Anxiety-Related Bleeding and Thrombosis

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