Lack of Association of Angiotensin-converting Enzyme and Angiotensinogen Genes Polymorphisms with Left Ventricular Structure in Young Normotensive Men

Abstract

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.

Polymorphism in gene coding for ACE determines different development of myocardial fibrosis in rats

“…In humans, some experimental evidence suggested an association between the ACE I/D polymorphism and LVH (40). However, recent careful studies have found that this association was inconsistent when additional populations were investigated (24,36,39).…”

Geographic variation in left ventricular mass and mass index: a systematic review

“…Not all studies in this review excluded subjects on this basis; however, of those that did 17,18,20,21,25,26,35 two studies of American men 17,35 and one of American women 17 still exceeded the upper ASE reference limit of LVM. Chinese men and women and Indian men were still lower.…”

“…Therefore of the 13 cohorts (12 studies) of normal healthy men that would be classified as including people with mild LVH, five would also contain men with moderate LVH. [13][14][15][16][17] The LVM from eight cohorts matched the upper ASE reference limit ( ± 10 g) 12,[18][19][20][21][22][23][24] (two studies included subjects from the cohorts used to create the reference range, 12,22 and one appears to be the study on which the twodimensional reference ranges were based 23 ), and LVM from seven cohorts was less than the upper ASE reference limit. 12,[25][26][27][28][29][30] Of those that were less than the upper ASE reference limit, three studies from Asia 25,26,30 had upper values on average 38 g less than the ASE reference limits for m-mode or two-dimensional measurements.…”

Polimorfismos genéticos determinantes da performance física em atletas de elite

“…In the heart, the Ang II is a potent factor of cellular growth (47) . Although increase in the left ventricular mass has not been verified in individuals with different genotypes for ACE (48)(49) , the local RAS activation with consequent increase of the Ang II in response to mechanical overload induced by physical exercise, seems to increase the protein synthesis in the cardiac myocyte via AT 1 receptors (50)(51) . Hypertrophy in the left ventricle (LV) is a remarkable characteristic in elite athletes (52) .…”