Neuroendocrine Control of the Cardiovascular System in Heart Failure

Neuroendocrine activation starts early in the natural history of left ventricular dysfunction, and the levels of circulating hormones increase in proportion to the severity of heart failure. The neurohormonal response evoked during congestive heart failure (CHF) is the same as that evolved to support the survival of the species under two main conditions which threaten life: hemorrhage and physical exercise. In these conditions, a short-term threat to blood pressure evokes a baroreceptor-mediated increase in sympathetic activity which causes venoconstriction, tachycardia, stimulation of the myocardium, and regional vasoconstriction. Augmented neuroendocrine activity in the syndrome of heart failure is initially beneficial, appears to be adaptive, and helps support blood pressure and cardiac output. Prolonged and excessive activation, however, has deleterious effects with adverse consequences at both cardiac and vascular levels which aggravate the clinical status of the syndrome and negatively affect its prognosis. Most studies suggest that high levels of neurohormones predict a poor prognosis, and antihormonal therapy is now the cornerstone of chronic heart failure treatment