Angiotensin Converting Enzyme Inhibitors (ACEI) has shown to reduce mortality in heart failure to the tune of 16-30 per cent in various large trials.

The renin-angiotensin-aldosterone system (RAAS) is activated early in the course of heart failure and plays an important role in the progression of heart failure. Hence, modulation of this system with Angiotensin Converting Enzyme (ACE) inhibitors should be the initial mode of therapy. 

ACE inhibitors modify neurohormonal activation in heart failure by inhibiting conversion of angiotensin I to angiotensin II (AII) through ACE. This results in the favourable hemodynamic effects of peripheral vasodilatation, reduced afterload, and decreased blood pressure. The reduction in AII, a potent myogenic agent, also may attenuate abnormal left ventricular remodeling; the subsequent reduction in aldosterone decreases sodium and fluid retention. ACE inhibitors also cause down-regulation of the sympathetic nervous system and improve baroreceptor function.

Angiotensin-converting enzyme is also involved in the degradation of bradykinin. So ACE inhibition result in higher bradykinin levels, which in turn stimulate synthesis of prostaglandins and nitric oxide, which may be beneficial.