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Titolo:
ANGIOTENSINOGEN GENE POLYMORPHISM IN JAPANESE PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY
Autore:
ISHANOV A; OKAMOTO H; YONEYA K; WATANABE M; NAKAGAWA I; MACHIDA M; ONOZUKA H; MIKAMI T; KAWAGUCHI H; HATA A; KONDO K; 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 HOKKAIDO UNIV,SCH MED,DEPT LAB MED,KITA KU SAPPORO HOKKAIDO 060 JAPAN HOKKAIDO UNIV,SCH MED,DEPT PUBL HLTH,KITA KU SAPPORO HOKKAIDO 060 JAPAN
Titolo Testata:
The American heart journal
fascicolo: 2, volume: 133, anno: 1997,
pagine: 184 - 189
SICI:
0002-8703(1997)133:2<184:AGPIJP>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEAVY-CHAIN GENE; ESSENTIAL-HYPERTENSION; MISSENSE MUTATION; ALPHA-TROPOMYOSIN; MOLECULAR-BASIS; BLOOD-PRESSURE; ASSOCIATION; VARIANT; RISK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
A. Ishanov et al., "ANGIOTENSINOGEN GENE POLYMORPHISM IN JAPANESE PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY", The American heart journal, 133(2), 1997, pp. 184-189

Abstract

To examine the contribution of the renin-angiotensin system to hypertrophic cardiomyopathy (HCM), we studied 96 patients with HCM (mean age50 years, 55% male), 105 of their unaffected siblings and offspring, and 160 healthy subjects without known hypertension and left ventricular hypertrophy (LVH) who were frequency matched to cases by age and sex. Patients were divided into familiar or sporadic HCM (FHCM or SHCM) groups with or without affected members of their family. The region ofinterest in the angiotensinogen (AGT) gene, the missense mutation with methione-to-threonine amino acid substitution at codon 235 in angiotensinogen (M235T), was amplified by polymerase chain reaction with theuse of allele-specific oligonucleotide primers flanking the polymorphic region of the AGT gene to amplify template deoxyribonucleic acid prepared from peripheral leukocytes. The T allele frequency was higher in the SHCM group than in unaffected siblings and offspring (88% vs 78%, X(2) = 4.6, P < 0.05). The M allele frequency was higher in unaffected siblings and offspring than in patients with SHCM (23% vs 12%, X(2)= 4.6, P < 0.05). The T allele frequency among unaffected siblings and offspring was similar to that observed in healthy subjects (78% vs 78%). We conclude that HCM, especially in sporadic cases, is partially determined by genetic disposition. The molecular variant of angiotensinogen T235 seems to be a predisposing factor for cardiac hypertrophy in HCM and carries an approximately twofold increased risk.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/01/21 alle ore 17:31:01