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Titolo:
ANGIOTENSIN-II TYPE-1 RECEPTOR GENE POLYMORPHISMS IN PATIENTS WITH CARDIAC-HYPERTROPHY
Autore:
ISHANOV A; OKAMOTO H; WATANABE M; YONEYA K; NAKAGAWA I; KUMAMOTO H; CHIBA S; HATA A; KAWAGUCHI H; KITABATAKE A;
Indirizzi:
HOKKAIDO UNIV,SCH MED,DEPT CARDIOVASC MED,KITA KU,KITA 15,NISHI 7 SAPPORO HOKKAIDO 060 JAPAN HOKKAIDO UNIV,SCH MED,DEPT CARDIOVASC MED,KITA KU SAPPORO HOKKAIDO 060 JAPAN
Titolo Testata:
Japanese Heart Journal
fascicolo: 1, volume: 39, anno: 1998,
pagine: 87 - 96
SICI:
0021-4868(1998)39:1<87:ATRGPI>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONVERTING ENZYME GENE; AT(1) RECEPTOR; BLOOD-PRESSURE; CARDIOMYOPATHY; HYPERTENSION; RENIN;
Keywords:
RENIN-ANGIOTENSIN SYSTEM; ANGIOTENSIN II RECEPTOR GENE; LEFT VENTRICULAR HYPERTROPHY; HYPERTROPHIC CARDIOMYOPATHY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
25
Recensione:
Indirizzi per estratti:
Citazione:
A. Ishanov et al., "ANGIOTENSIN-II TYPE-1 RECEPTOR GENE POLYMORPHISMS IN PATIENTS WITH CARDIAC-HYPERTROPHY", Japanese Heart Journal, 39(1), 1998, pp. 87-96

Abstract

Chronic mechanical stress of the heart secondary to arterial hypertension is a primary cause of left ventricular hypertrophy (LVH). The renin-angiotensin system (RAS) plays an important role in the cardiovascular system, regulating the expression of cardiac hypertrophy, in part,independent of the effects of systemic hypertension. A major component of RAS is angiotensin converting enzyme (ACE), which is upregulated in pressure overload-induced cardiac hypertrophy as well as heart failure. In a recent study, we found that the T allele of the M235T polymorphism of the angiotensinogen gene in sporadic hypertrophic cardiomyopathy (HCM) patients is associated with LVH. The present study was designed to assess the contribution of the polymorphisms of the angiotensin II type 1 receptor (AGT(1)R A(1166)C) genes on development of left ventricular hypertrophy. Patients with hypertensive LVH and relatives of HCM without manifesting the disease, showed higher C allele frequency compared to patients with HCM (11.3% vs 4.2%, chi(2) = 5.3, p < 0.05and 10.5% vs 4.2%, chi(2) = 5.3, 1,< 0.05, respectively), but healthycontrols did not (11.3% vs 7.5%, chi(2) = 1.42, NS and 10.5% vs 7.5%,chi(2) = 1.2, NS). The strong interaction between ACE I/D and AGT(1)RA(1166)C gene polymorphisms has been found in groups of relatives of HCM patients; odds ratio associated with ACE D allele was significant in subjects carrying the AGT(1)R C allele (OR = 7.3, 95% CI 1.6-33.1; chi(2) = 7.9, P < 0.02) compared with healthy subjects. We conclude that the molecular variant of the AGT(1)R A(1166)C gene is not contributing to the development of cardiac hypertrophy in hypertensive LVH and HCM patients, whereas carriers of both C and D alleles had a four-foldincrease in the odds ratio for family history of HCM without manifesting the disease.

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Documento generato il 17/01/21 alle ore 18:25:56