Role of the renin-angiotensin system as a risk factor for control of morbidity and mortality in coronary artery disease.

Coronary heart disease is a multifactorial disease, influenced by environmental and genetic factors. Experimental and clinical data show that the renin-angiotensin system has important indications in coronary artery disease by influencing progressive ventricular dilatation, ventricular function, and outcome. Angiotensin II may have direct toxic effects on myocardial cells, induce hypertrophy in noninfarcted areas, activate the sympathetic nervous system, stimulate fibroblast proliferation, vasoconstrict coronary vessels, increase left ventricular afterload, and impair diastolic relaxation. Associations between a polymorphism of the angiotensinogen gene and angiotensin-converting enzyme gene and the occurrence of myocardial infarction have been reported. Patients with the DD genotype (ACE gene) have higher plasma ACE and myocardial ACE activity. Preliminary data suggest that the DD genotype is associated with more progressive ventricular dilatation post myocardial infarction and with a greater response after ACE inhibition. The DD genotype is also associated with a higher incidence of left ventricular hypertrophy, which may have implications for the induction of hypertrophy in noninfarcted areas. Whatever the mechanisms, chronic ACE inhibition, started early after myocardial infarction, improves survival and reduces mortality and morbidity for major cardiovascular events.