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  • Updated 01.18.2023
  • Released 03.18.1997
  • Expires For CME 01.18.2026

Hypercoagulable states and cerebrovascular disease



In this update, the author discusses advancements in the epidemiology, diagnosis, treatment, and prognosis of patients with arterial ischemic stroke and cerebral venous thrombosis associated with genetic and acquired thrombophilia, including the antiphospholipid antibody syndrome.

Key points

• Genetic and acquired hypercoagulable states, such as factor V Leiden deficiency, prothrombin G20210A mutation, and antiphospholipid syndrome, are associated with cerebrovascular events, including cerebral venous thrombosis and ischemic stroke.

• Understanding the pathophysiology of the hypercoagulable state is essential to understand the associated stroke syndromes and appropriate treatments.

• Study of the epidemiology, pathophysiology, and treatment of many recently described hypercoagulable states is an active and important area of research in neurology.

• The use of direct oral anticoagulants (DOACS) in the treatment of patients with cerebral venous thrombosis has been established by recent research.

• Recent clinical trials and metaanalyses have established warfarin as the first-line treatment to prevent thrombotic complications in the antiphospholipid syndrome. Direct oral anticoagulants are associated with an increased risk of thrombosis in comparison to warfarin.

Historical note and terminology

Rudolf Virchow proposed in 1862 that the pathophysiology of thrombosis involved a triad of interrelated factors: damage to blood vessel endothelium, stasis of blood flow, and disorders of blood coagulability.

Virchow triad

In 1862, Rudolf Virchow proposed the pathophysiology triad of thrombosis: blood vessel wall lesion, blood flow stasis, and alterations in blood coagulability. (Contributed by Dr. Steven Lentz.)

Today, thrombophilia is broadly defined as both inherited and acquired conditions that predispose to venous or arterial thrombosis. The term "hypercoagulable state" is defined as a prothrombotic condition resulting from any specific disorders of blood coagulation. Although the clinical concept of hypercoagulability has been appreciated for decades, only since the 1980s has it been possible to identify an underlying disorder of coagulation in a subset of patients with thrombosis. These disorders may be hereditary or acquired. Activated protein C resistance due to factor V Leiden mutation, prothrombin 20210A gene mutation, protein C deficiency, protein S deficiency, and antithrombin III deficiency are the most frequently seen causes of a hereditary hypercoagulable state; antiphospholipid antibody syndrome is the most common acquired disorder.

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