The effect of different mechanisms of myocardial ischemia on left ventricular function.

Myocardial ischemia may be produced by limitation of blood flow as in abrupt coronary occlusion, termed supply-type ischemia, or by increasing myocardial oxygen demand in the setting of restricted flow, termed demand-type ischemia. To examine the comparative extent and severity of the dysfunction related to both forms of ischemia, we studied anesthetized, open-chest dogs by means of two-dimensional echocardiography and tracer microspheres. Supply-type ischemia was produced by total occlusion of the LCx (n = 7); demand-type ischemia was induced by infusion of dobutamine after creation of a critical LCx stenosis (n = 6). At the time of the production of ischemia, the group with demand-type ischemia had significant increases in both heart rate (p less than 0.05) and mean arterial pressure (p less than 0.05), whereas the group with supply-type ischemia had a decrease in mean arterial pressure (p less than 0.05). Subendocardial blood flow in the LCx region was severely depressed in supply-type ischemia (0.09 +/- 0.04 ml/min/gm) compared to demand-type ischemia (1.04 +/- 0.07 ml/min/gm; p less than 0.01). Although both groups of animals had an abnormality of left ventricular function during ischemia, as determined by two-dimensional echocardiography, the extent of the dysfunction in the group with supply-type ischemia was greater (146 +/- 12 degrees) compared to the group with demand-type ischemia (99 +/- 9 degrees; p less than 0.01). Similarly, the degree of left ventricular dysfunction in the group with supply-type ischemia was greater than that for the group with demand-type ischemia (p less than 0.05). Thus these data suggest that supply-type ischemia produced by coronary occlusion results in a greater extent and degree of left ventricular functional abnormality than pharmacologically induced demand-type ischemia.