Key result
Stress-induced neurohormonal responses promote hypercoagulation and potential CV harm by activating clotting and inhibiting fibrinolysis.
Why the study?
To provide an overview of current views on changes in the hemostasis system in response to stress.
This review highlights the physiological mechanisms by which acute psychological stress induces hypercoagulation, potentially increasing cardiovascular risk.
May support stress reduction counseling in CV prevention; leaves open randomized trials on coagulation outcomes.
The article presents an overview of current views of changes in the hemostasis system in response to stress. Stress-induced neurohormonal responses activate the clotting system and inhibit the fibrinolysis system, leading to hypercoagulation. An evolutionary interpretation of such responses is that hypercoagulation under stress protects a healthy body from excessive bleeding in case of trauma in fight-or-flight situations. Acute psychological stress can cause significant hemoconcentration and prothrombotic changes in the blood, which can have potentially harmful effects on the cardiovascular system.
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Салухов et al. (2023) conducted a review in Stress-induced hemostatic changes. Acute and chronic stress was evaluated. Stress-induced neurohormonal responses activate the clotting system and inhibit the fibrinolysis system, leading to hypercoagulation and potential cardiovascular harm.
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