title: [Clinico-genetic aspects of the hypotensive response and regression of left ventricular hypertrophy in arterial hypertension patients].
abstract: OBJECTIVE
  To study clinicogenetic determinants of left ventricular hypertrophy (LVH) regress in 52-week antihypertensive therapy to achieve the target arterial pressure (AP) < 140/90 mm Hg.
  
  
  METHODS
  I/D-polymorphism of angiotensin converting enzyme gene, T174M-polymorphism of angiotensinogen gene, A1166C-polymorphism of angiotensin II ATI-receptor gene (ATII), 4a/b-polymorphism of endothelial NO-synthetase gene (eNOS) were determined in 64 patients (24 males, 40 females, mean age 54 +/- 1.1 years) with arterial hypertension (AH) and LVH. Echocardiography, laboratory tests, clinical measurements of blood pressure (BP) and 24-h AP monitoring were made after 4 weeks of placebo and 52 weeks of treatment.
  
  
  RESULTS
  Baseline values of LV myocardium mass index (LVMMI) correlated significantly with mean 24 hour and night systolic arterial pressure; 24-h, day and night pulse pressure (PP). In patients with regress of LVH the degree of LVMMI reduction significantly correlated with lowering of day and night PP, baseline level of neutrophils, uric acid and creatinine 52 weeks after treatment. Groups made by polymorphism, did not significantly differ by initial LVMMI, frequency of achievement of target AP. In patients with genotypes ID/II and aa, the level of achieved diastolic arterial pressure was significantly lower than in other groups. Resistant LVH was seen in 42.2% patients. Frequency of AP normalization was higher in the group of patients with LVH regress (48.6% vs 25.9%; p < 0.05). Resistant LVH occurred more frequently in patients with genotype DD (64.0 vs 28.2% in patients with II/ID, p < 0.05) and in patients with genotype 4ab (62.9 vs 30.4% in patients with genotype aa and 21.4%--with genotype bb; p < 0.05 in both cases). In patients with resistant LVH frequency of DD genotype increased (59.3 vs 24.3% in patients with regress of LVH; p < 0.01), genotype AA (74.5 vs 48.6%; p < 0.01) and genotype ab (63.0 vs 27.0%, p < 0.01).
  
  
  CONCLUSIONS
  Regress of LVH in AH patients depends on dynamics and complex interactions of some hemodynamic, laboratory and genetic parameters.
authors.forename: V S
authors.initials: VS
authors.lastname: Moiseev
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Kotovskaia
authors.forename: Zh D
authors.initials: ZhD
authors.lastname: Kobalava
authors.forename: V V
authors.initials: VV
authors.lastname: Nosikov
authors.forename: E P
authors.initials: EP
authors.lastname: Korovina
authors.forename: S G
authors.initials: SG
authors.lastname: Timofeeva
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000959:Antihypertensive Agents / Q000627:therapeutic use; D006332:Cardiomegaly / Q000150:complications / Q000473:pathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000235:genetics; D052250:Nitric Oxide Synthase Type III; D011110:Polymorphism, Genetic; D011945:Receptors, Angiotensin / Q000235:genetics / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000235:genetics
chemical_list: D000959:Antihypertensive Agents; D011945:Receptors, Angiotensin; D000804:Angiotensin II; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III