Two German studies published today in JAMA Cardiology They show abnormal imaging findings of the heart in newly recovered COVID-19 patients and heart infections in those who have died from their infections.
The first, an observational cohort study, involved 100 unselected coronavirus patients identified by the COVID-19 Registry of the Frankfurt University Hospital from April to June, 57 patients with risk factors and 50 healthy volunteers.
Cardiac magnetic resonance imaging (CMR) revealed cardiac involvement in 78 patients and active cardiac inflammation in 60, regardless of underlying conditions, disease severity, general course of disease, and time from diagnosis to CMR.
Thirty-three out of 100 patients required hospitalization. Detectable levels of highly sensitive troponin were found in 71 patients with COVID-19, while significantly elevated levels were detected in five patients. Patients recovered from COVID-19 had a lower left ventricular ejection fraction, higher left ventricular volumes, higher left ventricular mass, and higher native T1 and T2 than controls, indicating cardiac dysfunction.
Seventy-eight coronavirus patients had abnormal CMR findings, including 73 with elevated native myocardial T1, 60 with elevated native myocardial T2, 32 with late myocardial gadolinium enhancement, and 22 with pericardial enhancement, all signs of cardiac damage. Biopsy of the heart muscle in patients with severe findings showed continued inflammation mediated by the immune system.
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 as it worsens. heart failure in patients with pre-existing heart disease.
In this study, CMR revealed several types of heart abnormalities, each of which may be related to underlying dysfunction and the worst outcomes, the authors said. They added that their study also showed that direct tissue characterization with CMR mapping measures is the most sensitive and clinically relevant way to detect early heart disease.
“Although the left and right ventricular ejection fraction was significantly reduced, there was a large overlap between recently recovered COVID-19 patients and both control groups, demonstrating that volumes and function are lower markers of detection of disease, “they wrote.
Cardiac infections, high viral loads.
The second study included autopsies of 39 patients with COVID-19 performed from April 8 to 18. Legal Medicine pathologists at the Hamburg Eppendorf University Medical Center identified evidence of the SARS-CoV-2 virus that causes COVID-19, but not clinically relevant inflammation of the heart muscle: in 24 cadavers (61.5%), 16 (41.0%) of which had high viral RNA loads.
Of the 24 corpses with heart infections, a cytokine response panel showed that the expression of six proinflammatory 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 in the heart muscle or tissue death in either group.
The 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 diseases were coronary artery disease (32). [82.0%]), high blood pressure (17 [43.6%]) and diabetes (7 [17.9%]) The median age of the patients 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, current data indicates that the presence of SARS-CoV-2 in heart 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 heart involvement.
