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Genetic aspects of the hemostatic system in cerebrovascular disease

From the Academic Unit of Molecular Vascular Medicine, Research School of Medicine, University of Leeds, Leeds, United Kingdom.

Address correspondence and reprint requests to Dr. Andrew J. Catto, Academic Unit of Molecular Vascular Medicine, Martin Wing, Leeds General Infirmary, Leeds, LS1 3EX UK.

Despite considerable research into the pathogenesis of cerebrovascular disease (CVD), acute stroke is the third most common cause of mortality in the Western world. The clinical management of acute stroke is largely supportive, although evidence is emerging for the benefit of early pharmacologic intervention. Even when the benefits of these therapies are accounted for, a significant proportion of patients remain disabled or die. Accordingly, stroke prevention is likely to offer the most effective manner of reducing stroke incidence. However, effective prevention depends on a reliable means of identifying and treating the risk factors associated with stroke and possibly targeting preventive measures at high-risk groups. Atherosclerosis is the process responsible for the development of ischemic CVD, and evidence is accumulating to suggest that these disorders are multifactorial, resulting from a complex series of interactions between genes and the environment. The outward expression of the disease, or the disease phenotype, is in part the product of gene–gene and gene–environment interactions. Research methods harnessing molecular biology techniques, including polymerase chain reaction (PCR) and sequencing have, in contrast to coronary artery disease (CAD), been under-utilized when it comes to furthering our understanding of the molecular epidemiology of CVD. This article reviews the evidence that stroke has a genetic basis and that the hemostatic system is an important risk factor for stroke. The genetic regulation of a number of these hemostatic proteins is evaluated.

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