Laboratory Investigation Myocardial Blood Flow

This study tested the hypothesis that in the chronically hypertrophied left ventricle pacing stress may cause abnormalities of perfusion that result in myocardial ischemia. Left ventricular hypertrophy (LVH) was produced by banding the ascending aorta of 10 dogs at 6 weeks of age, and studies were carried out after the animals had reached adulthood and when mean left ventricular/body weight ratio was 74% greater than in eight control dogs. Myocardial blood flow was measured with microspheres during pacing at 100, 200, and 250 beats/min, while aortic and coronary sinus blood samples were obtained for determination of concentrations of lactate and the adenosine metabolites inosine and hypoxanthine. In the control dogs, increasing heart rates were associated with an increase in mean myocardial blood flow while subendocardial flow was maintained at a level equal to or greater than subepicardial flow. Myocardial lactate uptake ranged from + 60% to -5%, and adenosine metabolites were not detected in coronary sinus blood (<0.5 ,uM/l). In four dogs that underwent aortic banding no production of lactate or adenosine metabolites was observed at any heart rate; in these animals subendocardial flow was maintained at a level equal to or greater than subepicardial flow at all pacing rates. The remaining six dogs with LVH demonstrated net lactate production significantly greater than control during pacing at 250 beats/min; five of these six animals also produced adenosine metabolites. In these six animals mean myocardial blood flow failed to increase as the pacing rate was increased from 200 to 250 beats/min, and pacing at 250 beats/min was associated with a transmural redistribution of perfusion away from the subendocardium (subendocardial/subepicardial blood flow ratio = 0.50 + 0.05). These findings demonstrate that perfusion abnormalities may occur in the chronically hypertrophied heart during rapid cardiac pacing and that these result in myocardial ischemia. Circulation 69, No. 2, 409-417, 1984. SEVERAL OBSERVATIONS suggest that the hypertrophied left ventricle may have increased vulnerability to ischemia. Thus, patients with severe left ventricular hypertrophy may experience angina pectoris and develop electrocardiographic repolarization abnormalities that are suggestive of myocardial ischemia. These findings may be accompanied by pathologic evidence of fibrosis or infarction of subendocardial myocardium or papillary muscle even in the presence of anatomically normal coronary arteries." 2 Although previous studies in the pressure-overloaded hypertroFrom the Department of Medicine, Cardiovascular Section, University of Minnesota Medical School, Minneapolis. This study was supported by U.S. Public Health Service grants HL21872, HL20598, and HL22152. Address for correspondence: Robert J. Bache, M.D., University of Minnesota Medical School, Box 388 Mayo Memorial Building, Minneapolis, MN 55455. Received Sept. 6, 1983; revision accepted Oct. 20, 1983. phied left ventricle have generally demonstrated a normal or slightly increased volume of blood flow per unit myocardial mass and a normal transmural distribution of perfusion under basal conditions,310 several investigators have reported that during the stress of exercise or rapid cardiac pacing, the hypertrophied heart may develop relative subendocardial hypoperfusion.5'6'"1'2 However, it is possible that alterations in the transmural distribution of myocardial blood flow could be related in part to changes in the transmural pattern of systolic stress (and therefore myocardial oxygen consumption) in the hypertrophied heart.9 For this reason, without information regarding myocardial metabolic demands it is not possible to determine whether relative subendocardial underperfusion in the hypertrophied heart represents inadequate subendocardial blood flow, or whether it results from a reduction of systolic stress in the subendocardium, thus representVol. 69, No. 2, February 1984 409 by gest on Jne 6, 2017 http://ciajournals.org/ D ow nladed from