title: Effect of 24-week treatment with telmisartan on myocardial structure and function: relationship to insertion/deletion polymorphism of the angiotensin-converting enzyme gene.
abstract: The aim of the present study was to assess the effect of treatment with the angiotensin II receptor blocker telmisartan for 24 weeks on myocardial structure and function in patients with essential hypertension, and the relationship between this effect and the structural polymorphism of the angiotensin-converting enzyme (ACE) gene. Thirty-five patients with essential hypertension and left ventricular hypertrophy (LVH) without other associated morbidity were included in an open-label, non-comparative study. The patients were treated with telmisartan 40-80 mg once daily. In the final analysis, there were 29 patients who received the full course of treatment and were evaluated echocardiographically before and after treatment by the same blinded investigator, and myocardial structure and function were analysed. The myocardial mass of the left ventricle was determined in M-mode. Assessment of diastolic function of transmitral blood flow was performed using pulsed Doppler echocardiography. All patients were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene. Telmisartan produced a significant reduction in left ventricular mass index from 140.4 +/- 48.6 to 128.7 +/- 40.6 g/m2 that was accompanied by an improvement in characteristics of diastolic function. The decrease in LVH was more significant in the ID genotype group than in the II and DD groups. Thus, prolonged treatment with telmisartan is accompanied by an improvement in myocardial structure, expressed as a reduction in left ventricular mass and function that is more marked in patients with ID genotype of the ACE gene.
authors.affiliation: Cardiovascular Research Institute, Pavlov State Medical University of St Petersburg, St Petersburg, Russian Federation. podiatr@inbox.ru
authors.forename: A O
authors.initials: AO
authors.lastname: Conrady
authors.forename: I O
authors.initials: IO
authors.lastname: Kiselev
authors.forename: N I
authors.initials: NI
authors.lastname: Usachev
authors.forename: A N
authors.initials: AN
authors.lastname: Krutikov
authors.forename: O I
authors.initials: OI
authors.lastname: Yakovleva
authors.forename: E V
authors.initials: EV
authors.lastname: Polunicheva
authors.forename: O A
authors.initials: OA
authors.lastname: Ovchinnikova
authors.forename: A V
authors.initials: AV
authors.lastname: Panov
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D015150:Echocardiography, Doppler; D005260:Female; D017353:Gene Deletion; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D000077333:Telmisartan; D013997:Time Factors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; D007703:Peptidyl-Dipeptidase A; D000077333:Telmisartan