Atherothrombotic disease arises secondary to a complex gene-environment interaction. In the initial stages, the condition is clinically silent but with more advanced disease, an occlusive thrombus is formed resulting in the classical clinical manifestations. Both environmental factors and genetic variations in elements of the clotting cascade influence thrombosis risk by inducing quantitative and qualitative changes in the mature protein, which may affect the final structure of the clot and determine its resistance to lysis. Understanding the fine details of gene-environment interactions in relation to thrombus formation will help to shed more light on disease pathogenesis. Consequently, this will allow the development of more efficacious treatment strategies and will also help to identify subjects at risk, thereby enabling the introduction of early preventative measures. © 2005 Elsevier Ireland Ltd. All rights reserved.
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