Acute mental stress and hemostasis: When physiology becomes vascular harm

Abstract

Stress-induced activation of the sympathoadrenal medullary system activates both the coagulation and fibrinolysis system resulting in net hypercoagulability. The evolutionary interpretation of this physiology is that stress-hypercoagulability protects a healthy organism from excess bleeding should injury occur in fight-or-flight situations. In turn, acute mental stress, negative emotions and psychological trauma also are triggering factors of atherothrombotic events and possibly of venous thromboembolism. Individuals with pre-existent atherosclerosis and impaired endothelial anticoagulant function are the most vulnerable to experience onset of acute coronary events within two hours of intense emotions. A range of sociodemographic and psychosocial factors (e.g., chronic stress and negative affect) might critically intensify and prolong stress-induced hypercoagulability. In contrast, several pharmacological compounds, dietary flavanoids, and positive affect mitigate the acute prothrombotic stress response. Studies are needed to investigate whether attenuation of stress-hypercoagulability through medications and biobehavioral interventions reduce the risk of thrombotic incidents in at-risk populations.

Psychosocial perspectives in cardiovascular disease

“…17 Low-grade inflammation and coagulation activation play particularly important roles, as they facilitate growth, vulnerability and haemodynamically induced erosion/rupture of an atherosclerotic plaque with thrombotic coronary occlusion. 18 As shown in Figure 2, the latter is a key mechanism in the biology of emotionally triggered ACS, such as with outbursts of anger. 19 Psychosocial factors and stress are associated with more adverse lifestyle behaviours related to smoking, physical activity, diet, alcohol consumption and sleep health.…”

The emotional stress and risk of ischemic stroke

“…prothrombin time and activated partial thromboplastin time. Exaggerated hypercoagulability in the response to acute mental stress may occur in the presence of modulators such as: older age, male sex, low socioeconomic status, cardiovascular disease, chronic psychosocial stress, negative affect, perceived threat and challenge [27,28]. In the healthy individuals the acute stress and subsequent increased coagulation does not have to be harmful for vessels leading to a vascular episode.…”

Psychokardiologische Grundlagen: Wie schädigt Stress das Herz-Kreislauf-System?

“…Akuter, wiederholter und chronischer Stress in verschiedenen Lebensbereichen ist geeignet, das Risiko für die Entstehung, die Manifestation und einen ungünstigen Verlauf kardiovaskulärer Erkrankungen zu erhöhen. [5].…”

“…Im Gegensatz zu stressinduzierten Veränderungen des Blutdrucks und des Kortisolspiegels findet man bei gesunden Individuen keine Anpassung hinsichtlich der Stärke der Gerinnungsreaktion bei wiederkehrenden Stressstimuli. Dies erklärt sich evolutionär am ehesten dadurch, dass die physiologische Hyperkoagulabilität zusammen mit der ebenfalls katecholamingetriggerten Vasokonstriktion zu hohe Blutverluste in einer Kampfsituation vermeiden soll [5].…”

“…Intimale Makrophagen phagozytieren oxidierte Lipoproteine und können zu Schaumzellen differenzieren, was als kritischer Vorläufer für die Entstehung der atherosklerotischen Plaque zu sehen ist. Mehr noch, Makrophagen sind entscheidende Mediatoren für die Entzündungsreaktion bei der Atherosklerose, indem sie Wachstumsfaktoren und verschiedene Zytokine produzieren [5,7,8].…”