BACKGROUND: Type 2 diabetic patients are at increased risk for cardiovascular morbidity and mortality. Increased left ventricular mass also predicts a higher incidence of cardiovascular events. Angiotensin II is a potent mediator of myocardial growth, and angiotensin II can be produced in the heart by angiotensin I-converting enzyme (ACE) and heart chymase (CMA). The aim of this study was to establish the role of ACE gene insertion/deletion (I/D) and CMA gene CMA/B polymorphisms in determining left ventricular mass in type 2 diabetic patients. MATERIAL/ METHODS: Echocardiographic measurements, ACE gene I/D and CMA/B genotypes were determined in 154 type 2 diabetic patients. RESULTS: Mean LVMI was higher among DD homozygotes compared to heterozygotes and II homozygotes (128.9 g/m2 vs. 120.5 g/m2 and 120.4 g/m2, respectively), but the difference was not statistically significant (ANOVA P=0.12). A similar effect was observed for the CMA/B polymorphism, where mean LVMI were 126.6 g/m2, 122.1 g/m2 and 118.2 g/m2, for carriers of AA, AG and GG genotype, respectively (not statistically significant, P=0.33). ACE I/D and CMA/B polymorphism were also analyzed jointly, and carriers of both DD and AA genotypes were found to have significantly higher LVMI values (P=0.05) than non-carriers (133.0 g/m2 and 121.2 g/m2, for 21 DD and AA carriers vs. 133 non-carriers). In multivariate analysis, the presence of DD and AA genotypes was independently associated with LVMI (P=0.04). CONCLUSIONS: Our results may suggest the additive effect of ACE and CMA gene polymorphisms on the increase in left ventricular mass in NIDDM patients.
BACKGROUND: Type 2 diabeticpatients are at increased risk for cardiovascular morbidity and mortality. Increased left ventricular mass also predicts a higher incidence of cardiovascular events. Angiotensin II is a potent mediator of myocardial growth, and angiotensin II can be produced in the heart by angiotensin I-converting enzyme (ACE) and heart chymase (CMA). The aim of this study was to establish the role of ACE gene insertion/deletion (I/D) and CMA gene CMA/B polymorphisms in determining left ventricular mass in type 2 diabeticpatients. MATERIAL/ METHODS: Echocardiographic measurements, ACE gene I/D and CMA/B genotypes were determined in 154 type 2 diabeticpatients. RESULTS: Mean LVMI was higher among DD homozygotes compared to heterozygotes and II homozygotes (128.9 g/m2 vs. 120.5 g/m2 and 120.4 g/m2, respectively), but the difference was not statistically significant (ANOVA P=0.12). A similar effect was observed for the CMA/B polymorphism, where mean LVMI were 126.6 g/m2, 122.1 g/m2 and 118.2 g/m2, for carriers of AA, AG and GG genotype, respectively (not statistically significant, P=0.33). ACE I/D and CMA/B polymorphism were also analyzed jointly, and carriers of both DD and AA genotypes were found to have significantly higher LVMI values (P=0.05) than non-carriers (133.0 g/m2 and 121.2 g/m2, for 21 DD and AA carriers vs. 133 non-carriers). In multivariate analysis, the presence of DD and AA genotypes was independently associated with LVMI (P=0.04). CONCLUSIONS: Our results may suggest the additive effect of ACE and CMA gene polymorphisms on the increase in left ventricular mass in NIDDMpatients.