(Hypertension. 2000;35:214.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
G-Protein ß3 Subunit Gene Variant and Left Ventricular Hypertrophy in Essential Hypertension
From the Servicio de Nefrología (E.P., D.G.), Unidad de Hipertensión Arterial del Servicio de Medicina Interna General (E.G.-A., A.d.l.S.), Laboratorio de Hormonología (D.G., F.R.), and Servicio de Cardiología (M.E., J.C.P.), Institut de Recerca Biomèdica August Pi i Sunyer, Hospital Clínic, Universidad de Barcelona, Barcelona, Spain.
Correspondence to Dr Esteban Poch, Servicio de Nefrología, Hospital Clinic, Universidad de Barcelona, Villarroel 170, 08036 Barcelona, Spain. E-mail epoch{at}medicina.ub.es
Abstract—A functional genetic variant consisting of a C825T substitution in the GNB3 gene, encoding for the G-protein ß3 subunit, has been associated with enhanced G-protein activation and cell growth. The aim of the study was to investigate the association of this polymorphism with left ventricular hypertrophy (LVH) in a sample of patients with essential hypertension. Left ventricular mass was assessed by 2-mode echocardiography in 86 patients with essential hypertension, and GNB3 C825T genotype was determined by polymerase chain reaction and restriction digestion. Thirty-seven (0.43) patients were homozygous for the C allele (CC), 40 (0.47) were heterozygous (CT), and 9 (0.10) were homozygous for the T allele (TT). The genotype distribution among the patients was in Hardy-Weinberg equilibrium. Values of left ventricular end-diastolic diameter (52.0±0.7 versus 48.9±0.9 mm, P=0.007), posterior wall thickness (11.3±0.2 versus 10.6±0.2 mm, P=0.042), and left ventricular mass index (152.7±4.4 versus 135.2±6.4 g/m2, P=0.023) were significantly higher in patients with CT and TT genotypes considered together (CT+TT) than in CC patients. The distribution of the genotypes was significantly different when comparing patients with LVH: 20 (0.33) CC and 40 (0.67) CT+TT patients had this complication, and 17 (0.65) CC and 9 (0.35) CT+TT patients did not (P<0.01). The frequency of the T allele was significantly different among patients with (0.40) and without (0.20) LVH (P<0.01). A logistic regression analysis showed that the association between the T allele and LVH was independent of age, mean blood pressure, body mass index, and alcohol consumption. The relative risk of LVH in patients bearing the T allele (CT+TT group) compared with CC hypertensive patients was 3.03 (95% CI 1.14 to 8.05). The findings suggest an association between LVH and the 825T allele in hypertensive patients.
Key Words: hypertrophy • G proteins • genes • hypertension, essential • polymorphism
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