Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.

No abstract

Ten normal volunteers and 38 patients with acute myocardial infarction were evaluated by biplane gated blood pool scanning. The mean left ventricular end-diastolic volume in those with infarction was 125 ± 41 ml/m 2 compared to 82 ± 10 ml/m 2 in the normals. The left ventricular end-systolic volume was 82 ± 35 ml/m 2 compared to 35 ± 4 ml/m 2 , and the left ventricular ejection fraction 36 ± 8% compared to 56 ± 3% in the normals. Thirty-six of the 38 patients with infarction had an area of akinesis which ranged from 15 to 59% of the left ventricular wall. Patients with acute myocardial infarction were found to have a significant increase in left ventricular end-systolic volume and decrease in ejection fraction compared to normals. The end-diastolic volume was, however, increased only in those with an elevated left ventricular filling pressure or decreased cardiac index. Follow-up studies obtained in 20 patients between one week and three months following infarction showed that in the 14 who improved clinically, left ventricular ejection fraction significantly increased from 38 to 45% ( P < 0.001) while in six who failed to show clinical improvement or worsened, left ventricular ejection fraction remained at 30%. Left ventricular ejection fraction was significantly greater and the extent of akinesis significantly less in the patients who survived compared to those who died.