Calcium antagonists and sympathetic activity in congestive heart failure

To review the sympathetic abnormalities occurring in heart failure, their pathophysiological importance and clinical relevance, and the effects of drug treatment, with particular reference to calcium antagonists.

Indirect and direct approaches to study sympathetic function in humans have documented conclusively that sympathetic activation represents a hallmark of cardiac failure syndrome. Evidence indicates that sympathetic overactivity is associated with, and probably caused by, a baroreflex impairment and that it has adverse effects on patients' prognosis and survival.

In the past, drug treatment in heart failure was aimed at improving patients' survival by ameliorating cardiac hemodynamics. It is now established that a major goal of therapeutic intervention is also to reduce sympathetic activation characterizing heart failure.

Studies with short-acting calcium antagonists show that they enhance sympathetic activation and that this has an adverse effect on patients' survival. In contrast, third generation calcium antagonists such as amlodipine, which have a slow onset and long duration of action, do not adversely affect sympathetic function and reflex cardiovascular control. Indeed, evidence suggests calcium antagonists with this profile may exert favorable clinical effects.