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longest ischemic events that culminated in myocardial infarction. No patient had ischemia (>10 min) during induction of anesthesia. Six patients had relatively short (≤34 min) intraoperative ischemia; only one of them sustained a longer episode of postoperative ischemia, which culminated in MI.Discussion Previous studies implied that prolonged ischemia is associated with postoperative cardiac complications. Frank et al. (19)and Ganz et al. (20)described two patients who died 9 h and 12 h after peripheral vascular surgery, following prolonged, silent ST depression-type ischemia on Holter monitoring. In a study of 151 patients, the cumulative duration of ST depression on Holter monitoring predicted postoperative cardiac complications (4). This study expands previous observations and shows that in vascular surgery patients the rise in cTn-I levels signifying PMI occurs during or immediately after prolonged, silent, stress-induced postoperative ischemia detected on continuous 12-lead ECG. The definition of PMI Postoperative MI was defined as a cTn-I level >3.1 ng/ml (12,17)after prolonged ST-segment deviation. This definition of MI conforms to the newly formulated European Society of Cardiology/American College of Cardiology consensus document redefining acute MI (18). Only 6 of the 12 patients with MI had either prolonged typical chest pain (5)or persistent new T wave inversion (1), thus fulfilling the traditional World Health Organization criteria for MI. Our ROC analysis of longest ischemia duration at different cutoff levels of cTn-I further confirmed that cTn-I levels between 3 and 3.5 ng/ml best defined PMI . Stress-induced postoperative ischemia The majority (67%) of ischemic events, including those culminating in PMI, started at the end of surgery and emergence from anesthesia (Fig. 3), a time characterized by an increase in heart rate, blood pressure, sympathetic discharge and procoagulant activity (21). This finding is supported by two recent studies (12,22)in which the increase in troponin occurred mostly within 12 h to 24 h after surgery and implies that 36 h of monitoring may suffice to capture most PMIs. Also in accordance with previous studies, ischemia was denoted by ST depression, not elevation, and was preceded in all cases by an increase in heart rate. In all but one patient, ischemic ECG changes were transient, emphasizing the importance of continuous ST monitoring for its detection. Pathophysiology of PMI The mechanism underlying PMI is not known. It is assumed to resemble that of nonsurgical MI (23), that is, acute plaque rupture and coronary thrombosis caused by the abrupt increases in blood pressure, heart rate, coronary tone and platelet aggregability (24)and the decrease in fibrinolytic activity (25)occurring postoperatively. However, total coronary occlusion and coronary thrombosis are found in only 26% to 43% of patients early after either ST elevation or ST depression–type non-Q-wave infarction (26), compared with >90% coronary occlusion in patients with Q-wave infarction. None of our patients had ST elevation or Q-wave infarction. Coronary angiography was performed in only three of our patients with PMI within seven days of the infarction, and in each case it showed chronic, severe CAD without angiographically visible thrombus or ruptured plaques. In one patient the postoperative angiogram was identical to a previous one obtained six months earlier. Is it possible, therefore, that PMI in these patients occurred secondary to prolonged postoperative ischemia in the presence of severe, yet stable, CAD and not as a consequence of acute coronary occlusion? Fuster et al. (27)proposed that, in contrast with the common thrombotic occlusion of a coronary artery after acute plaque disruption, thrombosis in a severe, but stable, coronary stenosis may
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