Synergistic effect of angiotensin II type-1 receptor 1166A/C with angiotensin-converting enzyme polymorphism on risk of acute myocardial infarction in north Indians

Abstract

Introduction:

This first study from north India investigated the synergistic effect of AT1R 1166A/C with the ACE I/D polymorphism on risk of acute myocardial infarction (AMI).

Materials and Methods:

Traditional coronary risk factors, ACE I/D and AT1R 1166A/C polymorphism were analyzed in 350 patients with AMI and 350 matched controls.

Results:

In univariate analysis, hypertension (52.9% vs. 11.1%; OR=8.9; 95%CI 6.0–13.3), diabetes mellitus (16.0% vs. 0.6%; OR=33.1; 95%CI 8.0–137), smoking (43.7% vs. 20.9%; OR=2.9; 95%CI 2.1–4.1), family history of coronary artery disease (22.3% vs. 14.0%; OR=1.8; 95%CI 1.2–2.6), high body mass index (64.3% vs. 51.4%; OR=1.7; 95%CI 1.3-2.3), high waist–hip ratio (46.2% vs. 2.3%; OR=37; 95%CI 16–85.8) and AT1R 1166AC genotype (20.6% vs. 12%; OR=1.9; 95%CI 1.3–2.9) were associated with AMI. In multivariate analysis, all these factors were found to be independent risk predictors for AMI. Subjects carrying the AT1R 1166AC+CC and ACE ID+DD combined genotype showed a twofold increased association (OR=2.1; 95%CI 1.2–3.5) compared with the AT1R 1166AA–ACE II combined genotype. Patients who smoked and who carried the ACE ID+DD genotype had 2.4-fold (OR=2.4; 95%CI 1.5–3.8), and with the AT1R 1166AC+CC genotype had 15-fold (OR=14.9; 95%CI 5.2–42.8) increased risk of AMI compared with non-smoking non-carriers.

Conclusions:

The AT1R 1166A/C polymorphism has association with AMI among north Indian patients, particularly if integrated with ACE I/D polymorphism and smoking.