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Drug Treatment of Congestive Heart Failure

Congestive heart failure (CHF), a syndrome with several pathologic backgrounds, is associated with a series of neuroendocrine (neurohumoral) processes that are triggered by the underlying problem of cardiac pump failure. Several important pathophysiologic systems are stimulated, including the reninangiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), the release of vasopressin from the hypothalamus/pituitary axis, and the release of atrial-brain natriuretic peptides from the heart. These neuroendocrine mechanisms are not only highly relevant from diagnostic and pathophysiologic viewpoints, but are also realistic targets for drug treatment. Over the years, it has become clear that drug treatment of CHF with inotropic agents, aiming at the improvement of pump failure, offers but modest benefit. It appears to be preferable to use drugs to target the neuroendocrine processes, and this approach will be the goal of this review. Accordingly, the following therapeutic principles may be applied: 1. Suppression of the hyperactivity of the RAAS, by means of angiotensin-converting enzyme (ACE) inhibitors or angiotensin type 1-receptor antagonists (AT,-blockers); 2. Antagonism of the effects of aldosterone, by means of spironolactone and (possibly) other aldosterone antagonists; 3. Suppression of the hyperactivity of the SNS by means of f-blockers, and (possibly) centrally acting agents such as clonidine, which cause peripheral sympatho-inhibition; and 4. Vasopressin antagonists. The validity of these various concepts will be the subject of the present review.