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Apolipoprotein E gene polymorphism and left ventricular function in Iranian patients with thalassemia major

^* Human Genetic Research Group, Iranian Academic Center for Education, Culture & Research, (ACECR), Fars Province Branch
^° Hematology Research Center, Shiraz University of Medical Sciences (SUMS)
^# Cooley’s Anemia Cardiac Clinic, Fatemeh-Zahra Hospital, SUMS, Shiraz, Iran

Correspondence: Masood Bazrgar, Human Genetic Research Group, ACECR, Fars Province Branch, Zand Ave., P.O. Box: 71345-1463, Shiraz, Iran. Phone: international +98 71123446723. Fax: international +98 7112337851, E-mail: mbazrgar{at}Yahoo.co.uk

Left ventricular (LV) failure is the main cause of death in thalassemia. Iron overload in patients with thalassemia leads to the formation of oxygen free radicals. Of the various apolipoprotein E (apoE) alleles, apoE4 is the least efficient in conditions of oxidative stress in comparison with apoE2 and apoE3. Our results showed that apoE4 is a genetic risk factor for LV dysfunction in thalassemia.

Key words: thalassemia, left ventricular function, apolipoprotein E.