PATHOPHYSIOLOGY OF TRANSIENT MYOCARDIAL-ISCHEMIA IN ACUTE CORONARY SYNDROMES - CHARACTERIZATION BY CONTINUOUS ST-SEGMENT MONITORING

Background Transient ischemia in stable coronary disease peaks in the morning, reflecting increased myocardial oxygen demand and coronary va somotor tone after waking. In acute coronary syndromes, however, ische mia may result from transient thrombus formation or coronary spasm at the site of a ruptured plaque. We report on the pathophysiological mec hanisms underlying transient ischemia in acute coronary syndromes desp ite optimal therapy, on the basis of analysis of heart rate changes pr e ceding ischemia and its circadian variation. Methods and Results Two hundred fifty-six patients with unstable angina or non-Q-wave myocard ial infarction underwent continuous ST-segment monitoring for 48 hours while receiving maximal medical therapy. All ischemic episodes were c haracter ized by their timing, duration, association with pain, and he art rate changes before the onset of ischemia. During 10 629 hours of monitoring, 44 patients (17.2%) had 176 episodes of transient ischemia . The mean heart rate at onset of ischemia was 68+/-12.8 bpm, and >55% of ischemic episodes were not preceded by a significant increase in h eart rare. Ischemic activity had a single nocturnal peak, with 64% of all episodes occurring between 10 Ph I and 8 AM, this nocturnal prepon derance being evident for episodes with or without a preceding increas e in heart rate. The characteristics and timing of transient ischemia were similar in unstable angina and non-Q-wave myocardial infarction, but transient ischemia was more frequent (27.3% versus 15.1%; P<.05) a nd prolonged (median, 20 versus 13.5 minutes; P<.01) in non-Q-wave myo cardial infarction.Conclusions In acute coronary syndromes, transient ischemia has a low threshold, occurs predominantly without an increase in myocardial oxygen demand, and is present mainly at night rather th an in the morning. These findings in patients receiving maximal medica l therapy suggest significant pathophysiological differences underlyin g transient ischemia compared with stable coronary disease.