Title of article :
Apolipoprotein E4 allele and the risk of left ventricular dysfunction in thalassemia major
Author/Authors :
Bazrgar، M نويسنده Human Genetic Research Group, Iranian Academic Center for Education, Culture and Research (ACECR), Fars Province Branch,, Shiraz, Iran , , Karimi، M نويسنده Hematology Research Center, Shiraz University of Medical Sciences , , Peiravian، F نويسنده Cooley’s Anemia Cardiac Clinic, Fatemeh-Zahra Hospital, Shiraz University of Medical Sciences, Kazerun Islamic Azad University , , Fathzadeh، M نويسنده Human Genetic Research Group, Iranian Academic Center for Education, Culture and Research (ACECR), Fars Province Branch,, Shiraz, Iran , , Fattahi، MJ نويسنده ,
Issue Information :
فصلنامه با شماره پیاپی 1 سال 2007
Pages :
7
From page :
13
To page :
19
Abstract :
Background: Left ventricular (LV) failure is the main cause of death in thalassemia. Iron overload in these patients leads to formation of oxygen free radicals. Apolipoprotein (ApoE) E4 allele is the least efficient in oxidative stress condition compared with apoE2 and apoE3 alleles. This study was performed to determine the association of three different ApoE alleles with LV dysfunction in thalassemia major patients in southern Iran. Methods: The present study comprised 202 patients with thalassemia major divided into three groups according to echocardiographic findings: Group 1 (n=135) had no cardiac impairment; Group 2 (n=38) exhibited LV dilatation but normal LV systolic function and Group 3 (n=29) showed LV systolic dysfunction. DNA was obtained from all patients and 198 healthy control subjects for ApoE genotyping. Results: Frequency of both apoE3/E4 genotype and apoE4 allele in Group 3 were higher than the control group with corresponding values of P < 0.05, Odds Ratio=2.97, 1.06 Conclusion: ApoE4 allele increases the risk of LV impairment in thalassemia major.
Journal title :
International Cardiovascular Research Journal
Serial Year :
2007
Journal title :
International Cardiovascular Research Journal
Record number :
2333558
Link To Document :
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