Thorac Cardiovasc Surg 2009; 57(7): 386-390
DOI: 10.1055/s-0029-1185876
Original Cardiovascular

© Georg Thieme Verlag KG Stuttgart · New York

CD14 Promoter Polymorphism (− 159C→t) is Not Associated with Myocardial Infarction or Coronary Artery Disease in Patients with Assumed High Genetic Risk

W. Haberbosch1 , K. Unkelbach2 , D. Schuster3 , A. Gardemann3 , H. Tillmanns2 , H. Hölschermann4
  • 1Department of Cardiology, Klinik für Innere Medizin I, SRH Zentralklinikum, Suhl, Germany
  • 2Department of Cardiology, Juistus-Liebig University, Giessen, Germany
  • 3Institute of Clinical Chemistry, Department of Pathobiochemistry, Otto-von-Guericke University, Magdeburg, Germany
  • 4Department of Cardiology, Hochtaunus-Kliniken, Bad Homburg, Germany
Further Information

Publication History

received January 19, 2009

Publication Date:
30 September 2009 (online)

Abstract

Objective: Inflammation plays a major role in the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI). CD14 is the receptor for bacterial lipopolysaccharide in monocytes and mediates the production of proinflammatory cytokines. The promoter of the CD14 gene has a polymorphic site in position − 159 (C→T) and T-homozygotes have been shown to express higher amounts of CD14 by some investigators. We and others have found an association of the T-allele with past MI in former studies, but reports in the literature are contradictory. Methods and Results: We investigated a study group with an assumed high genetic risk by selecting 200 patients suffering from angiographically verified CAD or MI who were younger than 50 years or who had only one or no risk factor (hypertension, smoking, elevated body mass index, impaired glucose tolerance or elevated cholesterol levels). We used 252 healthy subjects as controls. Additionally, the levels of soluble (s) CD14 in plasma and amount of membranous (m) CD14 on the surface of monocytes were determined in different genotypes. We found no association of either genotype with CAD, extent of CAD, or a history of MI. No significant correlation was found after adjustment for vascular risk factors. In addition, no significant differences in the density of monocyte mCD14 or in plasma levels of sCD14 were detectable among the various genotypes. Conclusions: The assumed weak association of the TT-genotype of the CD14 promoter polymorphism with MI could not be not established in a well-defined group of young patients with a high genetic risk. The association of the polymorphism with expression of sCD14 or mCD14 was not confirmed.

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Prof. Dr. Werner Haberbosch

Dept. of Cardiology
Klinik für Innere Medizin I
SRH Zentralklinikum Suhl gGmbH

Albert-Schweitzer-Str. 2

98527 Suhl

Germany

Phone: + 49 36 81 35 54 00

Fax: + 49 36 81 35 54 01

Email: werner.haberbosch@zs.srh.de