Progressive epicardial coronary blood flow reduction fails to produce ST-segment depression at normal heart rates

Abstract

ST-segment depression is commonly seen in patients with acute coronary syndromes. Most authors have attributed it to transient reductions in coronary blood flow due to nonocclusive thrombus formation on a disrupted atherosclerotic plaque and dynamic focal vasospasm at the site of coronary artery stenosis. However, ST-segment depression was never reproduced in classic animal models of coronary stenosis without the presence of tachycardia. We hypothesized that ST-segment depression occurring during acute coronary syndromes is not entirely explained by changes in epicardial coronary artery resistance and thus evaluated the effect of a slow, progressive epicardial coronary artery occlusion on the ECG and regional myocardial blood flow in anesthetized pigs. Slow, progressive occlusion over 72 min (SD 27) of the left anterior descending coronary artery in 20 anesthetized pigs led to a 90% decrease in coronary blood flow and the development of ST-segment elevation associated with homogeneous and transmural myocardial blood flow reductions, confirmed by microspheres and myocardial contrast echocardiography. ST-segment depression was not observed in any ECG lead before the development of ST-segment elevation. At normal heart rates, progressive epicardial stenosis of a coronary artery results in myocardial ischemia associated with homogeneous, transmural reduction in regional myocardial blood flow and ST-segment elevation, without preceding ST-segment depression. Thus, in coronary syndromes with ST-segment depression and predominant subendocardial ischemia, factors other than mere increases in epicardial coronary resistance must be invoked to explain the heterogeneous parietal distribution of flow and associated ECG changes.

Dissociation of hemodynamic and electrocardiographic indexes of myocardial ischemia in pigs with hibernating myocardium and sudden cardiac death

“…Animal studies directly measuring myocardial perfusion during acute ischemia have also confirmed the insensitivity of the ECG to detect ischemia that is restricted to the subendocardium. de Chantal et al (7) found no electrocardiographic evidence of ischemia in swine when subendocardial perfusion was reduced by up to 50% by an acute partial LAD occlusion. Collectively, the findings in humans and animal models of acute ischemia support the notion that electrocardiographically silent myocardial ischemia is common and could explain the development of extensive intrinsic adaptations of the myocardium to chronic repetitive ischemia in the absence of ST segment changes in swine with hibernating myocardium.…”

“…Since the ECG may be relatively insensitive to detect subtle degrees of subendocardial ischemia (7), hemodynamic indexes such as LV end-diastolic pressure (LVEDP) or indexes of LV contractility might provide more sensitive indicators of ischemia since they change quickly after total coronary occlusion (27) and before the development of ST segment changes or angina in patients (5). We therefore performed the present study to determine if LV hemodynamic variables at the onset of a spontaneous episode of VT/VF in swine with hibernating myocardium differ from animals that survive.…”

The role of extracellular potassium transport in computer models of the ischemic zone

“…One reason for the uncertainty is the difficulty of reproducing it in animal models at normal heart rate [8,28,29]. Understanding of subendocardial ischemia therefore depends on careful analysis of the limited data that can be obtained from patients, and on computer modeling.…”