Lack of association polymorphisms and cardiac among five genetic of the renin-angiotensin system hypertrophy in patients with aortic stenosis

Citation
Jr. Ortlepp et al., Lack of association polymorphisms and cardiac among five genetic of the renin-angiotensin system hypertrophy in patients with aortic stenosis, AM HEART J, 141(4), 2001, pp. 671-676
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
AMERICAN HEART JOURNAL
ISSN journal
00028703 → ACNP
Volume
141
Issue
4
Year of publication
2001
Pages
671 - 676
Database
ISI
SICI code
0002-8703(200104)141:4<671:LOAPAC>2.0.ZU;2-5
Abstract
Background Patients with aortic stenosis (AS) have left ventricular hypertr ophy (LVH). it is thought that LVH in these patients is a consequence of ch ronic left ventricular pressure overload. However, there is only a poor cor relation between the degree of AS and the degree of LVH. Genetic polymorphi sms of the renin-angiotensin-aldosterone system (RAAS) have been considered to trigger the response of the left ventricle to chronic pressure overload and determine the degree of LVH in patients with AS. Methods One hundred five consecutive patients with symptomatic AS were exam ined by echocardiography and left heart catheterization to determine the se verity of AS and LVH. Five genetic polymorphisms of the RAAS (ACE, AGTR1, A GT, CMA, CYP11 B2) were analyzed in all patients and the results of genetic analysis were correlated to severity of AS and LVH to determine the import ance of the polymorphisms for LVH. Results All tested genotypes were in Hardy-Weinberg equilibrium and allele frequencies were similar to other study populations. There was no correlati on between the severity of AS and the severity of LVH. There was no associa tion between the five tested genotypes of the RAAS and the severity of AS ( mean gradient and area of the aortic valve) or LVH (LV muscle mass). Conclusion We conclude that LVH in patients with AS is not determined by th e tested genetic polymorphisms of the RAAS.