The aim of the study was to evaluate the influence of pharmacogenetically determined treatment of essential arterial hypertensive patients (EAH) on ultrasonography data depending on polymorphism of 5 genes: I/D in
angiotensin-converting enzyme gene (ACE), А1166С in gene of the first type receptor of angiotensin II (AGTR1), T894G in gene of endothelial NO-synthase (eNOS), Pro12Ala in gene of PPAR-γ2 receptor, Arg389Gly in gene of β1-adrenergic receptor (ADRb1). 249 patients with EAH І–ІІІ stages severities (EAH I – 26.5 % (66) patients; EAH ІІ – 45.8 % (114); EAH ІІІ – 27.7 % (69); women – 48.2 % (120), men – 51.8 % (129), mean ages 50.5±10.4 years) were observed. All subjects were examined by genetic polymorphisms analysis for five genes by polymerase chain reaction based method. DRA extracted from venous blood, genes’ alleles (AGTR1, eNOS, PPAR-γ2, ADRb1) split by restriction enzymes Ddel, BanII, CseI and FaqI. Standard linear structural myocardial data evaluated with Echo-KG (ASE, Penn Convention). Patients were split depending on ACE gene genotypes and combo therapy type prescription for 6 groups: 1st gr. – I-allele carriers (n=60) took hydrochlorothiazide (HCTZ) and angiotensin II type-1 receptor blocker (ARB); 2nd gr. – I/D-genotype carriers (n=34) took HCTZ+β1-adrenoblockers (β1-AB); 3rd gr. – I/D-genotype carriers (n=50) took HCTZ+ACE inhibitor (ACEI); 4th gr. – DD-genotype carriers (n=15) took calcium channel blocker (CCB)+ ARB; 5th gr. – DD-genotype carriers (n=15) took CCB+β1-AB; 6th gr. – DD-genotype carriers (n=27) took CCB+ACEI. Pharmacogenetically determined treatment significantly increased number of patients with normal LV myocardial geometry (Р=0.02) with decreasing of patients amount with hypertrophic LV myocardial models (Р<0.01). More effective organ-protection (after LVMI normalization) in EAH patients was under CCB+ARB II (13.3 %) and CCB+β1-АB (20.0 %) combination treatment.