Acute effects of oral pirbuterol on myocardial oxygen metabolism and systemic hemodynamics in chronic congestive heart failure.

Abstract

Pirbuterol hydrochloride, an orally effective beta-adrenergic agonist, improves hemodynamic abnormalities in patients with congestive heart failure, but its effects on myocardial oxygen consumption (MVO2) and coronary blood flow have not been characterized. We studied the effects of 20-30 mg of oral pirbuterol on myocardial metabolic and hemodynamic parameters in 12 patients (six with coronary artery disease) with chronic CHF refractory to standard medical therapy. Pirbuterol induced an increase in cardiac index (1.7 +/- 0.1 to 2.3 +/- 0.2 l/min/m2, p less than 0.05) and a fall in systemic vascular resistance (1884 +/- 118 to 1391 +/- 69 dyn-sec-cm-5, p less than 0.01) 2 hours after administration. Pulmonary capillary wedge pressure fell from arterial and right atrial pressures did not change. Heart rate remained constant. Arterial-coronary sinus oxygen content difference narrowed (from 12.9 +/- 0.4 to 11.1 +/- 0.3 vol%, p less than 0.05), while no significant change occurred in MVO2. Myocardial oxygen extraction ratio and myocardial lactate extraction ratio did not change, and no patient developed angina or electrocardiographic evidence of myocardial ischemia. Patients with coronary artery disease had hemodynamic and myocardial metabolic responses similar to those without coronary artery disease. Pirbuterol effects substantial acute hemodynamic improvement in patients with chronic congestive heart failure without increasing requirements for coronary blood flow or myocardial oxygen delivery and without provoking myocardial ischemia.