COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
Practically from the beginning of the COVID-19 pandemic, researchers and medical experts feared–and often loudly warned–that the virus wasn’t like other infections that people might encounter during, say, flu season. SARS-CoV-2 was different. It was worse. And the potential long-term effects, as we reported two years ago, were even more worrisome.
A new large-scale study puts those longer-range concerns into bold relief. The results are as unforgiving as many experts had hypothesized.
Abstract:
BACKGROUND:
COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post–COVID-19 are not known.
RESULTS:
The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94–2.25]; P<0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51–4.24]; P<0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08–1.37]; P<0.005). A significant genetic interaction was observed between the ABO locus and hospitalization for COVID-19 (Pinteraction=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29–2.09]; P=4.8×10−5) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66–1.39]; P=0.82).
CONCLUSIONS:
Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post–acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events.
