Mental Stress-Induced Platelet Activation Among Patients With Coronary Artery Disease

Abstract

Experimentally induced mental stress induced platelet activation in patients with CAD. This mechanism may partially explain the link between psychosocial variables and the development of adverse cardiac outcomes in patients with CAD.

Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects

“…Nevertheless, total PLAs and platelet-monocyte aggregates were positively related to SBP changes immediately after stress, implicating the sympathetic nervous system, at least in part, in the PLA response to acute stress [134]. Two studies have been published that examined stress-induced PLA changes in patients with CHD [17,128]. Both studies reported that PLAs increased after acute stressors.…”

“…Additionally, many studies report increases in the levels of the platelet activation markers circulating platelet factor 4 (PF4) and beta-thromboglobulin (BTG) among healthy individuals [6,[116][117][118][119][120][121] and among individuals with essential hypertension [122] and with angina pectoris [123]. However, not all studies have reported significant changes in platelet aggregability [124][125][126] and platelet activation markers [123,127,128] in response to acute stress. For example, Wallén and colleagues [123] reported that acute stress did not elicit elevations in these platelet activation markers in elderly healthy volunteers.…”

“…In another study [120], BTG levels increased significantly following a structured interview and speech task in the control group, but not in postinfarction patients. Similarly, Reid et al [128] found no change in BTG in CHD patients following a stressor protocol that included mental arithmetic and anger recall. Conversely, Wallén et al [123] found that BTG levels increased significantly following a Stroop task among angina patients.…”

Pathogenetic relationship between personality traits and mental derangement with coronary heart disease

“…Однако установить связь данных явлений с психологическими переменными авторам не удалось, в данном исследовании отсутствовала группа контроля [106].…”

“…Из описанных выше экспериментов известно, что психологический стресс вызывает увеличение лейко-цитарно-тромботических агрегатов с преобладанием ней-трофилов и моноцитов [133,135], активацию фибриноге-новых рецепторов, увеличение концентрации Р-селектина [106], который в свою очередь обеспечивает адгезию ней-трофилов и моноцитов к активированному сосудистому эндотелию.…”