The pathophysiology of peri-operative myocardial infarction.

Abstract

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.