Neurohormonal modulation in chronic heart failure

During the past 50 years there have been vast improvements in the treatment of chronic heart failure (CHF). CHF was initially considered to be a cardio-renal problem - an acute disorder leading to volume expansion and oedema. Diuretics and digitalis were the only available treatments. Subsequently, CHF was considered to be the result of both myocardial dysfunction and increased tone in the pulmonary and peripheral circulations. The presence of peripheral vasoconstriction suggested that circulatory failure was an important component of the disease, and vasodilators were added to therapy. In the more recent past, experimental and clinical studies have demonstrated that CHF is also characterized by increased neurohormonal activation. This has led to the use of angiotensin-converting enzyme inhibitors, beta-blockers and spironolactone in CHF. Increased neurohormonal activity is now recognized as one of the major pathophysiological factors that contribute to the progression of CHF. Activation of neurohormonal mechanisms is only compensatory in the short term; chronic activation produces detrimental changes in the myocardium, kidneys and peripheral vasculature. This article provides an overview of the key neurohormonal systems that are activated in CHF.