dressed extremely tiring.

The patches are meant to be sewn into place on the damaged heart, where they will offer physical support to the damaged muscle and help it pump more efficiently. At the same time, the patch delivers compounds that stimulate its healing and regeneration. Eventually, the team hopes, these patches will be incorporated into the heart muscle.

The patches start to beat spontaneously after three days, and start to mimic the structure of mature heart tissue within one month, the team explains. After this, they can be grafted into the damaged heart to help it repair and recover normal functionality.

Rabbit trials showed these patches to be safe and that they lead to an improvement in the functioning of the heart after a heart attack. Four weeks after the patches were applied, heart scans showed that the heart’s left ventricle (the one which pumps blood out to the body) was recovering nicely, without any abnormal heart rhythms. Other stem cell delivery methods run the risk of such abnormal rhythms developing, the team explains.

So far, the patches have proven their efficacy. The next steps include a clinical trial with human subjects, first to test how safe they are, then to see if they can achieve the same levels of healing in humans. They were developed as an alternative to the more traditional approach of injecting stem cells directly into damaged hearts, which has had mixed results. In the absence of a patch, the stem cells are quickly cleared from the heart before they can produce any significant repairs.

“One day, we hope to add heart patches to the treatments that doctors can routinely offer people after a heart attack,” says Dr Richard Jabbour, who carried out the research at the London BHF Centre of Regenerative Medicine said.

“We could prescribe one of these patches alongside medicines for someone with heart failure, which you could take from a shelf and implant straight in to a person.”

The findings were presented at the British Cardiovascular Society (BCS) Conference in Manchester on Monday, June 3rd.

Researchers 3D print a miniature heart — using a patient’s own cells

The heart is still too small to be useful, but this represents an important proof of concept, researchers say.

We’ve all seen how 3D printers can be used to produce a wide variety of materials, but human body parts weren’t exactly on the expectation list — and a heart is probably the last thing you’d expect. But in a new study, researchers from Tell Aviv University have done just that: they’ve 3D printed a miniature version of a human heart, using material from a patient.

“It’s completely biocompatible and matches the patient,” said Tal Dvir, the professor who directed the project.This greatly reduces the chances of rejection inside the body,

Dvir and colleagues harvested fatty tissue from a patient, then separated it into cellular and non-cellular components. The cellular components were then reprogrammed into stem cells and subsequently turned into heart tissue cells. The non-cellular cells were also processed and used as a gel that served as the bio-ink for printing.

The process was lengthy. A massive 3D printer sent a small stream of this bio-ink to print, and the cells were then left to mature for another month. For now, the heart is very small and doesn’t “work” — but this is still an important breakthrough. Previously, only simple tissues had been printed.

A simplified diagram of the heart-printing process. Image credits: Tel Aviv University.

“We need to develop the printed heart further,” Dvir said. “The cells need to form a pumping ability; they can currently contract, but we need them to work together. Our hope is that we will succeed and prove our method’s efficacy and usefulness.”

The potential for this invention is tremendous. Cardiovascular diseases are the number one cause of death in industrialized nations, and heart transplants face a number of hurdles, ranging from the lack of donors to challenging surgery and potential rejection. This would not only ensure that there is always a donor (the patient himself) but also eliminate the risk of rejection.

A human-sized heart might take a whole day to print and would require billions of cells, compared to the millions used to print these mini-hearts, Dvir said. This is still just the very first stage of the project, but it’s still a promising one. Even though it will be a long time before functional hearts can be produced thusly, researchers are also considering printing “patches” to address localized heart problems.

“Perhaps by printing patches we can improve or take out diseased areas in the heart and replace them with something that works,” Dvir concluded.

The study “3D Printing of Personalized Thick and Perfusable Cardiac Patches and Hearts” has been published in Advanced Science.

Common painkiller linked to major heart problems

According to a recent study, the painkiller diclofenac could be associated with an increased risk of major cardiovascular events, such as heart attack and stroke. The risk seems to be higher not only when compared to no usage, but also when compared to some of its substitutes.

Diclofenac is a medicine that reduces inflammation and pain. It’s commonly used to treat a wide variety of aches and pains. Depending on the country and the type of drug it is administered in, it’s either available over the counter or requires a prescription. But the authors of a new study argue that diclofenac shouldn’t be allowed as an over-the-counter drug, or at the very least, should be accompanied by appropriate warnings.

[panel style=”panel-default” title=”Painkillers” footer=””]Diclofenac is part of a class of painkillers called nonsteroidal anti-inflammatory drugs (NSAID). The most prominent NSAIDs are aspirin, ibuprofen and naproxen, all available over the counter in most countries.

Although these drugs are generally efficient not only in reducing pain and inflammation but also in preventing some blood clots, they come with a few well-known side effects. Side effects depend on the specific drug, but largely include an increased risk of gastrointestinal ulcers and bleeds, as well as heart attack and kidney disease.


In the new study, Morten Schmidt at Aarhus University Hospital in Denmark examined the cardiovascular risks of starting diclofenac compared with no non-steroidal anti-inflammatory drugs (NSAIDS) — other drugs in diclofenac’s category. The results included data for more than 6.3 million adults in Denmark with at least one year of prescriptions. Diclofenac was associated with an increased risk of adverse cardiac events such as irregular heartbeat or flutter, ischaemic stroke, heart failure, and heart attack.

However, researchers point out that, while the relative risk increased significantly, the overall risk was still pretty small.

Also, it’s important to note that this is an observational study, so no cause-effect relationship was established. But even so, researchers say that the risk is not really justified. They recommend using other similar painkillers that come without the increased risk.

“Treatment of pain and inflammation with NSAIDs may be worthwhile for some patients to improve quality of life despite potential side effects,” they write. “Considering its cardiovascular and gastrointestinal risks, however, there is little justification to initiate diclofenac treatment before other traditional NSAIDs,” they conclude.

The study has been published in the British Medical Journal.

Want to keep a young heart? Try exercising 4-5 times a week

Exercising at least 4 times a week is necessary for maintaining a young heart, a new study concludes.

That exercising helps keep us healthy should be a secret to no one. But how much you should exercise — that’s a different problem. In a new study, authors carried out an examination of 102 people over 60 years old, with a consistently-logged, lifelong exercise history. Researchers also gathered detailed measures of arterial stiffness from all participants — a key index of arterial health. Based on the results, participants were split into the following groups:

  • Sedentary: less than 2 exercise sessions/week;
  • Casual Exercisers: 2-3 exercise sessions per week;
  • Committed Exercisers: 4-5 exercise sessions/week; and
  • Masters Athletes: 6-7 exercise sessions per week.

They found that exercising 2-3 times a week helps keep the middle-sized arteries young. Notably, these are the arteries which supply oxygenated blood to the head and neck. However, in addition to this, people who exercised 4 times per week or more also kept their main arteries healthy — the arteries which provide blood to the chest and abdomen.

So the conclusion is that even a couple of weekly workouts is good, but if you really want to keep your heart going, you should probably push it to about 4 or 5 a week.

The good thing about this study is that it could be an important step towards developing exercise strategies to slow down such aging.

“This work is really exciting because it enables us to develop exercise programmes to keep the heart youthful and even turn back time on older hearts and blood vessels,”  says Benjamin Levine, one of the authors of the study.

“Previous work by our group has shown that waiting until 70 is too late to reverse a heart’s ageing, as it is difficult to change cardiovascular structure even with a year of training. Our current work is focussing on two years of training in middle aged men and women, with and without risk factors for heart diseases, to see if we can reverse the ageing of a heart and blood vessels by using the right amount of exercise at the right time”.

There are still significant drawbacks of this study. For starters, 102 people is not the largest sample size you can ask for. Secondly, even though the data was very thorough, it didn’t include any information about the intensity and duration of the workout, which could have significant vascular consequences.

However, while researchers still aren’t sure exactly how much exercise is enough, even a bit is better than nothing. So if you want to maintain a healthy and young body, you’d best start working.

Journal Reference: Shibata, S et. al. The Effect of Lifelong Exercise Frequency on Arterial Stiffness. JPhysiol. 21 May 2018. doi: 10.1113/JP275301

Generic drugs for heart conditions work just as well as brand name drugs

Credit: Pixabay.

Generic anti-platelet drugs, which are effective for arterial circulation, work just as well for heart patients as the established brand-name drugs, according to Canadian researchers. The study found that the switch saved the Ontario Drug Benefit Program $32 million Canadian dollars on medications alone.

Just as good — for the fraction of a cost

Dennis Ko, who is the lead study author and senior scientist at the Institute for Clinical Evaluative Sciences (ICES) in Toronto, and colleagues devised a methodology to evaluate the safety of generic medications in the real world setting. They analyzed outcomes from a study cohort, which included 24,530 patients over age 65, of whom 12,643 received Plavix and 11,887 received generic clopidogrel. The patients were prescribed the drugs after hospitalization for a heart attack or heart-related chest pain in Ontario, Canada. In 2012, the patent for Plavix expired and the Ministry of Health began to automatically prescribe the generic alternative in favor of the brand name drug.

The researchers found that generic version, which is far cheaper, did not cause any significant difference in health outcomes for heart-attack and chest pain patients. Clopidogrel patients were no more likely to die from any cause or be re-hospitalized for heart problems within a year than those who were prescribed Plavix (17.9 percent vs. 17.6 percent).

“People can safely use generic clopidogrel. This large and real-world study should be reassuring to physicians and healthcare organizations who have been concerned about changing what is prescribed,” Ko said in a statement.

In 2010, Plavix cost $2.58 Canadian dollars per pill. The generic version costs only $0.39 per pill, resulting in huge savings for the healthcare system. The results should apply to the United States, even if the generic drug offerings are slightly different, according to the researchers.

“I think the biggest limitation of our study is that we were unable to look at this aspect in patients under 65 years old. However, older patients are at highest risk of complications and we do not think our finding should differ among younger patients,” Ko told ZME Science.

[panel style=”panel-info” title=”Generic drugs have to work just as well as brand-name drugs” footer=””]

In the United States, the FDA requires drug companies to demonstrate that the generic medicine can be effectively substituted and provide the same clinical benefit as the brand-name medicine that it copies. To get approved, generic drugs must meet the following requirements:

  • The active ingredient in the generic medicine is the same as in the brand-name drug/innovator drug.
  • The generic medicine has the same strength, use indications, form (such as a tablet or an injectable), and route of administration (such as oral or topical).
  • The inactive ingredients of the generic medicine are acceptable.
  • The generic medicine is manufactured under the same strict standards as the brand-name medicine.
  • The container in which the medicine will be shipped and sold is appropriate, and the label is the same as the brand-name medicine’s label.


In other words, a generic must work exactly as a brand name drug to be on the market in the first place. As billions of dollars worth of brand-name drugs go off patent, the market will increasingly become available to far-cheaper generic copies. Between 2010 and 2014, patent-protection ended for prescription drugs worth an estimated $7-billion a year in Canada, according to one estimate. Even so, generic drug adoption is still sluggish.

Ko told me that there are two main factors that slow down generic drug adoption.

“Patients and clinicians do not trust generic medications, maybe, in part, because there are not enough studies to show their safety. The brand name drug manufacturers also likely continue to exert an influence on the market to protect the market share of the drugs — such as providing incentives so that patients continue their drugs,” Ko told ZME Science.

“It is difficult to pinpoint exactly why brand name medications are continued to be used frequently, but it is correct that we need more studies on generic medications so that they are used frequently to reduce health care costs,” he added.

Next, Ko and colleagues plan on investigating the generic drug’s effectiveness in other groups of patients.

“We are continuing to conduct additional research on effectiveness and safety of the medical treatment in post myocardial infarction patients. We have developed a very extensive dataset on a population level of myocardial infarction and unstable angina patients in Ontario and will work towards ensuring that the safety and effectiveness of the drugs are translated in a real-world setting,” Ko said.

Findings appeared in the journal Circulation: Cardiovascular Quality and Outcomes.



artificial heart

Silicon 3D-printed heart looks and functions much like the real deal

Each year, about 26 million people worldwide suffer a heart failure and donors barely cover a fraction of the demand. Swiss researchers at ETH Zurich want to make heart transplants a lot easier and safer. While their solution isn’t meant to replace a heart, the artificial silicon heart they developed is set to increase the rate of success of transplant operations.

artificial heart

Credit: Zurich Heart.

In the crucial minutes between when a patient’s heart stops beating and doctors prepare the transplant of a new heart from a donor, surgeons use blood pumps to bridge this gap. Sometimes, however, the mechanical parts of the pump can cause unwanted complications that can ruin the operation, threatening the life of the patient.

The 390-gram artificial heart is designed to have the size as the patient’s own one so it can fit. Because it’s 3-D printed, it could actually completely mimic the patient’s own heart both in appearance and function.

It’s comprised of a left and right ventricle which are separated by another chamber that inflates and deflates with air pressure, thus mimicking the pumping action of the human heart. It came to life during the doctoral studies of Nichals Cohrs, who is now part of the Zurich Heart project which focuses on improving existing blood pumps.

Tests show the heart can last around 3,000 beats or 30 to 45 minutes of operation, after which the material starts to collapse under the strain. The findings were reported in the journal Artificial Organs.

“This was simply a feasibility test. Our goal was not to present a heart ready for implantation, but to think about a new direction for the development of artificial hearts,” said Cohrs.

For the next prototype, the researchers plan on significantly improving the tensile strength so the artificial heart can beat on for hours if it has to.

“As a mechanical engineer, I would never have thought that I would ever hold a soft heart in my hands. I’m now so fascinated by this research that I would very much like to continue working on the development of artificial hearts,” said Anastasios Petrou, a doctoral student of the Product Development Group Zurich.

It’s efforts such as this that lend hope one day we’ll be able to make artificial hearts that can be fitted instead of a patient’s own heart. Already, there are some options but they’re not there yet in terms of functionality. For instance, a 25-year-old man from the US lived without a heart for more than a year, carrying his artificial heart in a backpack with him. You can read more about his amazing story in a previous ZME article.

The amazing see-through frog. Credit: Jaime Culebras.

Incredible new Amazon glass frog is so transparent you can see its beating heart

Deep in the Amazonian lowlands, biologists stumbled across a peculiar glass frog species completely new to science. What makes glass frogs so interesting, unique even, is their chest which varies in different levels of transparency. This trait is so pronounced in some individuals that you can see their beating hearts straight through the limpid chest. Unfortunately, the new species called Hyalinobatrachium yaku may already be threatened with extinction by oil exploitations in the area.

The amazing see-through frog. Credit: Jaime Culebras.

The amazing see-through frog. Credit: Jaime Culebras.

Glass frog or “see-through frog” is a unique type of frog that is named that way because of its translucent skin. These usually live in Central and South America, preferring tropical rainforests where they rest high in the treetops right above the water. These unique amphibians are usually tiny, typically 0.78 inches long, though some can reach 3 inches in length.

The body of the frog is usually bright green or olive green in color, and it’s the belly that’s covered in transparent skin. Liver, heart, and intestines can be seen when the glass frog is looked from the underneath.

Glass frogs are arboreal animals, meaning they spend most of their lives in trees and will come to the ground only during the mating season which takes place right after the rainy season. Females lay 20 to 30 eggs on the underside of leaves that hang right above the water. Males, on the other hand, guard the eggs until these are ready to hatch and fall on the below water stream. The males are also very protective of their mates’ eggs and will watch them 24/7. Nothing will sway the males from their jobs and no intrududer is intimidating enough for them. Some males have even been known to kick away wasps that get too close to the egg cluster!

More than 60 different species of glass frogs are known to science, the latest being Hyalinobatrachium yaku which was identified as unique by researchers at the Universidad San Francisco de Quito, in Ecuador. The team led by biologist Juan Guayasamin performed DNA sequencing on samples taken from the glass frog and found the genome didn’t match other species. They also found that the dark green spots on its back, its call, and reproductive behavior were different from other known frogs.

A juvenile H. yaku, stands out with its dark green spots and atypical reproductive behaviours.

A juvenile H. yaku, stands out with its dark green spots and atypical reproductive behaviours.

‘All species in this genus have a completely transparent ventral peritoneum, which means that organs are fully visible in ventral view,’ researchers explain in a new paper, published to ZooKeys.

‘The reproductive behaviour is also unusual, with males calling from the underside of leaves and providing parental care to egg clutches.’

Nobody’s sure why the see-through skin appeared in glass frogs but the discovery of H. yaku might help shed light in the matter. The more members scientists can draw on a family tree, the easier it becomes to identify out evolutionary traits and mechanisms.

Might be already endangered

All in all, Hyalinobatrachium yaku looks like a fine addition to the 100 to 200 of so new amphibian species discovered each year — far more than new birds or mammals. However, this joy might be short-lived. Like other glass frogs, this amphibian needs pristine streams to breed but these are beginning to dry up or get polluted from nearby oil wells.

“For example, even though a high proportion of the Ecuadorian Amazon is already concessioned to several extractive activities, the Government of Ecuador is planning to intensify oil extraction in the region,” the researchers wrote.

“Aside from obvious concerns such as water pollution, extraction of natural resources increased the level of regional road development, which could threaten populations of H. yaku.”



A muffin a day might keep the doctor away — if you eat this special muffin

Eating healthy foods just became much easier, after researchers develop a new type of muffin which is delicious and very good for you.

These are cholesterol-lowering muffins that can lower your cholesterol and keep your health healthy. Image credits: University of Queensland (UQ).

We all know we should eat healthy foods, but quite often, the problem is that we fall for the tasty foods, which are often not as good for us. After all, who can resist good cake? But what if instead of being not-particularly-good-for-you, the cake would actually really healthy? That’s what UQ Centre for Nutrition and Food Sciences scientist and keen baker Dr. Nima Gunness had in mind when she designed the ‘good health’ muffin.

The good heart muffin contains three grams of beta-glucans — soluble fibers which emerge naturally in the walls of oats and other cereals. Beta-glucans are also natural components of the cell walls of bacteria, fungi, and yeast. The good thing about them is that meet the food standard guidelines for lowering cholesterol.

“There is good evidence that three grams or more of oats beta glucan consumption a day can help reduce cholesterol levels,” Dr Gunness said.

The idea is not groundbreaking, but it crosses a much-needed bridge. Researchers often focus on understanding the benefits of certain compounds, but rarely concern themselves with delivering that compound to the public in an attractive form. Dr. Gunness chose a different approach, and we’re happy she did.

This is Dr. Nima Gunness with her healthy heart muffin. Image credits: University of Queensland.

This is how she developed the ‘good heart’ muffin, as an attractive product which people would naturally want to buy.

“I wanted to turn my discovery into a product, like a muffin, that people could eat to help reduce the amount of cholesterol in their blood stream, lowering the risk of heart disease.”

She didn’t just jam the beta-glucans into a classical muffin recipe. Instead, she spent months trying to figure out how to achieve the best taste and texture while not sacrificing the ‘good heart’ part.

“The trick was to avoid making the muffin gluggy from all the extra oat bran and beta glucan fibre.”

She says that so far, customer feedback has been highly encouraging, and this has a real shot at providing a cheap, desirable, and delicious way to boost people’s heart health. We can only hope her muffin will be a commercial success. After all, who doesn’t like muffins?

“It’s very exciting to see a simple everyday product come out of some fairly complex research.

Atrioventricular node with macrophages.

Macrophages conduct electricity through the heart to keep it beating properly

Macrophages seem to not only help keep the body safe and clean but also make sure it stays very much alive by helping the mammalian heart beat in rhythm, new research reveals.

Colorized scanning electron micrograph of a macrophage.
Image credits NIAID / Flickr.

They’re the champion eaters of our bodies, gulping up pathogens and waste wherever they find them — they’re the macrophages. These white cells play a central part in our immune systems, for which we’re all thankful. But they may play a much more immediately vital role for us than we’ve suspected. Researchers from the Massachusetts General Hospital have discovered that these cells play a central part in regulating cardiac activity by conducting electrical signals through the heart.

“This work opens up a completely new view on electrophysiology; now, we have a new cell type on the map that is involved in conduction,” says senior author Matthias Nahrendorf, a systems biologist at Massachusetts General Hospital, Harvard Medical School.

“Macrophages are famous for sensing their environment and changing their phenotype very drastically, so you can think about a situation where there is inflammation in the heart that may alter conduction, and we now need to look at whether these cells are causally involved in conduction abnormalities.”

Researchers have known for some time now that macrophages can be found in and around hearts battling an infection — cause that’s what they do. But Nahrendorf team found that they still hang around in healthy hearts, in much greater numbers than would be required for simple maintenance or defense. So he and his team set out to understand why.

After performing MRI and electrocardiogram studies on model depleted of macrophages, the team found that the heart was arrhythmic and beat too slowly. By analyzing the heart tissue of a healthy mouse, they found that there’s a high density of macrophage cells at atrioventricular node, which carries electricity from the atria to the heart’s ventricles.

Working with David Milan and Patrick Ellinor, both electrophysiologists at Massachusetts General Hospital, the researchers found that the macrophages extend their membranes between cardiac cells and create pores, known as gap junctions, for electricity to flow through. This helps prepare the heart’s conducting cells (the ‘wiring’) for the next burst of electricity — allowing them to maintain a fast contraction rhythm.

Atrioventricular node with macrophages.

Cardiomyocytes (heart muscle cell, red) densely interspersed with macrophages (green).
Image credits Maarten Hulsmans / Matthias Nahrendorf.

“When we got the first patch clamp data that showed the macrophages in contact with cardiomyoctes were rhythmically depolarizing, that was the moment I realized they weren’t insulating, but actually helping to conduct,” Nahrendorf says.

“This work was very exciting because it was an example of how team science can help to connect fields that are traditionally separated — in this case, immunology and electrophysiology.”

The researchers say that the next step is to see whether macrophages have a hand to play in common conduction abnormalities in the heart. There are potential ties between macrophages and anti-inflammatory drugs, which are widely reported to help with heart disease. If macrophages do play a role in disease, the researchers say it can open up a new line of therapeutics, as these immune cells naturally consume foreign molecules in their presence and are easy to target as a result.

The full paper “Macrophages Facilitate Electrical Conduction in the Heart” has been published in the journal Cell.

New soft heart robot could save many lives from heart failure

A soft, customizable robot fits around a human heart and helps it beat. Without actually touching any blood, it augments cardiovascular functions, reducing the risk of clots and eliminating the need for dangerous blood thinning medication. All this sounds like Science Fiction — but it’s very much real. The technology was developed by researchers from Harvard University and Boston Children’s Hospital as a treatment for people suffering from heart failure.

In vivo demonstration of cardiac assist in a porcine model of acute heart failure (Video courtesy of Ellen Roche/Harvard SEAS)
Credit: Courtesy of Ellen Roche/Harvard SEAS

Heart failure affects over 40 million people every year. Today, we have some possibilities to mechanically aid the heart through pumps called ventricular assist devices (VADs) which pump blood from the ventricles into the aorta, and heart transplant. While this is spectacular in itself, patients using VADs are still at risk of blood clots and stroke, so scientists wanted a different option, a robot which isn’t in contact with any blood.

“This work represents an exciting proof of concept result for this soft robot, demonstrating that it can safely interact with soft tissue and lead to improvements in cardiac function. We envision many other future applications where such devices can delivery mechanotherapy both inside and outside of the body,” said Conor Walsh, senior author of the paper and the John L. Loeb Associate Professor of Engineering and Applied Sciences at SEAS and Core Faculty Member at the Wyss Institute.

To create the device, they took inspiration from the heart itself. It features soft pneumatic actuators placed around the heart, mimicking the outer muscle layers of the mammalian heart. They’re covered with a thin silicone sleeve, and the actuators pull and compress the sleeve in a similar fashion to a real heart. Everything is connected to an external pump which uses air to power the actuators. In other words, it stimulates the heart just like the real muscles do, but from the outside – not from within.

Researchers have really big plans for this technology, and soft robots seem like a great fit for this type of invasive yet delicate interventions.

“This work represents an exciting proof of concept result for this soft robot, demonstrating that it can safely interact with soft tissue and lead to improvements in cardiac function. We envision many other future applications where such devices can delivery mechanotherapy both inside and outside of the body,” said Conor Walsh, senior author of the paper and the John L. Loeb Associate Professor of Engineering and Applied Sciences at SEAS and Core Faculty Member at the Wyss Institute.

So far, the work has only been tested in a lab and on animal models — there’s still a way to go before it will be tested on humans. But the research opens intriguing possibilities: can we truly augment human organs with soft, external robots? The answer will likely be ‘yes.’


Harvard pushes the boundaries and fully 3-D prints a heart-on-a-chip device


Image courtesy of Lori K. Sanders and Alex D. Valentine, Lewis Lab/Harvard University

Scientists at Harvard University used novel inks and 3-D printing techniques to make the first entirely 3-D printed organ-on-a-chip. Such devices are very valuable for modeling the function of human tissues and are used to collect data. The downside is that they’re very expensive, but the newly printed heart-on-chip is easily customizable and manufactured. One day, such microphysiological systems could be widely used because they can be quickly tailored to match the properties of diseases or even the cells of individual patients.

“This new programmable approach to building organs-on-chips not only allows us to easily change and customize the design of the system by integrating sensing but also drastically simplifies data acquisition,” said Johan Ulrik Lind, first author of the paper, postdoctoral fellow at the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS), and researcher at the Wyss Institute for Biologically Inspired Engineering at Harvard University.

3d printed heart on chip

The heart-on-a-chip is entirely 3D printed with built-in sensors that offer new possibilities for studying the musculature of the heart. Image courtesy of Johan Lind, Michael Rosnach, Disease Biophysics Group/Lori K. Sanders, Lewis Lab/Harvard University

Lind and colleagues designed six different inks that can be integrated with soft strain sensors with a microarchitecture. In one single go, the Harvard researchers 3-D printed these inky materials into a cardiac device with integrated sensors — the heart on a chip.

“We are pushing the boundaries of three-dimensional printing by developing and integrating multiple functional materials within printed devices,” said Lewis. “This study is a powerful demonstration of how our platform can be used to create fully functional, instrumented chips for drug screening and disease modeling.”Jennifer Lewis, co-author of the new study published in Nature Materials and the Hansjorg Wyss Professor of Biologically Inspired Engineering.

Inside the chip, we can find multiple wells which separate tissues and integrated sensors. This design allows scientists to study multiple engineered cardiac tissues at once.

A couple of experiments were performed to demonstrate the new technology, including drug studies and long-term studies of cardiac tissue response to contractile stress.

Cardiac tissue self assembles on the chip, guided into place by the printed microstructures. Credit: Johan Lind, Francesco S. Pasqualini, Disease Biophysics Group/Harvard University

Cardiac tissue self assembles on the chip, guided into place by the printed microstructures. Credit: Johan Lind, Francesco S. Pasqualini, Disease Biophysics Group/Harvard University

“Researchers are often left working in the dark when it comes to gradual changes that occur during cardiac tissue development and maturation because there has been a lack of easy, noninvasive ways to measure the tissue functional performance,” said Lind. “These integrated sensors allow researchers to continuously collect data while tissues mature and improve their contractility. Similarly, they will enable studies of gradual effects of chronic exposure to toxins.”

“Translating microphysiological devices into truly valuable platforms for studying human health and disease requires that we address both data acquisition and manufacturing of our devices,” said Kit Parker, Tarr Family Professor of Bioengineering and Applied Physics at SEAS, who co-authored the study. Parker is also a core faculty member of the Wyss Institute. “This work offers new potential solutions to both of these central challenges.”