A new study finds SARS-CoV-2 directly infects the coronary vasculature and causes plaque inflammation, which could help explain why people with COVID-19 have an increased risk for ischemic cardiovascular complications up to 1 year after infection.
METHODOLOGY:
Researchers obtained 27 coronary autopsy specimens from eight patients who died from COVID-19, mean age 70 years and 75% male. All had coronary artery disease and most had cardiovascular risk factors such as hypertension, were overweight or obese, and had hyperlipidemia and type 2 diabetes.
All but one patient, who was pronounced dead before hospital admission, were hospitalized for an average of 17.6 days.
To identify SARS-CoV-2 viral RNA (vRNA) in the autoptic coronary vasculature, researchers performed RNA fluorescence in situ hybridization (RNA-FISH) analysis for the vRNA encoding the spike (S) protein; they also probed the antisense strand of the S gene (S antisense), which is only produced during viral replication.
TAKEAWAY:
The study found evidence of SARS-CoV-2 replication in all analyzed human autopsy coronaries regardless of their pathological classification, although viral replication was highest in early-stage lesions that progress to more advanced atherosclerotic plaques.
Findings indicated that more than 79% of macrophages (white blood cells that help remove lipids) and over 90% of foam cells (lipid-laden macrophages that are a hallmark of atherosclerosis at all stages of the disease) are S+, and more than 40% of both cell types are S antisense+, indicating SARS-CoV-2 can infect macrophages at a high rate.
SARS-CoV-2 induced a strong inflammatory response as evidenced by release of cytokines (including interleukin-1 beta and interluekin-6 that are linked to myocardial infarction) in both macrophages and foam cells, which may contribute to the ischemic cardiovascular complications in patients with COVID-19.
IN PRACTICE:
"Our data conclusively demonstrate that SARS-CoV-2 is capable of infecting and replicating in macrophages within the coronary vasculature of patients with COVID-19," write the authors, adding that SARS-CoV-2 preferentially replicates in foam cells compared to other macrophages, suggesting these cells "might act as a reservoir of SARS-CoV-2 viral debris in the atherosclerotic plaque."
SOURCE:
The study was led by Natalia Eberhardt, PhD, postdoctoral fellow, Department of Medicine, Division of Cardiology, New York University, New York City, and colleagues. It was published online September 28 in Nature Cardiovascular Research.
LIMITATIONS:
Findings are relevant only to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021, and are not generalizable to patients younger and healthier than those from whom samples were obtained for the study.
DISCLOSURES:
The study received support from the National Institutes of Health (NIH). The authors report no relevant financial relationships.
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