ItHome Cardiac Arrest COVID-19’s consequences for the heart – Harvard Gazette

COVID-19’s consequences for the heart – Harvard Gazette

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COVID-19’s consequences for the heart – Harvard Gazette

Third, some people may experience heart damage that mimics heart attack injury even if their arteries lack the fatty, calcified flow-limiting blockages known to cause classic heart attacks. This scenario can occur when the heart muscle is starved for oxygen, which in the case of COVID-19 may be triggered by a mismatch between oxygen supply and oxygen demand. Fever and inflammation accelerate heart rate and increase metabolic demands on many organs, including the heart. That stress is compounded if the lungs are infected and incapable of exchanging oxygen and carbon dioxide optimally. This impaired gas exchange can further diminish oxygen supply to the heart muscle.

Finally, there is a subset of people with COVID-19 — some of them previously healthy and with no underlying cardiac problems — who develop fulminant inflammation of the heart muscle as a result of the virus directly infecting the heart. This type of inflammation could lead to heart rhythm disturbances and cardiac muscle damage as well as interfere with the heart’s ability to pump blood optimally. 

The propensity of certain viruses to attack the heart muscle and cause viral myocarditis is well known, Libby said, adding that the most notorious viral offender has been the Coxsackie B virus. A recent case report from Italy underscores the notion that the new coronavirus could also infect the heart and affect heart muscle function in healthy adults even after the acute phase of the infection has resolved and even in the absence of lung damage.

“There are definitely some people who develop acute fulminant myocarditis — in which the virus infects the heart muscle itself or the cells within the heart — and causes a horrible inflammatory reaction,” said Libby, the Mallinckrodt Professor of Medicine at Brigham and Women’s Hospital. “This can be life threatening, and it can happen in people who don’t have any preexisting risk factors.”

Libby and Ridker, however, say this out-of-the-blue scenario in otherwise healthy individuals is likely rare relative to the overall number of people with COVID-19 who experience heart problems. 

The frenemy within

For Ridker and Libby, the cardiac involvement in COVID-19 is yet another striking example of the widespread effects of inflammation on multiple organs and systems. Inflammation is a critical defense response during infection, but it has a dark side. Infections can set off a cascade of immune signals that affect various organs. 

Libby and Ridker hypothesize that any infection in the body — a festering boil, an injured joint, a virus — can become a source of inflammation that activates the release of inflammatory proteins known as cytokines and calls up armies of white blood cells and other messenger molecules that, in an effort to fight the infection, disrupt normal processes. When these inflammatory molecules reach the welcoming soil of a fatty deposit in the blood vessel wall — one that is already studded with resident inflammatory white blood cells — the cytokines can boost the local inflammatory response and trigger a heart attack.

“Our work has shown that cytokines can impinge on these cells in the plaque and push it through a round of further activation,” Libby said.

The inflammatory chemicals released during infection can also induce the liver to ramp up the production of important proteins that defend the body from infection. These proteins, however, make the blood more prone to clotting, while also reducing the secretion of natural clot-dissolving substances. The tiny clots that may form can clog the small blood vessels in the heart and other organs, such as the kidneys, depriving them of oxygen and nutrients and setting the stage for the multisystem failure that can occur in acute infection.

Thus, immune-mediated injury to the heart and other organs could be collateral damage because of the body’s overwhelming systemic immune response — a condition known as cytokine storm, which is marked by the widespread release of cytokines that can cause cellular demise, tissue injury and organ damage.

COVID-19 and blood pressure medications

SARS-CoV-2 invades human cells by latching its spike protein onto the ACE2 receptor found on the surface of cells in the airways, lungs, heart, kidneys and blood vessels. The ACE2 protein is an important player in the renin-angiotensin-aldosterone system, which regulates blood vessel dilation and blood pressure. Two classes of drugs widely used to treat high blood pressure and heart disease — ACE inhibitors and angiotensin receptor blockers — interact with the ACE2 receptor. A possible concern related to COVID-19 stems from the notion that these blood pressure medications could increase the number of ACE2 receptors expressed on cells, possibly creating more molecular gates for the virus to enter. Some experts have wondered whether the use of such drugs could render people who take them more susceptible to infection. Conversely, others have postulated that the abundance of ACE2 receptors may enhance cardiovascular function, exercising a protective effect during infection.

The answer is far from clear, but a recent review suggests these medicines may play a dual role in COVID-19 — on the one hand, enhancing susceptibility to infection and, on the other, protecting the heart and ameliorating lung damage from the disease.

Libby and Ridker cautioned that patients who take such life-saving medications should stay on them or at least have a careful discussion with their cardiologists. This is because these drugs have clear and well-established benefits in hypertension and certain forms of heart disease, while their propensity to make humans more susceptible to SARS-CoV-2 remains speculative for the time being.

But what remains speculative today will crystalize in the weeks and months to come, Ridker and Libby said, because the science is moving forward rapidly, with new papers coming out daily and a growing pool of patients to draw observations from.

“In 12 to 18 months we’re going to have a great deal of information, but right now our job is to, number one, keep people from getting COVID-19 by strict adherence to now-familiar containment measures,” Libby said. “Then, we need to get people who get the disease through this acute phase.”

The need for rigorous randomized trials done quickly and effectively is acute, they said. Until the evidence from these trials begins to coalesce, clinicians will have to navigate the uncharted territory of delivering cardiac care in the time of pandemic with caution but also with resolve.

“We don’t have the comfort of our usual databases, so we have to rely on our clinical skills and judgment. But we have to do so in all humility because often data don’t bear out our logical preconceptions,” Libby said. “Yet, we must act.”

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