Abstract
Combined Effects of Thrombosis Pathway Gene Variants Predict Cardiovascular Events
Highlights
The genetic basis of complex diseases like coronary heart disease and ischemic stroke probably consists of several predisposing risk factors that can interact with environmental factors to produce the disease phenotype
As in other complex diseases, the genetic risk is thought to consist of several genetic variants and their possible interactions
Our study explores the role in cardiovascular disease of four thrombosis genes: coagulation factor V, intercellular adhesion molecule 1, protein C, and thrombomodulin
Summary
The genetic basis of complex diseases like coronary heart disease and ischemic stroke probably consists of several predisposing risk factors that can interact with environmental factors to produce the disease phenotype To address such polygenic structure is a challenge likely requiring simultaneous analysis of several risk factors, including genetic variants, in large study samples rich in phenotypes. Gene– gene and gene–environment interaction studies have recently attempted to answer this challenge by analyzing the interacting relations of putative risk loci [1,2,3,4,5] The majority of these studies, use two to three genetic markers, failing to address the physiological entities or the underlying complex genetic profiles. Whether THBD gene variants act as independent CVD risk factors remains unclear [15]
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