Catecholamines and their blockade in congestive heart failure.

The hemodynamic effects of sympathetic nervous system stimulation and the benefits of catecholamine blockade in patients with congestive heart failure (CHF) are discussed. Prolonged stimulation of the sympathetic nervous system promotes disease progression in patients with CHF. The level of circulating norepinephrine is the factor most closely correlated with prognosis. Long-term catecholamine stimulation of beta-receptors in the myocardium reduces the ability of catecholamines to improve cardiac contractility. CHF patients have higher vascular resistance (afterload) than healthy persons, increasing the strain on the heart. Also, beta 1-adrenergic activity stimulates renin release, which is deleterious in CHF. Clinical trials suggest that long-term (greater than one month), carefully dose-adjusted therapy with beta-blockers improves symptoms, ventricular ejection fraction, exercise time, and quality of life in patients with CHF, but it is unclear whether beta-blockers reduce mortality. Some patients cannot tolerate even the lowest starting dosages of beta-blockers, and withdrawal of these agents may result in clinical and hemodynamic deterioration. Carvedilol, which has beta-blocking, alpha-blocking, and antioxidant properties, is associated with a reduction in hospitalizations and symptoms and improvements in ejection fraction it also appears to reduce mortality, although confirmatory studies are needed. Initiation of carvedilol therapy can cause symptomatic and hemodynamic worsening in the short term, and some patients cannot tolerate it. Adrenergic blocking agents are important components of therapy for CHF. Carvedilol may prove useful in reducing symptoms and improving survival in these patients.