SARS-CoV-2 infection may not elicit inflammatory response linked to myocarditis
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A lower SARS-CoV-2 virus load within the cardiac tissue may not prompt the inflammatory response associated with clinical myocarditis, researchers reported.
In an analysis of consecutive autopsies, compared with patients with no cardiac infection, patients with more than 1,000 copies of SARS-CoV-2 per micrograms of RNA had no cardiac inflammatory cell infiltrates or differences in leukocyte numbers per high-power field.
“Fulminant myocarditis was not associated with SARS-CoV-2 infection in this study, with no significant change in transendothelial migration of inflammatory cells in the myocardium in patients with high virus load vs. no virus,” Diana Lindner, PhD, of the department of cardiology at the University Heart and Vascular Centre in Hamburg, Germany, and colleagues wrote. “Our findings emphasize no increased inflammatory cells in consecutive COVID-19 cases without clinical myocarditis. Whether myocardial viral activity in the absence of clinical evidence of myocarditis might result in long-term consequences is unknown.”
For this study, published in JAMA Cardiology, investigators used data from consecutive autopsy cases (April 8 to April 18) of 39 SARS-CoV-2-positive patients (median age, 85 years; 59% women) to determine the presence of the virus within the myocardial tissue and document a possible cardiac response.
Pneumonia was documented as cause of death in 89.7% of the cohort, whereas 10.2% died from other causes, including necrotizing fasciitis, cardiac decompensation with prior HF and bacterial bronchitis. The cause of death for one patient was unknown.
Hypertension (43.6%), CAD (82%) and diabetes (17.9%) were the most common comorbidities.
Overall, 38.5% of autopsies were free from SARS-CoV-2 RNA in the myocardium. Among those with viral presence, 33.3% had virus load of less than 1,000 copies per micrograms of RNA. The remainder (n = 16) had virus load above 1,000 copies per micrograms of RNA. In situ hybridization confirmed presence of SARS-CoV-2 in interstitial cells within cardiac tissue.
Reduced proinflammatory gene expression of growth factor-alpha, interferon-gamma, chemokine ligand 5, and interleukin-6, interleukin-8 and interleukin-18 was found among patients with a virus load of less than 1,000 copies per micrograms of RNA compared with those with higher virus load.
“Importantly, virus presence was not associated with increased infiltration of mononuclear cells into the myocardium compared with the virus negative group,” the researchers wrote. “According to the Dallas criteria, no myocarditis was present because no massive cell infiltrates or necrosis could be documented.”
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