title: [Association between angiotensin converting enzyme gene, chymase gene and regression of left ventricular hypertrophy in patients treated with angiotensin converting enzyme inhibitors].
abstract: OBJECTIVE
  To investigate the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and the A/B polymorphism of the chymase (CMA) gene with regression of left ventricular hypertrophy (LVH) in patients with essential hypertension and left ventricular hypertrophy. The study subjects had been participants in along-term trial of therapy with an ACE inhibitor.
  
  
  METHODS
  Follow-up data of 157 patients with essential hypertension and left ventricular hypertrophy were collected. DNA fragments of ACE gene and CMA gene were amplified by PCR and analysed by RFLP. LVDd, IVST and LVPWT were measured by Ultrasonic Cardiogram (UCG).
  
  
  RESULTS
  (1) When long-term treatment with Benazepril was carried out, the blood pressure was markedly decreased and the heart rate was maintained steadily. (2) Regression of left ventricular hypertrophy was improved. (3) The magnitudes of regression of LVM and LVMI during therapy were greater in the DD group than in the II and ID group. No significant differences of other indices were found in the different genotype groups of ACE. (4) No significant differences of all indices were found in the different genotype groups of CMA. (5) No interaction appeared between the genotypes of the ACE and the genotypes of the CMA.
  
  
  CONCLUSIONS
  Hypertensive patients with DD genotype were more likely to have regression of left ventricular hypertrophy when treated with ACE inhibitors than patients with other ACE genotypes. No evidence was found to support an association between CMA genotype and regression of LVH in those patients.
authors.affiliation: Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing 100083, China.
authors.forename: Hong
authors.initials: H
authors.lastname: He
authors.forename: Li-ming
authors.initials: LM
authors.lastname: Li
authors.forename: Wei-hua
authors.initials: WH
authors.lastname: Cao
authors.forename: Mei-zhen
authors.initials: MZ
authors.lastname: Liu
authors.forename: Ning-ling
authors.initials: NL
authors.lastname: Sun
authors.forename: Jun
authors.initials: J
authors.lastname: Lü
authors.forename: Yong-hua
authors.initials: YH
authors.lastname: Hu
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D001552:Benzazepines / Q000008:administration & dosage* / Q000627:therapeutic use; D053818:Chymases; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000235:genetics; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D012697:Serine Endopeptidases / Q000096:biosynthesis / Q000235:genetics*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001552:Benzazepines; D007703:Peptidyl-Dipeptidase A; D012697:Serine Endopeptidases; D053818:Chymases; C044946:benazepril