Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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

Authors: Ortlepp, JR  Breithardt, O  Ohme, F  Hanrath, P  Hoffmann, R 
Citation: Ortlepp JR, etal., Am Heart J. 2001 Apr;141(4):671-6.
Pubmed: (View Article at PubMed) PMID:11275936
DOI: Full-text: DOI:10.1067/mhj.2001.113394

BACKGROUND: Patients with aortic stenosis (AS) have left ventricular hypertrophy (LVH). It is thought that LVH in these patients is a consequence of chronic left ventricular pressure overload. However, there is only a poor correlation between the degree of AS and the degree of LVH. Genetic polymorphisms 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 examined by echocardiography and left heart catheterization to determine the severity of AS and LVH. Five genetic polymorphisms of the RAAS (ACE, AGTR1, AGT, CMA, CYP11B2) were analyzed in all patients and the results of genetic analysis were correlated to severity of AS and LVH to determine the importance 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 correlation between the severity of AS and the severity of LVH. There was no association 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 the tested genetic polymorphisms of the RAAS.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 4891151
Created: 2011-01-10
Species: All species
Last Modified: 2011-01-10
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.