Coagulopathies and Ischemic Stroke

Chang, Dae il

Abstract

The etiology of ischemic stroke remains undetermined in nearly 40% of patients despite extensive evaluations. Coagulopathies associated with cerebrovascular ischemia may be familial or acquired and account for 4% of all strokes. The four important naturally occurring circulation proteins that inhibit coagulation are protein C, protein S, antithrombin III, and heparin cofactor II. A carefully balanced interaction between these proteins and normal vascular endothelial cells comprise a major barrier inhibiting thrombosis. The true deficiencies of these proteins are usually inherited although many conditions such as DIC, malignancy, malnutrition, infection, and neutropenia can be associated with acquired deficiencies. Although some data suggest an association between arterial strokes and the deficiency of these proteins in young adults, cerebral venous thrombosis and venous infarcts gave been reported far more commonly with deficiencies of any of these proteins. The understanding of the molecular events underlying coagulation has improved in recent years. This has led to development of specific assays that can identify genetic abnormalities which can cause coagulopathies. Although the technology has improved the fundamental approach to the patient has not changed. A primary care physician requires a basic knowledge of the principles of blood coagulation so as to treat patients with simple problems and refer patients with more unusual or complex disorders on to the specialist. The recognition that hypercoagulable states are sometimes found in ischemic stroke patients has led to testing for these rare conditions. Coagulopathies related to protein C, protein S, or antithrombin III deficiencies, activated protein C resistance, prothrombin gene mutation, anticardiolipin antibodies, or lupus anticoagulant can be evaluated with various coagulation testing strategies.