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COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type
James R Hilser1,2, Neal J Spencer1,2, Kimia Afshari1,2
1Department of Population and Public Health Sciences (J.R.H., N.J.S., K.A., F.D.G., H.H., J.A.H., H.A.), Keck School of Medicine, University of Southern California, Los Angeles.
Insights
COVID-19 hospitalization significantly increases the long-term risk of major adverse cardiac events (MACE), acting as a coronary artery disease risk equivalent. Non-O blood types face a heightened risk of thrombotic events post-COVID-19, indicating a gene-pathogen interaction.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Genetics
Background:
- COVID-19 (Coronavirus Disease 2019) is linked to an increased risk of major adverse cardiac events (MACE), including heart attack, stroke, and death.
- The long-term cardiovascular disease (CVD) risk and MACE determinants following COVID-19 infection remain unclear.
Purpose of the Study:
- To assess the long-term risk of MACE after COVID-19 infection.
- To determine if COVID-19 hospitalization is a risk equivalent for coronary artery disease (CAD).
- To investigate potential interactions between genetic factors and COVID-19 in MACE development.
Main Methods:
- Utilized UK Biobank data from February 1, 2020, to December 31, 2020.
- Identified COVID-19 cases (n=10,005) via PCR testing or ICD-10 codes.
- Employed proportional hazard models and propensity score-matched controls (n=38,860) to analyze long-term MACE risk (>1000 days).
Main Results:
- COVID-19 cases exhibited elevated MACE risk across all severities (HR 2.09), significantly higher in hospitalized cases (HR 3.85).
- Hospitalization for COVID-19 was a CAD risk equivalent, with higher MACE risk in non-CVD patients than in CVD patients without COVID-19 (HR 1.21).
- A significant interaction between the ABO blood group locus and COVID-19 hospitalization was found (P=0.01), increasing thrombotic event risk in non-O blood types (HR 1.65).
Conclusions:
- Hospitalization for COVID-19 equates to a CAD risk equivalent, with elevated post-acute myocardial infarction and stroke risk observed.
- Non-O blood types show a particularly heightened risk for thrombotic events after COVID-19 hospitalization.
- This study presents one of the first documented gene-pathogen interactions influencing thrombotic events.
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 (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.
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