The primary cause of heart failure is an impairment of the heart's ability
to fill or empty the left ventricle properly. A reduction in the ejection f
raction is the hallmark of chronic systolic dysfunction, and leads to a neu
rohumoral activation with the kidney participating to retain sodium. This r
etention of sodium is facilitated by an increased intrarenal formation of a
ngiotensin II, and is accompanied initially by a normal glomerular filtrati
on rate that can later fall as a consequence of the progression of heart fa
ilure. Drugs blocking the renin-angiotensin system have proved to be of gre
at value in the therapy of chronic heart failure because of their positive
effects on systemic haemodynamics and also on renal function through the fa
cilitation of renal sodium handling. There is a relevant concern about the
possibility of renal functional impairment when the renin-angiotensin syste
m is blocked in patients with heart failure. This concern partly accounts f
or the underutilization of drugs such as angiotensin-converting enzyme inhi
bitors or angiotensin T1 receptor antagonists in this syndrome. The knowled
ge of the reversibility of the fall in renal function will encourage a wide
r utilization of this therapy, leading to a better outcome in heart failure
patients. Curr Opin Nephrol Hypertens 8:153-156. (C) 1999 Lippincott Willi
ams & Wilkins.