Lack of association of angiotensin-converting enzyme and angiotensinogen genes polymorphisms with left ventricular structure in young normotensive men.
Left ventricular (LV) hypertrophy is a strong predictive factor for cardiovascular morbidity and mortality. LV structure and function are influenced by many variables, including genetic background. The potential role of gene polymorphisms of different components of the renin angiotensin system remains controversial. The aim of this study was to determine the influence of deletion/insertion (D/I) polymorphism of the angiotensin-converting enzyme (ACE) gene and M235-->T polymorphism of the angiotensinogen (AG) gene on left ventricular morphology and function in young normotensive men. The study included 110 normotensive healthy males (mean age 24 +/- 4 years, age range 18 to 34 years) who were assessed by echocardiography for LV structure and function. In all subjects ACE D/I polymorphism was evaluated using a polymerase chain reaction (PCR) method. M235-->T polymorphism assessment was available in 98 individuals. Significant differences between groups according to ACE I/D or AG M235-->T polymorphisms were not found for parameters of LV morphology or for parameters of systolic and diastolic function. When subjects with DD or ID genotypes were grouped, their LV mass index was higher than that in subjects with II genotypes (86 +/- 14 vs 79 +/- 15, r = 0.033, p = 0.05). There were no significant differences among other variables. In a population of young normotensive men where the influence of confounding variables such as age, gender and associated pathological conditions is minimized, the gene polymorphisms of ACE I/D and AG M235-->T are not important determinants of LV structure and function.
Linhart
A
A
2nd Department of Internal Medicine, 1st School of Medicine, Charles University, Prague, Czech Republic.
Sedlácek
K
K
Jáchymová
M
M
Jindra
A
A
Beran
S
S
Vondrácek
V
V
Heller
S
S
Horký
K
K
D000328:Adult; D000808:Angiotensinogen / Q000235:genetics*; D004251:DNA Transposable Elements / Q000502:physiology; D004452:Echocardiography; D017353:Gene Deletion; D005838:Genotype; D006352:Heart Ventricles; D006801:Humans; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics / Q000502:physiology*; D012016:Reference Values
D004251:DNA Transposable Elements; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A