Stress-induced hemostasis: mechanisms and implications for health

Stress, encompassing both psychological and physical dimensions, profoundly affects the hemostatic system, which is responsible for maintaining the delicate balance between blood fluidity and clot formation. The interplay between stress and hemostasis involves intricate mechanisms where stress hormones like cortisol, adrenaline, and noradrenaline interact with coagulation factors and platelets, promoting a hypercoagulable state. This review delves into the various pathways through which stress influences hemostasis, highlighting the critical roles of the sympathetic nervous system, the hypothalamic-pituitary-adrenal axis, and inflammatory mediators. Psychological stress, arising from anxiety, depression, and acute mental stress, has been shown to elevate levels of coagulation factors such as fibrinogen and D-dimer, increasing the risk of thrombotic events. Similarly, physical stress from intense exercise or trauma enhances platelet reactivity and the expression of procoagulant factors. The body's response to severe physical stress, such as trauma or burns, can overwhelm the hemostatic system, leading to conditions like disseminated intravascular coagulation, characterized by widespread clotting and subsequent bleeding. The health implications of stress-induced hemostatic changes are significant, particularly concerning cardiovascular diseases. Chronic stress contributes to persistent hypercoagulability, elevating the risk of myocardial infarction and stroke. Acute stress episodes can precipitate acute coronary syndromes, especially in individuals with preexisting conditions like hypertension or diabetes.