Difference in fibrinolytic capacity in young patients with venous thrombosis or ischaemic stroke

Jane Skov1, Johannes J Sidelmann, Else-Marie Bladbjerg

  • 1aUnit for Thrombosis Research, Institute of Public Health, University of Southern Denmark bDepartment of Clinical Biochemistry, Hospital of South West Denmark, Esbjerg, Denmark.

Many recent studies focus on the common pathophysiological mechanisms and risk factors for arterial and venous thrombosis. We investigated the hypothesis that fibrinolytic capacity is similar in patients with ischaemic stroke and venous thromboembolism. Retrospective study of 604 consecutive patients (age <50 years) referred to systematic thrombophilia testing at a single regional centre. The thrombophilia test included clinical variables, genetic polymorphisms, biomarkers of coagulation and a global assay of fibrinolysis that tested the patient's blood fibrinolytic capacity by application of the euglobulin fraction of plasma to a preformed clot of plasminogen-rich bovine fibrin. The patients with venous thromboembolism (n = 284) were slightly younger (32.3 vs. 33.9 years; <0.01) than those with ischaemic stroke (n = 320), had a significantly higher prevalence of obesity (28 vs. 18%; P < 0.01), higher plasminogen activator inhibitor 1 (PAI-1) activity (12.3 vs. 11.1 IU/ml; P = 0.049) and a significantly lower fibrinolytic capacity (3.4 vs. 3.9 IU/ml; P < 0.01). The lower fibrinolytic capacity in patients with venous thromboembolism was also observed in the subgroup of patients with PAI-1 activity within the normal range (n = 430, 3.7 vs. 4.1IU/ml; P < 0.01). After adjustment for age, BMI, fibrinogen concentration, PAI-1 activity and tissue plasminogen activator activity, fibrinolytic capacity still differed significantly between the two groups. Our results indicate that the capacity for fibrinolysis is lower in young patients with venous thromboembolism than ischaemic stroke, suggesting a different mechanistic role of fibrinolysis in arterial and venous thromboembolism.

Related Concept Videos

Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies01:20

Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies

The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...