Psychological stress induces different alterations in the organism in order to maintain homeostasis, including changes in hematopoiesis and hemostasis. In particular, stress-induced hyper activation of the autonomic nervous system and hypothalamic-pituitary-adrenal axis can trigger cellular and molecular alterations in platelets, coagulation factors, endothelial function, redox balance, and sterile inflammatory response. For this reason, mental stress is reported to enhance the risk of cardiovascular disease (CVD).
However, contrasting results are often found in the literature considering differences in the response to acute or chronic stress and the health condition of the population analyzed. Since thrombosis is the most common underlying pathology of CVDs, the comprehension of the mechanisms at the basis of the association between stress and this pathology is highly valuable.
The aim of this work is to give a comprehensive review of the studies focused on the role of acute and chronic stress in both healthy individuals and CVD patients, focusing on the cellular and molecular mechanisms underlying the relationship between stress and thrombosis.
All the data from the literature did not provide unequivocal evidence that both acute and chronic stress alone suffice to provoke acute coronary thrombosis events, whereas they strongly suggest that in presence of other risk factors stress may confer a greater risk for CVD. Stress response determines a pro-thrombotic state characterized by autonomic and neuroendocrine dysfunction, platelet activation, dysregulation of coagulation, fibrinolysis, and endothelial dysfunction and inflammation. However, this physiological stress response can be considered a pathological trigger only in susceptible patients, worsening the prognosis and the outcome in the ones with pre-existing CVD. Burg et al. proposed the conceptual model of a “perfect storm” in which only the co-occurrence of different pathophysiologic and psychosocial factors, each acting in tandem with one another, can explain the increased risk induced by stress.