title: ACE and AGTR1 polymorphisms and left ventricular hypertrophy in endurance athletes.
abstract: OBJECTIVE
  This study aimed to evaluate the role of angiotensin type 1 receptor gene (AGTR1) polymorphism (A1166C) in left ventricular hypertrophy (LVH) mediated by the angiotensin-converting enzyme (ACE) in endurance athletes.
  
  
  METHODS
  A group of 74 white, healthy male endurance athletes, aged between 25 and 40 yr, were enrolled in this study. All of them participated primarily in isotonic sports, training for at least >10 h x wk(-1), for at least 5 yr. The ACE genotype (insertion [I] or deletion [D] alleles) was ascertained by polymerase chain reaction (DD in 35, ID in 36, and II in 3). Group II was excluded from the analysis because of its small size. No difference was found between the two groups as regards age, blood pressure, HR, and echocardiographic data.
  
  
  RESULTS
  The left ventricular mass index (LVMI) was significantly higher in group DD rather than in group ID (P = 0.029). The group DD showed a slightly higher prevalence of subjects with LVH (LVMI > 131 g x m(-2); 62.9%) than group ID (44.4%, P = 0.120). No association was found between ACE-DD and LVH (odds ratio (OR) = 2.12, 95% confidence interval = 0.82-5.46). Concerning the role of AGTR1 polymorphism, the highest LVMI was found in 15 athletes with ACE-DD and AGTR1-AC/CC genotypes (150 +/- 23 g x m(-2)); the lowest value of LVMI was found in the case of ACE-ID and AGTR1-AA (127 g x m(-2) +/- 18 g x m(-2)), whereas LVMI in subjects with ACE-DD + AGTR1-AA was similar to that in the ACE-ID + AGTR1-AC/CC group (134 +/- 18 g x m(-2) vs 133 +/- 20 g x m(-2), P = 0.880). The presence of ACE-DD + AGTR1 + AC/CC was strongly associated with LVH (OR = 4.6, P = 0.029). Moreover, subjects with LVH showed longer left ventricular isovolumetric relaxation time and higher end-systolic wall stress. The latter was strongly correlated to LVMI (r = 0.588), especially in the presence of ACE-DD + AGTR1 + AC/CC (r = 0.728).
  
  
  CONCLUSIONS
  LVMI may be greater in the presence of ACE- DD and AGTR1-AC/CC polymorphisms.
authors.affiliation: Department of Human Movement, University G. D'Annunzio, Chieti-Pescara, Italy.
authors.forename: Michele
authors.initials: M
authors.lastname: Di Mauro
authors.forename: Pascal
authors.initials: P
authors.lastname: Izzicupo
authors.forename: Francesco
authors.initials: F
authors.lastname: Santarelli
authors.forename: Stefano
authors.initials: S
authors.lastname: Falone
authors.forename: Alfonso
authors.initials: A
authors.lastname: Pennelli
authors.forename: Fernanda
authors.initials: F
authors.lastname: Amicarelli
authors.forename: Antonio M
authors.initials: AM
authors.lastname: Calafiore
authors.forename: Angela
authors.initials: A
authors.lastname: Di Baldassarre
authors.forename: Sabina
authors.initials: S
authors.lastname: Gallina
mesh_terms: D000328:Adult; D056352:Athletes; D004452:Echocardiography; D005838:Genotype; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010807:Physical Endurance / Q000502:physiology*; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*
chemical_list: C544065:AGTR1 protein, human; D044140:Receptor, Angiotensin, Type 1; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A