The pathophysiology of peri‐operative myocardial infarction

Summary It is generally believed that plaque rupture and myocardial oxygen supply‐demand imbalance contribute approximately equally to the burden of peri‐operative myocardial infarction. This review critically analyses data of post‐mortem, pre‐operative coronary angiography, troponin surveillance, other pre‐operative non‐invasive investigations, and peri‐operative haemodynamic predictors of myocardial ischaemia and/or myocardial infarction. The current evidence suggests that myocardial oxygen supply‐demand imbalance predominates in the early postoperative period. It is likely that flow stagnation and thrombus formation is an important pathway in the development of a peri‐operative myocardial infarction, in addition to the more commonly recognised role of peri‐operative tachycardia. Research and therapeutic interventions should be focused on the prediction and therapy of flow stagnation and thrombus formation. Plaque rupture appears to be a more random event, distributed over the entire peri‐operative admission.