Published online before print March 27, 2006, doi: 10.1161/01.HYP.0000215180.32274.c8
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(Hypertension. 2006;47:920.)
© 2006 American Heart Association, Inc.
Original Articles |
Association of the Ghrelin Receptor Gene Region With Left Ventricular Hypertrophy in the General Population
Results of the MONICA/KORA Augsburg Echocardiographic Substudy
From the Clinic for Internal Medicine II (A.B., M.F., M.K., W.R., G.R., C.H.), University of Regensburg, Regensburg, Germany; Medical College of Wisconsin (A.E.K.), Milwaukee, Wis; Clinic for Internal Medicine II (J.E., H.S.), University of Luebeck, Luebeck, Germany; and GSF-Research Center for Environment and Health (A.D.), Institute of Epidemiology, Neuherberg, Germany.
Correspondence to Andrea Baessler, Clinic for Internal Medicine II, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany. E-mail andrea.baessler{at}klinik.uni-regensburg.de
Growth hormone (GH) can influence left ventricular myocardial growth, structure, and function. The GH secretagogue receptor (GHSR, ghrelin receptor) is known to be involved in GH release and is expressed in the myocardium. We hypothesized that genetic variants within the GHSR are associated with parameters of left ventricular mass (LVM) and geometry. Ten single-nucleotide polymorphisms (SNPs) covering the gene region were genotyped in 1230 members of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Augsburg Echocardiographic Substudy). Linkage disequilibrium analysis revealed a linkage disequilibrium block consisting of 5 SNPs forming 2 common haplotypes. One haplotype was found significantly more often in subjects without left ventricular hypertrophy ([LVH] 69% versus 59%; permutated P=0.0015), whereas the second haplotype was significantly more frequent in individuals with LVH (32% versus 26%; P=0.019). Homozygous subjects presented with an increase of risk with respect to all heart size parameters. A significantly increasing frequency of the risk haplotype could be observed from the lowest (20.9%) to the highest quintile (31.0%) of gender-specific LVM distributions (P=0.0096). We found association of the minor alleles of individual single nucleotide polymorphisms contributing to the haplotypes with higher LVM indices, septal wall thickness, and different LVH criteria consistent in men and women in matched cases and controls (LVM, women: 144.8±30.9 [noncarrier] versus 171.3±36.0 [homozygous], P=0.001; men: 186.7±42.4 versus 236.3±64.5, P=0.002). These data suggest that common variants in the GHSR region are associated with parameters of LVM and geometry independent of blood pressure and body mass in the general population and, thus, may be involved in the pathogenesis of LVH.
Key Words: ventricular function, left • genetics • growth substances • hypertrophy
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