Recent clinical data from the SOLVD (Studies on Left Ventricular Dysfunction) and SAVE (Survival and Ventricular Enlargement) studies have shown a significant reduction in ischaemic events with ACE inhibition. When the results of the two SOLVD and the SAVE trials were combined, the overall risk reduction in myocardial infarction with long-term ACE inhibitor treatment was 23% (P < 0.001) and the overall risk reduction for hospitalizations for unstable angina 15%. The time frame of the clinical effects suggests that ACE inhibitors may be working through an antiatherosclerotic mechanism, and genetic, epidemiological and mechanistic data suggest that the renin-angiotensin-aldosterone system may play a role in the atherosclerotic process. Genetic and epidemiological evidence has shown that an activated renin-angiotensin aldosterone system is associated with a higher incidence of myocardial infarction, and mechanistic studies have demonstrated that ACE inhibition can produce antiatherosclerotic effects in animal models. The antiatherosclerotic effects of ACE inhibitors may be mediated at one of several steps in the atherosclerotic pathway: blocking plaque formation, plaque rupture, or thrombus formation.