title: Deletion polymorphism of angiotensin-converting enzyme gene and left ventricular hypertrophy in southern Italian patients.
abstract: OBJECTIVE
  This study sought to evaluate the possible association of polymorphism of the angiotensin-converting enzyme (ACE) gene with blood pressure and left ventricular mass index (LVMI).
  
  
  BACKGROUND
  The renin-angiotensin system seems to be involved in the pathogenesis of essential hypertension. Moreover, recent epidemiologic observations demonstrate that many subjects with left ventricular hypertrophy have normal blood pressure levels, suggesting that factors other than hemodynamic overload may contribute to the hypertrophy.
  
  
  METHODS
  The study included 140 untreated hypertensive outpatients who underwent ambulatory blood pressure monitoring, echocardiographic evaluation and analysis for insertion (I)/ deletion (D) polymorphism in intron 16 of the ACE gene by polymerase chain reaction. Blood pressure was measured at 24 h, and LVMI was calculated by the Devereux formula, in each patient.
  
  
  RESULTS
  Left ventricular mass index values (mean +/- SD) were 137 +/- 28 g/m2 in patients with the DD genotype, 125 +/- 27 g/m2 in those with the ID genotype and 115 +/- 27 g/m2 in those with II genotype. The frequencies of the DD, ID and II genotypes were 45.71% (n = 64), 46.42% (n = 65) and 7.85% (n = 11), respectively, and were in Hardy-Weinberg equilibrium. The strongest association between left ventricular mass and DD genotype in our cohort appeared to be an independent cardiovascular risk factor (DD vs. ID: odds ratio [OR] 2.497, 95% confidence interval [CI] interval 1.158 to 5.412, p < 0.05; DD vs. II: OR 6.577, 95% CI 1.169 to 28.580, p < 0.02).
  
  
  CONCLUSIONS
  Our data show that the LVMI was significantly enhanced in patients with the DD genotype.
authors.affiliation: Department of Experimental and Clinical Medicine, University of Reggio Calabria, Catanzaro, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Perticone
authors.forename: R
authors.initials: R
authors.lastname: Ceravolo
authors.forename: C
authors.initials: C
authors.lastname: Cosco
authors.forename: M
authors.initials: M
authors.lastname: Trapasso
authors.forename: A
authors.initials: A
authors.lastname: Zingone
authors.forename: P
authors.initials: P
authors.lastname: Malatesta
authors.forename: N
authors.initials: N
authors.lastname: Perrotti
authors.forename: D
authors.initials: D
authors.lastname: Tramontano
authors.forename: P L
authors.initials: PL
authors.lastname: Mattioli
mesh_terms: D000328:Adult; D000368:Aged; D004452:Echocardiography; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D017379:Hypertrophy, Left Ventricular / Q000235:genetics*; D007558:Italy; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D007703:Peptidyl-Dipeptidase A