(Hypertension. 2001;38:1199.)
© 2001 American Heart Association, Inc.
Fourth International Seminar on Cardiovascular Biology |
From the "Angela Valenti" Laboratory of Genetic and Environmental Risk Factors for Thrombotic Disease, Department of Vascular Medicine and Pharmacology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy.
Correspondence to Licia Iacoviello, MD, PhD, "Angela Valenti" Laboratory of Genetic and Environmental Risk Factors for Thrombotic Disease, Department of Vascular Medicine and Pharmacology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy. E-mail: iaco{at}cmns.mnegri.it
Abstract
Abstract The role of fibrinogen in cardiovascular disease has been extensively studied, and meta-analyses have definitively confirmed that high levels of fibrinogen are associated with an increased risk of the disease. In recent years, several polymorphisms have been identified in the fibrinogen chain genes that contribute to determine the levels of fibrinogen in the general population. The fibrinogen ß-chain gene has been more extensively studied because the ß-chain synthesis is the limiting step in the production of mature fibrinogen. Overall, the studies show an association between ß-fibrinogen chain polymorphisms and the levels of fibrinogen. In contrast, the majority of the studies did not find any relation with the risk of cardiovascular disease. The individual responses to gender or to environmental stimuli such as smoking, physical exercise, or infections may be genetically determined, and genetic variability underlies changes in biological reactions that contribute to differences in cardiovascular risk. In the future, gene-environment interactions should be considered in evaluating the relevance of genetic variations on the risk of cardiovascular disease.
Key Words: fibrinogen polymorphisms gene-environment interactions risk factors cardiovascular disease
This article has been cited by other articles:
![]() |
E. S. Ganotakis, I. F. Gazi, J. A. Papadakis, I. A. Jagroop, D. R. Nair, and D. P. Mikhailidis The Relationship Between Circulating Fibrinogen and Lipoprotein (a) Levels in Patients With Primary Dyslipidemia Clinical and Applied Thrombosis/Hemostasis, January 1, 2007; 13(1): 35 - 42. [Abstract] [PDF] |
||||
![]() |
S. Kathiresan, Q. Yang, M. G. Larson, A. L. Camargo, G. H. Tofler, J. N. Hirschhorn, S. B. Gabriel, and C. J. O'Donnell Common Genetic Variation in Five Thrombosis Genes and Relations to Plasma Hemostatic Protein Level and Cardiovascular Disease Risk Arterioscler Thromb Vasc Biol, June 1, 2006; 26(6): 1405 - 1412. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Staiger, K. Staiger, N. Stefan, H. G. Wahl, F. Machicao, M. Kellerer, and H.-U. Haring Palmitate-Induced Interleukin-6 Expression in Human Coronary Artery Endothelial Cells Diabetes, December 1, 2004; 53(12): 3209 - 3216. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Sankar, M. K. Cho, C. M. Condit, L. M. Hunt, B. Koenig, P. Marshall, S. S.-J. Lee, and P. Spicer Genetic Research and Health Disparities JAMA, June 23, 2004; 291(24): 2985 - 2989. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. H Reinhart Fibrinogen - marker or mediator of vascular disease? Vascular Medicine, August 1, 2003; 8(3): 211 - 216. [Abstract] [PDF] |
||||
![]() |
L. H. Kuller Hormone Replacement Therapy and Risk of Cardiovascular Disease: Implications of the Results of the Women's Health Initiative Arterioscler Thromb Vasc Biol, January 1, 2003; 23(1): 11 - 16. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Sehnal and J. Slany Fibrinogen--the key to familial CHD or just another shadow in Plato's Allegory? Eur. Heart J., August 2, 2002; 23(16): 1231 - 1233. [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2001 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |