title: The effect of different mechanisms of myocardial ischemia on left ventricular function.
abstract: 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.
authors.affiliation: Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0366.
authors.forename: R E
authors.initials: RE
authors.lastname: Carlson
authors.forename: K M
authors.initials: KM
authors.lastname: Kavanaugh
authors.forename: A J
authors.initials: AJ
authors.lastname: Buda
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D004285:Dogs; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D013318:Stroke Volume