First-Line Treatment of Left Ventricular Failure Complicating Acute Myocardial Infarction

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Abstract
A prospective randomised trial compared the immediate haemodynamic effects of intravenous diuretic (frusemide), venodilator (isosorbide dinitrate), arteriolar dilator (hydralazine), and positive inotropic stimulation (prenalterol) as first-line therapy for acute left ventricular (LV) failure following myocardial infarction. Forty-eight patients with transmural myocardial infarction and a pulmonary artery occluded pressure (PAOP) of > 20 mm Hg were studied within 18 h of admission to a coronary care unit. Both frusemide (-4 mm Hg; p < 0.01) and isosorbide dinitrate (-6 mm Hg; p < 0.01) reduced LV filling pressure without change in cardiac index and heart rate. Although both hydralazine and prenalterol increased cardiac index (p < 0.01), the reduction in LV filling pressure (-2 mm Hg; p < 0.05) was less than with frusemide and isosorbide dinitrate, and was associated with an increased heart rate (+8 and +13 beats min-1; p < 0.01). These data suggest that in acute heart failure following myocardial infarction the four treatment modalities could be ranked in descending order of potential benefit as follows: (a) venodilation (isosorbide dinitrate).sbd.decrease of LV pressure/work; (b) diuretic therapy (frusemide).sbd.decrease of LV pressure/work offset by a transient pressor effect; (c) arteriolar dilatation (hydralazine).sbd.decrease of LV pressure/work and of PAOP, but offset by tachycardia; and (d) positive inotropic therapy (.beta.1-agonist prenalterol).sbd.tachycardia and augmented LV afterload. Combination of the former and latter agents, because of their differing modes of action, should offer haemodynamic advantages over monotherapy and deserves further evaluation.