Acute effects of beta-endorphin on cardiovascular function in patients with mild to moderate chronic heart failure

Cardiomyocytes produce opioid peptides and receptors. beta-Endorphin is increased in the plasma of patients with congestive heart failure (CHF). We evaluated whether an intravenous infusion of beta-endorphin exerted any effect on cardiovascular function and on the neurohormonal milieu in patients with mild to moderate CHF.

According to a double-blind, placebo-controlled design, 10 patients (5 men, age 46.9 +/- 8.2 years [mean +/- SD]) with CHF and New York Heart Association functional class II to III received, in random order, 1-hour intravenous infusion of beta-endorphin (500 microg/h) and, on a separate occasion, received placebo and underwent echocardiographic and laboratory measurements at baseline and during infusions.

beta-Endorphin significantly increased left ventricular ejection fraction (LVEF) (P =.0001) and stroke volume (P =.0001), and reduced systemic vascular resistance (P =.031) in patients with CHF. These changes were paralleled by a significant increase in plasma levels of glucagon (P =.0001), GH (P =.0001), and IGF-1 (P =.0001), and a significant decrease in plasma levels of endothelin (P =.0001) and catecholamines (P =.01). No hemodynamic and neurohormonal changes were observed during the placebo study in any patient.

We conclude that a short-term, high dose infusion of beta-endorphin improves LVEF, reduces systemic vascular resistance, blunts the neurohormonal activation, and stimulates the GH/IGF-1 axis in patients with mild to moderate CHF.