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(Hypertension. 2002;40:162.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Relation of the G Protein ß₃-Subunit Polymorphism With Left Ventricle Structure and Function

Kamil Sedláek; Marcus Fischer; Jeanette Erdmann; Christian Hengstenberg; Stephan Holmer; Susanne Kürzinger; Michael Muscholl; Andreas Luchner; Günter A. Riegger; Hans-Werner Hense; Heribert Schunkert

From the Klinik und Poliklinik für Innere Medizin II, Universität Regensburg (K.S., M.F., J.E., C.H., S.H., S.K., M.M., A.L., G.A.R., H.S.), Regensburg, Germany; and Institut für Epidemiologie und Sozialmedizin, Universität Münster (H-W.H.), Münster, Germany.

Correspondence to Heribert Schunkert, MD, Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, Franz-Josef-Strauss Allee 11, D-93042 Regensburg, Germany. E-mail heribert.schunkert{at}klinik.uni-regensburg.de

The G protein ß₃-subunit C825T polymorphism results in a truncated splice variant protein that is associated with enhanced transmembrane signaling, increased proliferative activity, and arterial hypertension. The aim of the present study was to further investigate the association of this polymorphism with left ventricular (LV) structure and function. A total of 2052 individuals from a large-scale population-based sample were investigated for the G protein ß₃-subunit C825T polymorphism and echocardiographic parameters of LV structure and function. Complete genotyping and echocardiographic data were available in 1720 individuals (829 men and 891 women). The mean LV mass indices in men with CC (n=384) and TT (n=84) genotypes were 98.3±1.2 g/m² and 100.0±2.8 g/m², respectively (P=0.64). In women, the corresponding values were 83.1±1.0 g/m² for the CC genotype (n=397) and 83.8±2.1 g/m² for the TT genotype (n=91, P=0.32). Likewise, LV dimensions or parameters of the diastolic function and serologic markers of LV mass were not associated with the C825T variant. Finally, multivariate analyses accounting for potentially confounding factors failed to show any influence of this polymorphism on echocardiographic parameters. In conclusion, we were not able to confirm the previously published associations of the G protein ß₃-subunit C825T polymorphism with LV structure and diastolic function.

Key Words: genetics • myocardium • hypertrophy • G proteins • signal transduction

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