{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T05:15:26Z","timestamp":1790226926151,"version":"4.1.0"},"reference-count":70,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","license":[{"start":{"date-parts":[[2024,11,1]],"date-time":"2024-11-01T00:00:00Z","timestamp":1730419200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>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\u2013COVID-19 are not known.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              Data from the UK Biobank was used to identify COVID-19 cases (n=10\u2009005) who were positive for polymerase chain reaction (PCR\n              <jats:sup>+<\/jats:sup>\n              )-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based\n              <jats:italic>International Classification of Diseases version-10 (ICD-10<\/jats:italic>\n              ) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217\u2009730) and propensity score\u2014matched controls (n=38\u2009860) 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 (&gt;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.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94\u20132.25];\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51\u20134.24];\n              <jats:italic>P<\/jats:italic>\n              &lt;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\u20131.37];\n              <jats:italic>P<\/jats:italic>\n              &lt;0.005). A significant genetic interaction was observed between the\n              <jats:italic>ABO<\/jats:italic>\n              locus and hospitalization for COVID-19 (\n              <jats:italic>P<\/jats:italic>\n              <jats:sub>interaction<\/jats:sub>\n              =0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29\u20132.09];\n              <jats:italic>P<\/jats:italic>\n              =4.8\u00d710\n              <jats:sup>\u22125<\/jats:sup>\n              ) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66\u20131.39];\n              <jats:italic>P<\/jats:italic>\n              =0.82).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post\u2013acute 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.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.124.321001","type":"journal-article","created":{"date-parts":[[2024,10,9]],"date-time":"2024-10-09T09:00:31Z","timestamp":1728464431000},"page":"2321-2333","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":66,"title":["COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type"],"prefix":"10.1161","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5849-7839","authenticated-orcid":true,"given":"James R.","family":"Hilser","sequence":"first","affiliation":[{"name":"Department 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 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