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Titolo:
Lack of association polymorphisms and cardiac among five genetic of the renin-angiotensin system hypertrophy in patients with aortic stenosis
Autore:
Ortlepp, JR; Breithardt, O; Ohme, F; Hanrath, P; Hoffmann, R;
Indirizzi:
Univ Hosp Aachen, Med Clin 1, D-52057 Aachen, Germany Univ Hosp Aachen Aachen Germany D-52057 Clin 1, D-52057 Aachen, Germany
Titolo Testata:
AMERICAN HEART JOURNAL
fascicolo: 4, volume: 141, anno: 2001,
pagine: 671 - 676
SICI:
0002-8703(200104)141:4<671:LOAPAC>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR HYPERTROPHY; CONVERTING-ENZYME GENE; DELETION POLYMORPHISM; JAPANESE PATIENTS; CARDIOMYOPATHY; MASS; GENOTYPES; VARIANTS; DISEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Ortlepp, JR Univ Hosp Aachen, Med Clin 1, Pauwelsstr 30, D-52057 Aachen, Germany Univ Hosp Aachen Pauwelsstr 30 Aachen Germany D-52057 Germany
Citazione:
J.R. 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

Abstract

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, CYP11 B2) 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 allelefrequencies 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 13:38:08