AT 1 Receptor A/C 1166 Polymorphism Contributes to Cardiac Hypertrophy in Subjects With Hypertrophic Cardiomyopathy

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Abstract
—The development of left ventricular hypertrophy (LVH) in subjects with hypertrophic cardiomyopathy (HCM) is variable, suggesting a role for modifying factors such as angiotensin II. We investigated whether the angiotensin II type 1 receptor (AT 1 -R) A/C 1166 polymorphism, the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and/or plasma renin influence LVH in HCM. Left ventricular mass index (LVMI) and interventricular septal thickness were determined by 2-dimensional echocardiography in 104 genetically independent subjects with HCM. Extent of hypertrophy was quantified by a point score (Wigle score). Plasma prorenin, renin, and ACE were measured by immunoradiometric or fluorometric assays, and ACE and AT 1 -R genotyping were performed by polymerase chain reactions. The ACE D allele did not affect any of the measured parameters except plasma ACE ( P P 1 -R C allele (190±8.3 g/m 2 ) than in AA homozygotes (168±7.2 g/m 2 ), and similar patterns were observed for interventricular septal thickness (23.0±0.7 versus 21.6±0.7 mm) and Wigle score (7.0±0.3 versus 6.3±0.3). Plasma renin was higher ( P =0.05) in carriers of the C allele than in AA homozygotes. Multivariate regression analysis, however, revealed no independent role for renin in the prediction of LVMI. Plasma prorenin and ACE were not affected by the AT 1 -R A/C 1166 polymorphism, nor did the ACE and AT 1 -R polymorphisms interact with regard to any of the measured parameters. We conclude that the AT 1 -R C 1166 allele modulates the phenotypic expression of hypertrophy in HCM, independently of plasma renin and the ACE I/D polymorphism.

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