{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T10:44:32Z","timestamp":1791974672812,"version":"4.4.0"},"reference-count":33,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Clin Appl Thromb Hemost"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Perioperative myocardial injury (PMI) and perioperative myocardial infarction (PMIn) are common, often clinically silent complications after noncardiac surgery and are associated with substantial short- and long-term mortality. Surgical stress promotes a prothrombotic milieu through platelet activation, coagulation cascade amplification, impaired fibrinolysis, endothelial dysfunction, and plaque destabilization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>This narrative review synthesizes current evidence on the thrombotic mechanisms, diagnostic challenges, and antithrombotic management of PMI\/PMIn, with emphasis on risk stratification using coronary computed tomography angiography (CCTA) and thrombogenicity biomarkers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Major perioperative cohort studies, randomized trials, scientific statements, and international guidelines were reviewed, including VISION, MANAGE, POISE, PANDA, the 2021 American Heart Association scientific statement, the 2024 American College of Cardiology\/American Heart Association (ACC\/AHA) perioperative guideline, and the 2022 European Society of Cardiology guideline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Most perioperative ischemic injury is clinically silent and frequently reflects oxygen supply-demand mismatch, whereas atherothrombotic plaque rupture with coronary thrombosis represents an important minority. Serial high-sensitivity troponin surveillance is central to detection, but interpretation requires exclusion of nonischemic causes and integration with electrocardiography, echocardiography, clinical context, and coronary anatomy. CCTA identifies vulnerable coronary anatomy, whereas D-dimer and thromboelastography-derived platelet-fibrin clot strength characterize a complementary vulnerable-blood phenotype. Antithrombotic therapy should be individualized: antiplatelet therapy and invasive evaluation are appropriate for Type 1 PMIn when bleeding risk permits, whereas dabigatran reduced major vascular complications in selected patients with myocardial injury after noncardiac surgery (MINS) in MANAGE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>A multimodal strategy integrating clinical risk, coronary anatomy, postoperative troponin surveillance, and thrombogenicity assessment may improve perioperative risk discrimination and guide individualized prevention and treatment.<\/jats:p>\n                  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