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07 August 2002

Angiotensin I-converting enzyme and chymase gene polymorphisms – relationship to left ventricular mass in type 2 diabetes patients

Janusz Gumprecht, Marcin Zychma, Władysław Grzeszczak, Beata Łącka, Wacław Burak, Mariusz Mosur, Jacek Kaczmarski, Ireneusz Otulski, Tomasz Stokłosa, Piotr Czank

Med Sci Monit 2002; 8(8): CR603-606 :: ID: 13605

Abstract

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).
Conclusion: Our results may suggest the additive effect of ACE and CMA gene polymorphisms on the increase in left ventricular mass in NIDDM patients.

Keywords: Chymases, Diabetes Mellitus, Type 2 - genetics, Diabetes Mellitus, Type 2 - pathology, Echocardiography, Genetic Predisposition to Disease, Genotype, Heart Ventricles - enzymology, Heart Ventricles - pathology, Heart Ventricles - ultrasonography, Organ Size, Peptidyl-Dipeptidase A - genetics, Polymorphism, Genetic, Serine Endopeptidases - genetics

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