Cardiac afferents and neurohormonal activation in congestive heart failure

Cardiac chambers have afferent connections to the brainstem and to the spin al cord, Vagal afferents mediate depressor responses and become activated b y volume expansion, increased myocardial contractility and atrial natriuret ic factor. Sympathetic afferents, on the contrary, are activated by metabol ic mediators, myocardial ischemia and cardiac enlargement. These opposite b ehaviors may lead to activation or suppression of the sympathetic nervous s ystem and of the renin-angiotensin-aldosterone system. As cardiac diseases progress, the heart dilates, plasma norepinephrine incr eases, atrial natriuretic factor is released and the renin-angiotensin-aldo sterone system is suppressed to maintain water and sodium excretion. This d issociation of the neurohormonal profile of cardiac patients, may be explai ned by coactivation of sympathetic afferents, by cardiac dilatation, and of vagal afferents by atrial natriuretic factor. in more advanced stages, atr ial natriuretic factor suppression of the renin-angiotensin-aldosterone sys tem is overridden by overt sympathetic activation and sodium and water rete ntion ensues. Digitalis, angiotensin-converting enzyme inhibitors and beta-blockers selec tively decrease cardiac adrenergic drive. A common mechanism of action, to all three groups of drugs, would be attenuation of sympathetic afferents an d partial normalization of vagal afferents. Consequently, heart size and ca rdiac afferents emerge as the key factors to understand the pathophysiology and treatment of the syndrome of congestive heart failure. (C) 2000 Harcou rt Publishers Ltd.