Although beneficial acute hemodynamic effects of calcium antagonists in heart failure have been reported, their use in this setting is still controversial because of the negative inotropic effects produced by these agents. The direct actions of calcium antagonists, that is direct depression of myocardial contractility and coronary and peripheral vasodilation, are modulated by systemic hypotension-induced baroreceptor activation of autonomic reflexes. Thus, at clinically relevant dosages, the baroreceptor-mediated cardiac stimulatory effects may counterbalance or override the direct negative-inotropic effects, as usually observed with nifedipine or diltiazem. By contrast, with verapamil significant depression of contractility may occur. Newer calcium antagonists with higher vasoselectivity such as nisoldipine or felodipine may be particularly interesting in the setting of congestive heart failure because of pronounced arterial vasodilatation and their additional effects on coronary blood flow, LV-regional wall motion and diastolic function and peripheral blood flow distribution with negligible myocardial effects. Due to their marked vasodilatating properties, newer derivatives may be advantageous in the treatment of heart failure due to coronary artery disease and hypertension. Although limited data concerning long-term efficacy are available, preliminary studies suggest long-term benefit in selected patients. It appears that verapamil should not be used for vasodilator therapy of severe heart failure, since deterioration of LV function may occur.