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Volume 192, Issue 1, Pages 62-66 (20 November 2009)


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Apolipoprotein E (apoE) polymorphism: A risk factor for fatal coronary sclerosis?

Steffen HeideaCorresponding Author Informationemail address, Kleiber Manfreda, Christiane Gläserb, Susanne Schulzc

Received 17 December 2008; received in revised form 7 May 2009; accepted 28 July 2009. published online 04 September 2009.

Abstract 

Objective

The association of apoE polymorphism and coronary heart disease has been examined in numerous clinical studies. However, there are only very few autopsy studies on this topic, there having been none in Germany for instance.

Methods

In a retrospective study, we examined 121 cases where the autopsy revealed premature coronary sclerosis. The collected data included the maximum degree of stenosis of the coronary arteries, the body mass index and a potential left heart hypertrophy. Coronary sclerosis was the cause of death in 47 and a relevant secondary finding in 74 of the cases. The control group consisted of 253 healthy blood donors and 79 patients who had undergone cardiac catheterization and did not show coronary macro-angiopathy. Genotyping of apoE polymorphism was performed by using blood.

Results

When assessing the influence of apoE genotype or allele no significant influence on premature death was found. However, a subdivision of deceased according to their coronary state showed that the carriers of apoE ɛ4-allele had a higher risk of coronary artery sclerosis with a significantly higher degree of stenosis.

Conclusion

In cases of fatal premature coronary sclerosis and proven apoE ɛ4-allele, blood relatives should receive advice.

a Institute for Forensic Medicine; Halle University, Franzosenweg 1, D-06112 Halle, Germany

b Institute for Human Genetics and Medical Biology; Halle University, Magdeburger Str. 2, D-06097 Halle, Germany

c University School of Dental Medicine, Department of Operative Dentistry and Periodontology; Halle University, Harz 42a, D-06108 Halle, Germany

Corresponding Author InformationCorresponding author. Tel.: +49 345 557 1588; fax: +49 345 557 1587.

PII: S0379-0738(09)00321-1

doi:10.1016/j.forsciint.2009.07.020


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