Vasodilators have a well-established role in the treatment of congestive heart failure. By virtue of their vasodilating properties, the calcium channel blockers have been advocated for use in the treatment of heart failure, in particular, in consideration of the fact that the left ventricular dysfunction in 60 to 70% of the patients with this condition is due to ischemic heart disease, the primary disorder for which the calcium channel blockers are intended to treat. The net hemodynamic effect of calcium channel blockade is the result of two opposing actions: negative inotropy and systemic vasodilation with reflex-induced sympathetic stimulation. The balance is dependent on the prevailing cardiovascular status prior to administration of the drug. In the presence of no or only mild-to-moderate left ventricular dysfunction and intact adrenergic reflexes, a small amount of negative inotropy is readily offset by afterload reduction and adrenergic stimulation. In the presence of severe left ventricular dysfunction sufficiently extensive to lead to heart failure, a condition in which homeostatic reflexes are already attenuated, even a slight amount of negative inotropy can lead to unequivocal deterioration of hemodynamics. Of the three conventional calcium channel blockers, verapamil exerts the most marked negative inotropic effects. Even verapamil, however, has been shown to lead to hemodynamic improvement in some patients, at least after acute administration. Apparently, the cut-off point between beneficial and adverse actions lies at an ejection fraction between 30 and 40% and a pulmonary capillary pressure of about 20 mm Hg. In patients beyond these limits, if treated with verapamil, worsening of heart failure is not uncommon.(ABSTRACT TRUNCATED AT 250 WORDS)