Key result
Severe COVID-19 hospitalization acts as a CAD risk equivalent, especially in non-O blood types.
Why the study?
The duration and determinants of heightened cardiovascular disease and MACE risk after COVID-19 infection were not known.
Does COVID-19 infection increase the long-term risk of MACE compared to matched controls?
Cohort (n=227,735)
Does COVID-19 infection increase the long-term risk of MACE compared to matched controls?
Hazard Ratio: 2.09 (95% CI 1.94–2.25)
p-value: p=<0.0005
Hospitalization for COVID-19 represents a coronary artery disease risk equivalent for long-term MACE, with thrombotic risk particularly heightened in patients with non-O blood types.
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. METHODS: Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR + )-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based International Classification of Diseases version-10 (ICD-10 ) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score—matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components. 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 ( P interaction =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.
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Hilser et al. (2024) conducted a cohort in COVID-19 (n=227,735). COVID-19 vs. Controls without COVID-19 was evaluated on major adverse cardiac events (MACE) (HR 2.09, 95% CI 1.94-2.25, p=<0.0005). COVID-19 infection was associated with an elevated long-term risk of major adverse cardiac events across all severity levels (HR 2.09; 95% CI 1.94-2.25; P<0.0005).
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