The Core Lesson of the COVID-19 Heart Debate
Last Monday, when I called the cardiologist Amy Kontorovich in the late morning, she apologized for sounding tired. “I’ve been in my lab infecting heart cells with SARS-CoV-2 since 6 a.m. this morning,” she said.
That might seem like an odd experiment for a virus that spreads through the air, and primarily infects the lungs and airways. But SARS-CoV-2, the new coronavirus behind the COVID-19 pandemic, can also damage the heart. That much was clear in the early months of the pandemic, when some COVID-19 patients would be hospitalized with respiratory problems and die from heart failure. “Cardiologists have been thinking about this since March,” said Kontorovich, who is based at Mount Sinai. “Data have been trickling in.”
Autopsies have found traces of the coronavirus’s genetic material in the heart, and actual viral particles within the heart’s muscle cells. Experiments have found that SARS-CoV-2 can destroy lab-grown versions of those cells. Several studies have now shown that roughly 10 to 30 percent of hospitalized COVID-19 patients had high levels of troponin—a protein released into the blood when the heart’s muscle cells are damaged. Such patients are more likely to die than others with no signs of heart injury.
[Read: America is trapped in a pandemic spiral]
This is worrying for people with severe symptoms, but more recently, a suggested that COVID-19 can cause heart inflammation, or myocarditis, even in people who showed mild symptoms, or had recovered. These results were controversial but concerning. Myocarditis is frequently caused by—the Big Ten and the Pac-12—to cancel their fall season. (The Big Ten has since , and the Pac-12 is )
