Two German studies published today in JAMA Cardiology show abnormal heart imaging findings in recently recovered COVID-19 patients, and cardiac infections in those who have died from their infections.
The first, an observational cohort study, involved 100 unselected coronavirus patients identified from the University Hospital Frankfurt COVID-19 Registry from April to June, 57 risk factor-matched patients, and 50 healthy volunteers.
Cardiac magnetic resonance (CMR) imaging revealed heart involvement in 78 patients and active cardiac inflammation in 60, independent of underlying conditions, disease severity, overall course of illness, and time from diagnosis to CMR.
Thirty-three of 100 patients required hospitalization. Detectable levels of high-sensitivity troponin were found in 71 COVID-19 patients, while significantly elevated levels were detected in five patients. Recovered COVID-19 patients had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and elevated native T1 and T2 than controls, all indicating heart dysfunction.
Seventy-eight coronavirus patients had abnormal CMR findings, including 73 with raised myocardial native T1, 60 with raised myocardial native T2, 32 with myocardial late gadolinium enhancement, and 22 with pericardial enhancement, all signs of heart damage. Biopsy of the heart muscle in patients with serious findings showed ongoing immune-mediated inflammation.
Exacerbation of underlying heart disease
The study authors noted that while most coronavirus research has focused on short-term respiratory complications, particularly in critically ill patients, mounting evidence suggests that COVID-19 has a significant impact on the cardiovascular system by worsening heart failure in patients with preexisting cardiac diseases.
In this study, CMR revealed several kinds of heart abnormalities, each of which can be tied to underlying dysfunction and worse outcomes, the authors said. They added that their study also showed that direct tissue characterization with mapping measures on CMR is the most sensitive and clinically relevant way to detect early heart disease.
"While left and right ventricular ejection fraction were significantly reduced, there was a large overlap between patients recently recovered from COVID-19 and both control groups, demonstrating that volumes and function are inferior markers of disease detection," they wrote.
Cardiac infections, high viral loads
The second study involved the autopsies of 39 COVID-19 patients conducted from Apr 8 to 18. Pathologists from the Legal Medicine at the University Medical Center Hamburg Eppendorf identified evidence of the COVID-19–causing SARS-CoV-2 virus—but not clinically relevant inflammation of the heart muscle—in 24 cadavers (61.5%), 16 (41.0%) of which had high loads of viral RNA.
Of the 24 cadavers with heart infections, a cytokine response panel showed that expression of six pro-inflammatory genes was higher in the 16 with high viral loads than in the 8 with low viral loads. But there were no signs of a massive influx of inflammatory cells into the heart muscle or tissue death in either group.
Cause of death was listed as pneumonia in 35 cases (89.7%), while the other four (10.2%) died of necrotizing fasciitis, cardiac decompensation with previous heart failure, bacterial bronchitis, or unknown causes. The most common underlying illnesses were coronary artery disease (32 [82.0%]), high blood pressure (17 [43.6%]), and diabetes (7 [17.9%]). Median patient age was 85 years, and 23 of 39 patients (59%) were women.
"Overt fulminant myocarditis has been reported in isolated patients with SARS-CoV-2 infection," the authors wrote. "However, the current data indicate that the presence of SARS-CoV-2 in cardiac tissue does not necessarily cause an inflammatory reaction consistent with clinical myocarditis."
They called for future research on the long-term complications of COVID-19 cardiac involvement.
