Finally, the muddied coronavirus waters are getting a little less murky — and revealing that the heart plays a major role in how COVID-19 affects people.
“When patients come in with something that seems non-COVID-related like a stroke or heart attack, we now know we should still be thinking of COVID as a player,” says Penn Medicine cardiologist Helene Glassberg, MD. “It’s important that we think in both directions. Don't miss a non-COVID diagnosis, but don't forget COVID when you're looking at something that doesn't look like it.”
Dr. Glassberg explains what we now know about the connection between heart disease and COVID-19.
How COVID-19 Affects the Heart
First came the studies out of Wuhan, China. One in March 2020 reported that 27.8 percent of hospitalized COVID-19 patients suffered heart damage. Some had preexisting heart problems, others didn’t. More research out of Europe and the U.S. has continued to shine a spotlight on the many ways COVID-19 affects the heart:
COVID-19 injures the heart
When you go to the hospital with heart concerns or a suspected COVID-19 infection, doctors will often check your cardiac enzymes. These tests measure the enzymes and proteins that increase when your heart is damaged, including troponin and creatine kinase (CK).
Damage to heart muscle cells causes troponin and creatine kinase to leak out of the heart into the blood. High levels of these enzymes on blood tests are a clear sign the heart’s in trouble. “The presence of these enzymes identifies heart attacks,” says Dr. Glassberg. “They also show when a COVID patient is having complications related to direct heart injury from the infection.”
COVID-19 causes myocarditis, which can lead to heart failure and arrhythmias
Coronavirus can also cause dangerous inflammation in the heart, or myocarditis, which prevents the heart from doing its job effectively. “We don’t yet know why or how, but COVID-19 infection can directly damage the heart and cause arrhythmias and heart failure. So it's an important risk factor to understand and use to monitor hospitalized patients.”
To determine if a patient is experiencing heart failure, doctors measure brain natriuretic peptide (BNP) levels. “When the heart muscle stretches, this protein gets released into the bloodstream,” explains Dr. Glassberg. “If BNP levels are elevated in COVID-19 patients, that means there’s heart injury and heart failure, which translates into potentially higher risks for worse outcomes.”
Dr. Glassberg also reports that about 10 to 20 percent of patients have arrhythmias related to COVID-19 infection.
COVID-19 infection increases blood clots
It’s becoming increasingly clear that the coronavirus can cause a dramatic increase in blood clots throughout the body. Blood clots happen when your blood forms gel-like clumps. Some European studies report that as many as 20 to 30 percent of the sickest COVID-19 patients are affected.
Too many blood clots lead to dangerous complications. “In patients coming in with a stroke or what looks like a heart attack, we need to consider if COVID is at play,” explains Dr. Glassberg. “We know from other infectious processes, such as sepsis or bacterial or viral illnesses, that people can have disruption of their clotting system. They either have bleeding problems or clotting problems. There’s some suspicion that the coronavirus has a direct effect on the clotting system as well. That may be why we're seeing not only stroke, but clots in small blood vessels and microclots in the lungs and heart.”
Who’s at Risk for Severe COVID-19 Illness and Related Heart Complications
The list of who’s most at risk for severe COVID-19 illness is now a familiar one:
- People age 65 and older
- Those with chronic medical conditions unrelated to COVID-19 infection
“Advanced age, established heart and lung disease, obesity, diabetes, high blood pressure (hypertension), and kidney disease put you at risk of having less wiggle room to tolerate any infection, but particularly COVID,” says Dr. Glassberg. “And surprisingly, heart disease seems to be an even greater risk factor than underlying lung disease.”
But in the ultimate catch-22, having a healthy immune system can sometimes backfire. It can overreact to the virus and cause inflammation that affects the organs — a response known as a cytokine storm. “We don't know what makes someone more hyperinflammatory than someone else. Decent control of your immune system might leave you with a low-grade fever and cough. But an immune system in overdrive seems to drive cellular effects that infiltrate the heart and take you over the edge, causing heart muscle inflammation and weakness.”
Solving the Mystery of High Blood Pressure and COVID-19 Risk
It’s a classic case of which came first: high blood pressure as a risk factor for COVID-19 — or blood pressure medications? The jury’s still out on whether high blood pressure itself or taking ACE (angiotensin-converting enzyme) inhibitors or ARB (angiotensin II receptor blocker) medications is more to blame. The key may lie in how the coronavirus invades the cells.
“The virus enters cells via a receptor called ACE2, or angiotensin converting enzyme-2. It's on the membrane of cells,” says Dr. Glassberg. “There's been a theory that if you take an ACE inhibitor or ARB, it might increase the activity of this ACE2, and in theory, increase the entry of the virus into the cell.”
But other researchers think it might be just the opposite. They propose that these medications help because they widen the blood vessels and have anti-inflammatory properties.
“On the other side, increasing ACE2 activity could actually help your immune system fight the virus,” says Dr. Glassberg. “Research is pointing to these blood pressure medications not increasing COVID-19 risk. That’s why the American Heart Association and the American College of Cardiology have maintained their position that people who take [blood pressure medications] should continue to do so unless their doctor says otherwise. What we don't want is untreated hypertension to go awry.”