Perioperative Myocardial Infarction

More than 230 million major surgeries are performed annually worldwide,1 and this number grows continuously. The 30-day mortality associated with moderate- to high-risk noncardiac surgery in recent large cohorts and population-based studies exceeds 2%2–4 and surpasses 5% in patients at high cardiac risk.5 Cardiac complications constitute the most common cause of postoperative morbidity and mortality,4,6 having considerable impact on the length and cost of hospitalization.7 As our population ages, more high-risk cardiac patients will undergo surgery, and perioperative myocardial infarction (PMI) can be an increasing problem. Traditionally, MI was defined by the World Health Organization criteria, ECG criteria, and cardiac enzymes. Defining PMI, however, is often difficult because most PMIs occur without symptoms in anesthetized or sedated patients, ECG changes are subtle and/or transient, and the creatine kinase-MB isoenzyme has limited sensitivity and specificity because of coexisting skeletal muscle injury.8 Consequently, PMI was often recognized late (postoperative day 3 to 5), resulting in high (30% to 70%9) mortality. Cardiac troponin assays have changed this definition.10 The recent universal definition of MI11 is based on a rise and/or fall of cardiac biomarkers (preferably troponin) in the setting of myocardial ischemia: cardiac symptoms, ECG changes, or imaging findings. Studies using serial troponin measurements demonstrate that most PMIs start within 24 to 48 hours of surgery during the greatest postoperative stress.12–15 Le Manach et al15 observed early ( 24 hours) peaks in troponin in 1136 patients after abdominal aortic aneurysmectomy. Yet, 90% of troponin elevations began within <24 hours. Two distinct mechanisms may lead to PMI: acute coronary syndrome and prolonged myocardial oxygen supply-demand imbalance in the presence of stable coronary artery disease (CAD), designated type 1 and type 2 by the universal definition of MI.11 This distinction …