Congestive Heart Failure: Neuroendocrine and Inflammatory Response

Overview

Congestive heart failure is a disorder that is set off by a noxious event which has damaged theheart muscle. The resulting loss of cardiac cells, i.e. the myocytes, diminishes the ability of themyocardium to perform work. The harmful event may have an abrupt onset, e.g. myocardialinfarction, or a gradual onset, e.g. valvular disease, or it may be of hereditary nature, e.g.cardiomyopathies. Most patients who survive the initial noxious event remain, for some timeat least, asympatomatic or minimally symptomatic. They develop signs and symptoms of heartfailure only after left ventricular dysfunction has been present for some period of time. Thisperiod is interindividually highly variable. Following the initial decline in pumping capacity ofthe heart, compensatory mechanisms are activated, like the adrenergic nervous system, therenin-angiotensin-aldosterone system, or the inflammatory cytokine system. In the short term,these compensatory systems are able to restore cardiovascular function to a near-normal range.However, in the long run, their sustained activation leads to secondary damage of the heartmuscle, resulting in left ventricular remodelling and cardiac decompensation. Consequently,patients exhibit transition from asymptomatic left ventricular dysfunction to full-blown heartfailure. Although there may be some modest declines in the overall pumping capacity of theheart preceding cardiac decompensation, novel evidence suggests that progression to heartfailure occurs independently of the hemodynamic status of the patients. The transition fromasymptomatic ventricular dysfunction to symptomatic heart failure is not any longer viewedas a result of further decline in mechanical function of the heart. Instead, it seems plausible toaccept the explanation that overexpression of compensatory mediators contributes to diseaseprogression, by virtue of their direct toxic effects on the heart and circulation.

Key words:
left ventricular dysfunction - neurohumoral response - inflammatory responseremodelling - cardiac failure.