Hypnosis as an Adjunct in the Treatment of Von Willebrand's Disease

Fung, Elizabeth H.; Lazar, Billie S.

doi:10.1080/00207148308406621

Cited by 2 publications

(5 citation statements)

References 17 publications

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“…One of the explanations for the increased risk of mucosal bleeding related to anxiety is vasospasm-related ischemia. 8 Different authors have confirmed a relationship between stressful life events and bleeding episodes in patients with coagulation abnormalities such as hemophilia and in von Willebrand disease, 10,11 strengthening the hypothesis of a role for increased fibrinolytic activity in the pathogenesis of anxiety-related bleeding.…”

Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 94%

“…8 The influence of anxiety on bleeding in sites other than the gastrointestinal tract has received less attention. It has been observed that anxiety is positively associated with epistaxis, with hypermenorrhea and with dysfunctional uterine bleeding in the general population, 9,10 but the pathogenic mechanisms are not well understood. One of the explanations for the increased risk of mucosal bleeding related to anxiety is vasospasm-related ischemia.…”

Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 99%

“…12 Since then, there have been many reports on the effectiveness of hypnosis, self-hypnosis, and other anxiolytic interventions in stopping bleeding in patients with hemophilia or von Willebrand disease. 10,13,14 Anxiety as a Risk Factor for Cardiovascular and Thrombotic Diseases Anxiety is a well-known risk factor for cardiovascular disease. A meta-analysis of 37 articles involving 1,565,699 individuals showed that anxiety increases the incidence of cardiovascular events by more than 50%, independent of smoking, sedentary lifestyle, hypertension, obesity, or depression.…”

Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 99%

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Anxiety-Related Bleeding and Thrombosis

Hoirisch-Clapauch

2018

Semin Thromb Hemost

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Anxiety, a normal response to stressful situations, is characterized by increased levels of factor VIII, fibrinogen, and von Willebrand factor, and by enhanced platelet aggregability. One would expect acute anxiety to be a prothrombotic state, but since acute mental stress induces tissue plasminogen activator (tPA) release from endothelial and chromaffin cells, fibrinolysis counteracts procoagulant stimuli. It could be said that procoagulant changes accompanying the fight-or-flight response reduce the risk of bleeding in case of potential injuries, while activation of fibrinolysis counteracts activation of hemostasis to prevent intravascular thrombus formation before injuries occur. Acutely anxious patients are prone to bleeding or thrombosis when the balance between hypercoagulation and hyperfibrinolysis is disturbed. Acute anxiety not only increases the risk of bleeding in hemophilia or von Willebrand disease, but many reports have shown that anxiolytic interventions such as hypnosis are effective in controlling bleeding in hemostatic disorders. The pathogenesis of cardiovascular and thrombotic diseases in highly anxious patients is multifactorial. An important element is α-adrenergic vasoconstriction, which increases viscosity due to leakage of intravascular fluid into the interstitium, and also causes hypertension, favoring plaque rupture. Paradoxical as it may seem, over secretion of tPA may increase cardiovascular risk. This is because tPA degrades the extracellular matrix, causing vascular stiffness that increases cardiac workload, and thus oxygen requirements. Anxious patients with conditions associated with increased plasminogen activator inhibitor-1 levels, such as depression or postprandial hyperinsulinemia, are at high risk of thrombosis. Postprandial hyperinsulinemia may result from consumption of high-carbohydrate foods, considered anxiolytic, combined with a sedentary life, which is common among anxious individuals. Preliminary evidence suggests that high anxiety combined with either depression or a lifestyle that results in hyperinsulinemia has an important role in the pathogenesis of thrombotic events currently classified as unprovoked.

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Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 94%

Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 99%

Section: Anxiety As a Risk Factor For Bleedingmentioning

confidence: 99%

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Anxiety-Related Bleeding and Thrombosis

Hoirisch-Clapauch

2018

Semin Thromb Hemost

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Section: Significance Of Stress-induced Hypercoagulability In Clinica...mentioning

confidence: 99%

“…50 Tissue plasminogen activator (t-PA) activity rises with acute stress, 51 so fibrinolysis could overwhelm coagulation when the concentration or function of clotting factors are diminished. 52 Stress-and anxiety-relieving techniques like hypnosis may mitigate bleeding in VWD 53 and hemophilia, 54 similarly to the antifibrinolytic drug tranexamic acid. 55 With the increasing recognition of stress and hypercoagulability as nontraditional cardiovascular risk factors, research has mainly focused on the role of acute and chronic stress-induced hypercoagulability in ASCVD and, to a lesser extent, VTE.…”

Section: Stress-induced Hypercoagulability Von Känelmentioning

confidence: 99%

Stress-Induced Hypercoagulability: Insights from Epidemiological and Mechanistic Studies, and Clinical Integration

von Känel

2024

Semin Thromb Hemost

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By integrating findings from comprehensive reviews, meta-analyses, and cutting-edge genetic studies, this article illuminates the significance of stress-induced hypercoagulability in clinical medicine. In particular, the findings from numerous prospective cohort studies indicate that stress and hemostatic factors of a hypercoagulable state are associated with increased incident risk and poor prognosis for atherosclerotic cardiovascular disease and venous thromboembolism. Mendelian randomization studies suggest that these associations are partially causal. The review synthesizes extensive research on the link between acute and chronic stress and hypercoagulability, outlining a potential pathway from stress to thrombosis risk. Consistent with the allostatic load concept, acute stress-induced hypercoagulability, initially adaptive, can turn maladaptive under chronic stress or excessive acute stress, leading to arterial or venous thrombotic events. Individuals with predisposing factors, including atherosclerosis, thrombophilia, or immobilization, may exhibit an increased risk of thrombotic disease during stress. Contextual sociodemographic characteristics, the stress experience, and coping resources additionally modulate the extent of stress-induced hypercoagulability. Research into the neuroendocrine, cellular, and molecular bases reveals how stress influences platelet activation coagulation and fibrinolysis. The activation of the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis, along with vagal withdrawal, and the effects of catecholamines, cortisol, and vasopressin, are the central mechanisms involved. Hemoconcentration, inflammation, endothelial dysfunction, and thrombopoiesis additionally contribute to stress-induced hypercoagulability. Further research is needed to prove a causal link between chronic stress and hypercoagulability. This includes exploring its implications for the prevention and management of thrombotic diseases in stressed individuals, with a focus on developing effective psychosocial and pharmacological interventions.

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Hypnosis as an Adjunct in the Treatment of Von Willebrand's Disease

Cited by 2 publications

References 17 publications

Anxiety-Related Bleeding and Thrombosis

Anxiety-Related Bleeding and Thrombosis

Stress-Induced Hypercoagulability: Insights from Epidemiological and Mechanistic Studies, and Clinical Integration

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