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Cardio-Vascular Heart Health Infectious Disease Inflammation

Mysterious Heart Damage Affecting COVID-19 Patients

4 weeks ago

1610  0
Posted on Jun 04, 2020, 6 p.m.

The majority of the focus of this outbreak has been placed upon the respiratory problems and securing enough ventilators for patients, but physicians on the front lines of this battle are struggling with medical mysteries. 

In addition to the lung damage many patients are developing heart problems and are dying of cardiac arrest. As more data emerges cardiac experts are coming to believe that this virus can infect the heart muscle, and an initial study has found cardiac damage 1 in 5 patients leading to heart failure and even death among those COVID-19 patients who are showing no signs of respiratory distress. 

This could change the way physicians and hospitals think about these patients, particularly in the early stages of illness. This may also open up a second front in the battle against this disease, creating a need for new precautions in those with preexisting heart problems, need for new equipment, and new treatments plans for damaged hearts in those who survive. 

“It’s extremely important to answer the question: Is their heart being affected by the virus and can we do something about it?” said Dr. Ulrich Jorde, the head of heart failure, cardiac transplantation and mechanical circulatory support for the Montefiore Health System in New York City. “This may save many lives in the end.”

A series of questions are emerging regarding whether heart problems are being caused by the virus or if they are a byproduct of the body’s reaction to the virus. This has become one of the critical unknowns that those brave souls on the frontlines are facing as they struggle to understand this novel illness. Determining how this virus affects the heart is proving to be difficult in part because severe illness alone is capable of influencing heart health. 

“Someone who’s dying from a bad pneumonia will ultimately die because the heart stops,” said Dr. Robert Bonow, a professor of cardiology at the Northwestern University Feinberg School of Medicine and editor of the medical journal JAMA Cardiology. “You can’t get enough oxygen into your system and things go haywire.”

Bonow and other cardiac specialists now believe that COVID-19 infection can lead to damage to the heart in 4 or 5 ways, with some patients being more affected by more than one of those pathways at the same time. 

Any serious medical event or even something as seemingly straightforward as hip surgery can create enough stress to damage the heart. Conditions such as pneumonia can cause widespread inflammation in the body which can lead to plaque in the arteries becoming unstable causing heart attacks. Inflammation can also cause myocarditis which can lead to the weakening of the heart muscle and heart failure. 

Damage observed in COVID-19 patients could be from the virus directly infecting the heart muscle, and initial research suggests that this virus attaches to certain receptors in the lungs, and these same receptors are also found in heart muscle, according to Bonow. 

Physicians in China recently published 2 studies demonstrating the first glimpses of how prevalent cardiac problems are among COVID-19 patients. The larger of the studies analyzed 416 hospitalized patients finding that 19% displayed signs of heart damage and those who did were significantly more likely to die.

51% of those with heart damage lost their battles with this disease versus 4.5% of those who did not have heart damage. Those who had heart disease before being infected were much more likely to show heart damage afterwards, but some with no previous heart disease also showed signs of cardiac damage. Those with no pre-existing heart conditions who incurred heart damage during infection were found to be more likely to die than those with previous heart disease but no COVID-19 induced cardiac damage. 

While it is unclear why some experience more cardiac effects than others, Bonow is not ruling out the possibility that it could be due to a genetic predisposition or being due to exposure to higher viral loads. 

All the uncertainties highlight the need for closer monitoring for cardiac markers in those who are infected suggests Jorde. If physicians and scientists are able to determine how the virus is affecting the heart they may be able to develop some sort of risk score or other guidance to help all clinicians manage the outbreak in patients around the globe. 

“We have to assume, maybe, that the virus affects the heart directly,” Jorde said. “But it’s essential to find out.”

Collecting data amid a crisis can be difficult, ideally biopsies of heart tissue would be taken to determine if the heart muscle has become infected with this virus. However, patients are often so ill it is difficult for them to undergo such invasive procedures, and more testing could expose additional healthcare workers. Electrocardiograms aren’t being used on isolated patients in many hospitals to avoid exposing more people and using limited supplies.

Amid the surge in patients physicians continue to gather data, compile trends, and publish their findings as quickly as they can.  Dr. Sahil Parikh, an interventional cardiologist at Columbia University Irving Medical Center in New York City and several colleagues have recently authored a compilation of what is known about these cardiac complications, making the report immediately available online and will be adding new findings before the article is put to print. 

A group of cardiologists from several states are also sharing the latest of information through WhatsApp. Even hospitals operating under crisis conditions are testing new drugs and treatments in clinical trials to ensure that what they are learning about this virus is being shared with others in the medical community with scientific validity. 

The work that groups such as these are doing is changing the way that hospitals are dealing with the cardiac implications of COVID-19 infection. These infections have been found to mimic heart attack, as patients brought to clear a suspected blockage have been found not to be experiencing a heart attack but they had COVID-19. Hospitals often rush suspected heart attack patients directly to a catheterization lab in an effort to shorten time for hospital entry to clearing the blockage with a balloon. This door to balloon time is important as a measure of how well hospitals treat heart attacks. Now new protocols are being developed, including bringing in a cardiologist and getting an EKG or ultrasound to confirm a blockage.

“We’re taking a step back from that now and thinking about having patients brought to the emergency department so they can get evaluated briefly, so that we could determine: Is this somebody who’s really at high risk for COVID-19?” Parikh said. “And is this manifestation that we’re calling a heart attack really a heart attack?”

About a month ago we also reported another mysterious and deadly complication that appears to be showing up in the front lines: “Microclots” - blood flow impeded by blood clots; the thrombotic events are occurring for a variety of reasons among those in intensive care, but the rates among COVID-19 patients are substantially higher than would otherwise be expected. 

Although it is not known exactly why this is happening there are several explanations such as those with severe forms of COVID-19 with underlying medical conditions such as heart or lung disease are linked to higher rates of clotting even without being infected. Also being in an ICU can make a person more likely to develop a clot as they are remaining still for too long. Infection with COVID-19 is associated with an abnormal cytokine storm immune reaction that research indicates is also linked to higher rates of blood clotting. 

This new mystery may help to solve the slightly older one, as lungs that are filled with microclots may explain why ventilators work so poorly for patients with low blood oxygen. Earlier into this outbreak doctors were treating patients with protocols developed for wet lungs, but in some cases it may not be due to the lungs being occupied with water, rather it may be that microclotting is blocking circulation and blood is leaving the lungs with less oxygen than it should. 

A study published in the Lancet has reported evidence of viral bodies of this novel coronavirus invading endothelial cells, which is the lining of our blood vessels that directs important functions of the vascular system, like clotting and swelling. Co-author Mandeep Mehra, MD, medical director of the Brigham and Women's Heart and Vascular Center in Boston suggests this virus can directly infect the endothelium, "This is actually a disease of the endothelium," he says.

Mehra thinks the infection only begins in the lungs because breathing is the easiest entry, once infected lungs cells begin to be destroyed and the virus then travels into the bloodstream where it infects endothelial cells causing endotheliitis. This comes from not only the direct infection but also from the cytokine storm that was launched to fight it off. Mehra believes his theory of infection may explain some of the puzzle to COVID-19. 

While there are many theories to these clots, and they may explain part of the mystery, but the clots themselves are just another part of a much larger problem, one that hopefully doctors can solve soon. Sorting out how this virus affects the heart will help doctors to determine which approaches to pursue in order to keep patients alive. 

After patients recover they could have long term effects from heart damage. Treatment options already exist for various forms of heart damage which will hopefully be effective once the infection has cleared. Here’s hoping that answers to these mysteries will be revealed sooner rather than later. 

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This article is not intended to provide medical diagnosis, advice, treatment, or endorsement.

https://worldhealth.net/news/latest-medical-findings-suggest-blood-clotting-covid-19/

https://khn.org/news/mysterious-heart-damage-not-just-lung-troubles-befalling-covid-19-patients/

https://www.onlinejacc.org/content/75/18/2352

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