Abstract
During acute myocardial infarction an increase in arterial pressure is common in patients who were previously normotensive and, therefore, do not have left ventricular hypertrophy. However, the effect of hypertension on infarct size in the absence of hypertrophy is uncertain. Thus, 32 open chest dogs underwent a 2 hour occlusion of the mid-left anterior descending coronary artery followed by 3 hours of reperfusion. Immediately after occlusion, 14 dogs were randomized to a hypertension group (intravenous phenylephrine infusion starting 5 minutes after occlusion and terminating at the time of reperfusion, with heart rate kept constant by atrial pacing) and 18 dogs to a control group (equivalent volumes of saline solution intravenously). Twelve of the 32 dogs were excluded from analysis because they developed ventricular fibrillation during coronary occlusion or reperfusion. In the hypertension group (n = 10), the mean arterial pressure increased significantly within 10 minutes of coronary occlusion (146 ± 7 versus 109 ± 11 mm Hg in 10 control dogs, p < 0.01) and was maintained approx- imately 40 mm Hg higher than in the control group (p < 0.01) throughout the ischemic period. Heart rate was similar in the two groups throughout the experiment. After the dogs were sacrificed, the region normally supplied by the occluded artery (anatomic “region at risk”) was identified by simultaneous perfusion of the aortic root and the coronary artery distal to the occlusion. The heart was sectioned transversely and stained with triphenyltetrazolium-chloride. The infarcted area and the anatomic risk area were determined by video planimetry. Control and hypertension groups did not differ significantly in the percent of left ventricle infarcted (14 ± 2 [mean ± standard error] and 13 ± 3%, respectively) or in the percent of anatomic risk region infarcted (41 ± 5 and 37 ± 7%, respectively). It is concluded that acute arterial hypertension un-associated with left ventricular hypertrophy has neither detrimental nor beneficial effects on the size of myocardial infarction resulting from a temporary coronary occlusion followed by reperfusion. © 1984, American College of Cardiology Foundation. All rights reserved.