Abstract

The circulatory effects induced by two sequential intravenous treatment programs with a diuretic, arteriolar or venodilator, and a positive inotropic drug were studied in a randomized between-group trial in 20 male patients with radiographic and hemodynamic evidence of left ventricular (LV) failure following acute myocardial infarction (AMI). Furosemide induced a substantial diuresis in both groups of patients, in association with reductions in LV filling pressure ( p < 0.01) and cardiac output ( p < 0.05), without significant change in heart rate or systemic arterial pressure. The addition of isosorbide dinitrate was followed by reductions in the systemic arterial ( p < 0.01) and LV filling pressures ( p < 0.01) without significant change in the heart rate or cardiac output. Hydralazine after furosemide reduced systemic vascular resistance ( p < 0.01), but the fall in mean blood pressure ( p < 0.01) was limited by the increase in cardiac output ( p < 0.01); heart rate was also increased ( p < 0.01) and LV filling pressure fell ( p < 0.05). The final addition of the beta-1 adrenoceptor agonist, prenalterol, increased systemic arterial systolic pressure ( p < 0.05), cardiac output ( p < 0.05), and heart rate ( p < 0.01), and reduced systemic vascular resistance ( p < 0.01) in both groups; these changes were greatest in those pretreated with furosemide and isosorbide dinitrate. In both treatment pathways compared with control the reductions in systemic vascular resistance and left heart filling pressure were accompanied by increases in heart rate and cardiac output without substantial changes in systemic blood pressure. Which of these hemodynamic pathways offers the optimum prognosis awaits further study.

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