Study: COVID-19 May Pose a Long-Term Cardiac Risk Comparable to Coronary Artery Disease

A new study found that COVID-19 significantly elevates the risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and all-cause mortality, particularly in individuals hospitalized with COVID-19.

The study addresses a critical gap in understanding the prolonged cardiovascular risk associated with COVID-19. While the acute cardiac risks of COVID-19 have been established, little is known about the extended duration and potential genetic influences on MACE risk.

Using data from the UK Biobank, researchers identified 10,005 individuals with confirmed COVID-19, verified through PCR tests or ICD-10 hospital codes, and matched them with both a general population control group (n = 217,730) and a propensity score–matched control group (n = 38,860). Proportional hazard models were employed to assess the association between COVID-19 and long-term MACE risk, with additional analyses examining genetic interactions. The study also investigated whether genetic determinants, particularly ABO blood group types, influenced MACE risk post-COVID-19.

The study results indicated an association between COVID-19 and elevated MACE risk across all infection severities, with the risk significantly accentuated in hospitalized cases. The researchers found that the hazard ratio (HR) for MACE in COVID-19 cases was 2.09 (95% CI, 1.94–2.25; P < .0005), and this risk increased substantially in those who required hospitalization, reaching an HR of 3.85 (95% CI, 3.51–4.24; P < .0005). In patients without prior cardiovascular disease, the risk of MACE following COVID-19 hospitalization surpassed that of individuals with preexisting cardiovascular disease, with an HR of 1.21 (95% CI, 1.08–1.37; P < .005). Specifically, COVID-19 hospitalization was correlated with an increased risk of thrombotic events, particularly among individuals with non-O blood types, suggesting a gene-pathogen interaction. For non-O blood types, the HR for thrombotic events was 1.65 (95% CI, 1.29–2.09; P = 4.8×10^−5), compared with 0.96 (95% CI, 0.66–1.39; P = .82) in individuals with blood type O.

A limitation of this study is its reliance on observational data. Additionally, the study did not account for potential behavioral or lifestyle changes post-COVID-19, which could also influence cardiovascular outcomes.

“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,” the authors concluded. “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.

Reference

Hilser JR, Spencer NJ, Afshari K, et al. COVID-19 is a coronary artery disease risk equivalent and exhibits a genetic interaction with ABO blood type. Arterioscler Thromb Vasc Biol. 2024;44(11):2321-2333. doi:10.1161/ATVBAHA.124.321001.