Heart and Vascular

How much damage does COVID-19 really cause on the heart?

Covid in Athletes

By Gregory Katz, MD


We can look at two studies published recently that investigated the effects of COVID-19 on the heart for some insight — one on cardiac MRIs done in survivors and one from an autopsy report of people who died from COVID-19.

The Cardiac MRI Study

This study looked at a randomly selected group of 100 patients with confirmed COVID-19 infection, about a third of whom required hospital admission. They did cardiac MRIs on the patients about 10 weeks after confirmed infection and compared the results to cardiac MRIs done on patients who weren’t infected. The top-line report is scary — more than three-fourths of the patients had “structural changes to their hearts” or “evidence of a biomarker signaling cardiac injury typically found after a heart attack.”

But when you dig into the numbers, things look a little bit less grave.

We measure cardiac function with something called an ejection fraction. A normal value is over 55%. The average patient in the COVID-19 group had an ejection fraction of 56%, compared to about 60% for the non-COVID-19 group. This was statistically significant but of questionable clinical significance.

The most notable part of the study is the description of scar tissue forming in the heart (late gadolinium enhancement, or LGE, for those MRI aficionados). Patients with COVID-19 were twice as likely as matched non-COVID-19 patients to have evidence of scar in the heart. The scar tissue data suggests the cardiac impact may be permanent.

The Autopsy Study

This study looked at 39 patients who had died with a confirmed diagnosis of COVID-19. They performed autopsies on the bodies and found viral genetic material (RNA) in the muscle tissue of the heart in 24 of them (around 60% of the patients). Two-thirds of the patients with viral RNA had very high levels, indicating a lot of virus in the heart. The patients in this study didn’t die of cardiac dysfunction — they predominantly died of pneumonia — and they didn’t even seem to have clinical evidence of cardiac dysfunction before death.

This is food for thought without clear real-world relevance. After all, the presence of viral particles in the heart may just reflect how sick you were. And who cares if you have viral fragments in your heart if you survive and go back to your regular life?

What should we take from this?

This doesn’t really change much about how we think of COVID-19 right now. We already know a lot of people have died. We already know there’s potential for long-term effects from this virus. But these findings do raise alarm bells.

The two studies put together start to tell a story of a physiologic explanation for cardiac dysfunction (viral particles found in the heart on autopsy) with evidence of cardiac dysfunction seen in patients (mildly reduced cardiac function on MRI).

But we probably don’t know enough to draw conclusions. Do the cardiac findings we’ve just discussed matter? They certainly raise several additional questions:

  • How does this cardiac damage evolve over a longer time frame?
  • Do these patients have increased risk of congestive heart failure? Of death from cardiac causes?
  • Does treating patients with cardio-protective medications such as beta blockers reduce the cardiac damage from COVID-19?
  • What is the long-term functional status of these patients? Are their lives limited by cardiac dysfunction?
  • Smart researchers are tackling these questions as we speak.

I’ll leave you with this: Just because something is statistically significant doesn’t mean it’s clinically significant. Conversely, just because you don’t want something to be clinically significant doesn’t mean it isn’t.

Dr. Gregory Katz is a cardiologist with The Heart Center, a division of Hudson Valley Cardiovascular Practice, P.C., now part of Nuvance Health. For more information on cardiovascular care and The Heart Center, visit www.nuvancehealth.org/heartcenter