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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:758-763
Published online before print January 17, 2008, doi: 10.1161/ATVBAHA.107.157842
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:758.)
© 2008 American Heart Association, Inc.


Clinical and Population Studies

Fibrinogen Genes and Myocardial Infarction

A Haplotype Analysis

Werner Koch; Petra Hoppmann; Janita Biele; Jakob C. Mueller; Albert Schömig; Adnan Kastrati

From the Deutsches Herzzentrum München and 1. Medizinische Klinik, Klinikum rechts der Isar (W.K., P.H., J.B., A.S., A.K.), Munich, and Max Planck Institute for Ornithology (J.C.M.), Department of Behavioural Ecology and Evolutionary Genetics, Starnberg (Seewiesen), Germany.

Correspondence to Dr Werner Koch, Deutsches Herzzentrum München, Lazarettstrasse 36, 80636 München, Germany. E-mail wkoch{at}dhm.mhn.de

Objective— Fibrinogen has a role in inflammatory processes and participates in atherosclerotic plaque formation. Despite intensive investigation, there is no clear evidence for a role of variations in the genes coding for the fibrinogen-{alpha}, fibrinogen-β, and fibrinogen-{gamma} polypeptide chains in myocardial infarction. We examined the association of haplotypes in the 50-kb fibrinogen gene region with myocardial infarction in 2 large case-control samples.

Methods and Results— Study sample 1 consisted of 3657 patients with myocardial infarction and 1211 control individuals and sample 2 comprised 1392 patients and 1392 controls. Haplotypes were inferred from genotype analyses of tagging single nucleotide polymorphisms dispersed among the fibrinogen genes. The frequencies of these haplotypes were not significantly different between the case and control groups in either sample (P≥0.07). In addition, haplotypes specific for individual fibrinogen genes were analyzed. No substantial differences in the frequencies of these haplotypes were observed between the groups (P≥0.13). Finally, haplotypes composed of SNPs that exhibited relatively low pairwise allelic associations among each other were examined. The proportions of the haplotypes were not significantly different between cases and controls (P≥0.12).

Conclusion— A haplotype analysis did not reveal a link between genetic variations in the fibrinogen gene region and myocardial infarction.

There is no clear evidence for a role of variations in the genes coding for the fibrinogen-{alpha}, fibrinogen-β, and fibrinogen-{gamma} polypeptide chains in atherosclerotic diseases. We examined 2 large case-control samples and found that haplotypes based on single nucleotide polymorphisms in the fibrinogen gene region on chromosome 4 were not associated with myocardial infarction.


Key Words: fibrinogen • myocardial infarction • risk factor • genetics • haplotype