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Angiology
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Hemodynamic Response to Oral Prenalterol in Dilated Decompensated Cardiomyopathy as a Result of Cardiac and Vascular Effects

Maurizio D. Guazzi

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

Pier Giuseppe Agostoni

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

Elisabetta Doria

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

Alessandro Loaldi

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

Mauro Pepi

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

Alvise Polese

Cattedra di Cardiologia, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "Monzino," Institute for Cardiovascular Research "G. Sisini," University of Milan, Milan, Italy

The initial antifailure efficacy of beta-adrenergic agonists is generally lost during prolonged treatment. The reasons are not fully understood. In 11 patients with advanced cardiac decompensation due to dilated cardiomyopathy, prenalterol, a selective beta 1 adrenergic agonist, improved the left ventricular contractility after acute intravenous and during prolonged oral administration. However, after periods of treatment ranging from 2 to 18 weeks, blood pressure and systemic vascular resistance were raised in each patient. These changes resulted in an increase of the left ventricular afterload which was such as to overwhelm the effects of the enhanced contractility, and to extinguish the initial improvement of the cardiac function and of the clinical condition.

Stimulation of the presynaptical beta-receptors facilitating norepinephrine release or of the renin secretion by this beta1 agonist, may be the causes of the systemic vasoconstriction and of the loss of effectiveness in the long run.

Angiology, Vol. 36, No. 12, 857-866 (1985)
DOI: 10.1177/000331978503601204
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