EFFICACY OF ENALAPRIL AND EPROSARTAN IN HYPERTENSIVE PATIENTS IN ACCOUNT WITH RAAS GENES POLYMORPHISMS: PP.24.479

Abstract

Aim: To study the association between I/D polymorphism of ACE gene, A1166C polymorphism of AT1R gene, M235T polymorphism of AGT gene, C344T polymorphism of CYP11B2 and blood pressure and left ventricular mass (LVM) regression during 3 month therapy with enalapril and eprosartan in Uzbek patients with essential hypertension (EH). Methods: We examined 120 men with I-II stage of EH (WHO, 2003) in the mean age of 49.3 ± 7.9 yr and 60 normotensive persons (45.1 ± 7.0 yr). LVM was measured by echocardiography. The LVM was indexed to the body surface area to determinate the LVM index (LVMI). Genomic DNA was extracted from peripheral blood. Followed PCR-RFLP analysis was performed. Results: Genetic models disclosed that the D-allele and the ID-genotype of ACE gene and the T-allele and TT-genotype of the CYP11B2 gene were associated with an increased risk for EH, but only the TT-genotype of the AGT gene was associated with an increased risk for LVH. Reliable association between the polymorphic markers and LVMI was found only for AGT gene. LVMI was significantly higher in TT homozygous than in MM homozygous: 168.0 ± 31.9 vs 140.8 ± 27.6 g/m2, p = 0.002. All patients were randomly divided on 2 groups: 1st was treated with Enalapril (En) in a dose of 20 mg/day, 2nd was treated with Eprosartan (Ep) in a 600 mg/day. Both drugs were significantly reduced systolic BP (on 17–20%) and diastolic BP (on 16–19%) after 12 weeks of therapy in all genotype carriers (p < 0.001). Regression of LVH in the course of En therapy reliable limited in DD genotype ACE gene, AC and CC genotype of AT1R gene and TT genotype of CYP11B2 gene. In the course of Ep therapy LVMI decreased on 8–9% regardless of GP. In conclusion, there is an association between EH in patients with ACE/ID and CYP11B2/C344T polymorphisms and LVH with AGT/M235T polymorphism. Antihypertensive efficacy both drugs did not depend from RAAS genes polymorphism. Cardioprotective effects of En unlike Ep associated with genes polymorphism.