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Reducing State Anxiety Using Working Memory Maintenance
Published on: July 19, 2017
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Anxiety-Related Bleeding and Thrombosis
1Hematology Department, Hospital Federal dos Servidores do Estado, Rio de Janeiro, Brazil.
Seminars in Thrombosis and Hemostasis
|May 4, 2018
Summary
Acute anxiety creates a prothrombotic state by increasing clotting factors, but also triggers fibrinolysis to prevent thrombosis. Imbalances in this system can lead to bleeding or clotting disorders in anxious patients.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Psychiatry
Background:
- Anxiety triggers procoagulant and fibrinolytic responses, creating a complex hemostatic balance.
- The fight-or-flight response involves increased clotting factors and platelet aggregation, counteracted by tissue plasminogen activator (tPA) release.
- Disturbances in this balance can predispose anxious individuals to bleeding or thrombotic events.
Purpose of the Study:
- To explore the multifactorial pathogenesis of cardiovascular and thrombotic diseases in highly anxious patients.
- To investigate the role of anxiety in modulating hemostasis and its clinical implications.
- To examine the contribution of hypercoagulation, hyperfibrinolysis, and associated conditions to thrombotic risk.
Main Methods:
- Review of existing literature on anxiety, hemostasis, and cardiovascular/thrombotic diseases.
- Analysis of physiological responses to acute mental stress, including clotting factor levels and fibrinolytic activity.
- Examination of the impact of comorbid conditions like depression and hyperinsulinemia on thrombotic risk in anxious individuals.
Main Results:
- Acute anxiety is characterized by increased clotting factors (factor VIII, fibrinogen, von Willebrand factor) and platelet aggregability.
- Mental stress induces tPA release, activating fibrinolysis to counteract procoagulant stimuli.
- Anxiety contributes to cardiovascular risk via α-adrenergic vasoconstriction, increased blood viscosity, hypertension, and plaque instability.
- Overproduction of tPA can paradoxically increase cardiovascular risk by degrading the extracellular matrix and causing vascular stiffness.
- Anxious patients with elevated plasminogen activator inhibitor-1 (PAI-1) levels, often seen in depression or hyperinsulinemia, face a high thrombosis risk.
Conclusions:
- The interplay between hypercoagulation and hyperfibrinolysis in anxiety dictates the risk of bleeding or thrombosis.
- Anxiolytic interventions may help manage bleeding in hemostatic disorders.
- High anxiety, particularly when combined with depression or lifestyle-induced hyperinsulinemia, plays a significant role in the pathogenesis of unprovoked thrombotic events.
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