Lack of association of G-protein subunit gene C825T polymorphism with leftventricular hypertrophy in essential hypertension.
Eugene I Shwartz, Yulia B Nefedova, Anna V Zukova, Eugene V Shlyakhto, Tatyana A Vinnic, Alexandra O Konrady
Med Sci Monit 2002; 8(5): CR337-340
BACKGROUND: The aim of the present study was to determine if there is anassociation of G-protein b3 subunit (GNB3) gene polymorphisms and left ventricular hypertrophy (LVH)in patients with essential hypertension (EH) in a St. Petersburg population. MATERIAL/METHODS: We examined135 patients (mean age 48 +/- 7 yrs) with mild to moderate EH recruited from the general population ofan outpatient hypertension clinic. Left ventricular mass was measured by echocardiography, and the leftventricular mass index (LVMI) was calculated. The GNB3 C825T genotype was determined by polymerase chainreaction and restriction digestion. RESULTS: 67 patients (50%) were homozygous for the C allele (CC),56 were heterozygous (CT) (41%) and twelve (9%) were homozygous for the T allele (TT). The distributionof genotypes among the patients was in Hardy-Weinberg equilibrium and did not differ significantly whencomparing patients with or without LVH. The frequency of the T allele was only slightly higher in patientswith LVH (32%) compared to those without LVH (28%), NS, and the LVMI was similar in patients with theCC, CT and TT genotypes (122.3 +/- 29.8; 118.8 +/- 29.9 and 115.2 +/- 18.3 g/m2, respectively). No significantdiscrepancies were found among the various genotype groups in posterior wall thickness, interventricularseptum thickness, or functional parameters such as ejection fraction, isovolumetric relaxation time andE/A ratio. CONCLUSIONS: These observations clearly suggest the lack of association between left ventricularstructure or function and the CNB3 gene variant in the studied population.
Keywords: Adult, Alleles, DNA Restriction Enzymes, Echocardiography, Genotype, Heterotrimeric GTP-Binding Proteins, Homozygote, Hypertension, Hypertrophy, Left Ventricular, Polymerase Chain Reaction, Polymorphism, Genetic