Evidence is mounting that COVID-19 also damages the heart, damage either caused by the virus itself, from inflammation triggered by the immune system’s response to the virus or a from increased clotting in heart vessels. Courtesy of
Intermountain Healthcare Heart Institute
One of the most harrowing effects of COVID-19 is severe damage to the lungs, which makes breathing hard or impossible for those who’re severely affected. However, evidence is mounting that COVID-19 also damages the heart, damage either caused by the virus itself, from inflammation triggered by the immune system’s response to the virus or a from increased clotting in heart vessels.
There is now evidence that heart damage may persist even after the patient recovers and, in some cases, that damage may be long lasting. Experts just don’t know how often the heart damage will occur at this point or whether it might affect people with only mild symptoms.
The worry is so grave that it was cited by some college football conferences as one of the reasons to postpone games for the year for fear that athletes who contract COVID-19 may suffer long-term cardiovascular problems.
In a prospectus review published this week in the Journal of Molecular and Cellular Cardiology, Kirk U. Knowlton MD, from the Intermountain Healthcare Heart Institute in Salt Lake City, examined more than 100 published studies related to COVID-19 and its effects on the heart.
While lung disease (severe acute respiratory distress syndrome, or ARDS) has been the most consistent problem with the virus, Knowlton found that many patients also suffer significant cardiovascular damage that might also persist after they have otherwise recovered.
“There’s clear evidence that COVID-19 can cause heart disease,” said Knowlton, who is director of cardiovascular research at the Intermountain Healthcare Heart Institute. “It does not affect all patients but affects around one in five patients admitted to the hospital with COVID-19.”
“When heart damage is present, patients have a greater chance of needing ventilators to support their breathing and they are at substantially higher risk of dying of COVID-19,” he added. “In addition to the acute effects, we still need to learn more about the long-term implications of the virus on the heart after people have otherwise recovered.”
In his review of published research, Knowlton found multiple reports of myocarditis or inflammation of the heart muscle that can damage the heart and affect the heart’s ability to pump blood.
In fact, leaders from the NCAA’s PAC-12 conference cited COVID-related myocarditis when announcing their decision to postpone sports for the fall 2020 season, after at least 10 football players developed the heart condition after being diagnosed with COVID-19.
Boston Red Sox pitcher Eduardo Rodriguez is also out indefinitely for the 2020 Major League Baseball season with COVID-related myocarditis.
Knowlton said additional data and follow up will be needed to understand the overall percentage of patients who might develop myocarditis.
Knowlton points out that there is considerable evidence that the COVID-19 infection can damage the heart in hospitalized patients via several mechanisms, including myocarditis. However, less is known about the effects of the virus on the heart in patients that do not require hospitalization or in those that do not develop significant lung disease.
While children are usually spared from the most ravaging effects of COVID-19, it can trigger a Kawasaki-like disease in children, that is referred to as Multisystem Inflammatory Syndrome in Children (MIS-C). This causes an inflammation of multiple body parts including the heart with evidence of myocarditis.
Other cardiovascular manifestations of COVID-19 include a thrombotic or clotting disorder that may manifest as deep-vein thrombosis, pulmonary embolism, stroke, and peripheral artery disease. Also, thrombosis of small and medium size vessels can contribute to cardiac injury.
Knowlton points out that this link between heart diseases and transmittable viruses isn’t new. Autopsies of patients who died during the 1918 flu pandemic found heart damage, and 50% of patients who died of polio from 1942 to 1951 had myocarditis, he said.
Heart damage has also been found in people infected with mumps, measles and enterovirus illnesses.
What’s less understood, he adds, is what role the virus-activated immune system plays in heart damage.
“Many patients with severe disease experience a cytokine storm, where the immune system goes into overdrive, attacks its own cells, and causes multi-organ failure,” he said. “These attacks to the heart are one of the ways that we believe the virus can cause heart damage and myocarditis, though the link is not absolutely clear.”
Treating COVID-19, he said, “is about finding a balance between allowing the immune system to fight the virus, but not so hard that it hurts the heart.”
Knowlton thinks treatments that disable the virus itself would stop it from replicating through the body (and being passed onto others) and that prevention of virus replication would prevent such a severe immune response.
This could be one of the most effective ways to treat patients that contract the virus, especially if started early. Most medications that treat other viral infections do so by preventing viral replication.
“Developing a more thorough understanding of the effects of the virus on the heart in the wider population of patients that are infected with SARS-CoV-2 is of paramount importance as we return to activities and events that involve large groups and athletes,” added Knowlton. “At the current time prevention continues to be the surest way to avoid the complications of heart disease caused by the virus.”
Source: Intermountain Healthcare