Baseline level of platelet-leukocyte aggregates, platelet CD63 expression, and soluble P-selectin concentration in patientswith posttraumatic stress disorder: A pilot study

Vidović, Anđelko; Vilibić, Maja; Markotić, Alemka; Sabioncello, Ante; Gotovac, Katja; Folnegović‐Šmalc, Vera; Dekaris, Dragan

doi:10.1016/j.psychres.2006.05.004

Cited by 15 publications

(4 citation statements)

References 36 publications

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“…68 Among civilians with war-related chronic PTSD, von Willebrand factor antigen levels were significantly higher in PTSD than in non-PTSD controls and, moreover, the most severe PTSD cases had higher von Willebrand factor antigen and clotting factor VIII activity levels than those with less severe PTSD symptoms and controls. 69 Baseline platelet activity did not differ between combat veterans with and without PTSD, 70 but platelets from PTSD patients showed exaggerated reactivity to in vitro epinephrine/ADP stimulation mediated by the α2-adrenergic receptor. 71 …”

Section: Mechanisms Of the Ptsd-cvd Associationmentioning

confidence: 95%

Post-traumatic stress disorder and cardiovascular disease

Edmondson

Känel

2017

The Lancet Psychiatry

260

197

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This work is a narrative review of the evidence for an association of PTSD with incident cardiovascular disease (CVD) risk and the mechanisms that may carry that association, as well as the prevalence of PTSD due to CVD events and its associated prognostic risk. We discuss new research conducted since the publication of previous relevant systematic reviews and survey currently funded research in the portfolios of the two most active funders in the field. We conclude that PTSD is a risk factor for incident CVD, and a common psychiatric consequence of CVD events that may worsen CVD prognosis. There are many candidate mechanisms for the PTSD-CVD link, and a number of ongoing studies may soon point to the most important behavioral and physiological mechanisms to target in early phase intervention development. Similarly, targets are emerging for both individual and environmental interventions that may offset PTSD risk after CVD events.

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Section: Mechanisms Of the Ptsd-cvd Associationmentioning

confidence: 95%

Post-traumatic stress disorder and cardiovascular disease

Edmondson

Känel

2017

The Lancet Psychiatry

260

197

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show abstract

“…73 Conversely, PTSD symptomatology was unrelated to baseline levels of PT, aPTT, FVII:C, D-dimer, fibrinopeptide A, and prothrombin fragments 1 þ 2 across several studies. [72][73][74] Baseline platelet activity and soluble P-selectin did not differ between combat veterans with and without PTSD 75 ; however, platelets from PTSD patients showed exaggerated reactivity to in vitro epinephrine/ADP stimulation mediated by the α 2 -adrenergic receptor. 76 Post-MI patients with PTSD caused by their MI showed a significant increase in soluble P-selectin during a trauma interview compared with non-PTSD controls 77 and increased fibrinogen and D-dimer reactivity if perceived stress before the interview was high.…”

Section: Posttraumatic Stress Disordermentioning

confidence: 99%

Stress and Hemostasis: An Update

Austin

Wissmann

Känel

2013

Semin Thromb Hemost

116

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, 62, is one psychoanalyst willing to declare that Richard Nixon's phlebitis is psychosomatic. The man has been under extraordinary pressure for more than a year, Dr. Silverman says. Mr. Nixon seems to keep his emotions under such control that we might have expected physical instead of emotional breakdown.Time Magazine, September 30, 1974, p. 65. This introductory "case vignette" raises the question of whether intense emotional stress, such as experienced by the United States President Nixon in the wake of the Watergate scandal, is capable of causing thrombosisassociated diseases and, if so, by which mechanisms. Thus, the aim of this review is to provide an update on the sizeable literature on stress-related changes in the Keywords ► blood coagulation ► fibrinolysis ► platelets ► psychological stress ► risk factor AbstractNumerous naturalistic, experimental, and mechanistic studies strongly support the notion that-as part of fight-or-flight response-hemostatic responses to acute psychosocial stress result in net hypercoagulability, which would protect a healthy organism from bleeding in case of injury. Sociodemographic factors, mental states, and comorbidities are important modulators of the acute prothrombotic stress response. In patients with atherosclerosis, exaggerated and prolonged stress-hypercoagulability might accelerate coronary thrombus growth following plaque rupture. Against a background risk from acquired prothrombotic conditions and inherited thrombophilia, acute stress also might trigger venous thromboembolic events. Chronic stressors such as job strain, dementia caregiving, and posttraumatic stress disorder as well as psychological distress from depressive and anxiety symptoms elicit a chronic low-grade hypercoagulable state that is no longer viewed as physiological but might impair vascular health. Through activation of the sympathetic nervous system, higher order cognitive processes and corticolimbic brain areas shape the acute prothrombotic stress response. Hypothalamic-pituitary-adrenal axis and autonomic dysfunction, including vagal withdrawal, are important regulators of hemostatic activity with longer lasting stress. Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response. Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed. Restoring normal hemostatic function with biobehavioral interventions bears the potential to ultimately decrease the risk of thrombotic diseases. hemostatic system (i.e., coagulation, fibrinolysis, and platelets) and their potential role in thrombosis. As a prerequisite for the notion that stress-associated hypercoagulability contributes to thrombotic events, 1 abundant epidemiological and experimental data exist supporting the role of enhanced coagulation, impaired fibrinolysis, and hyperactive platelets in the development of atherogenesis, atherothrombosis, and acute coronary...

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“…An analysis of data from a large sample of Vietnam veterans with PTSD found no association between dissociative symptoms and a number of physiological symptoms, including heart rate, skin conductance, electromyographic data, and blood pressure (170). Another study comparing 20 male Croatian combat veterans to non-PTSD males matched on age and BMI found no differences in blood platelet function (171). However, the authors cautioned that this study was designed as a pilot study with low power to detect group differences.…”

Section: Influences Of Hostility and Health Behaviors On Cardiovasculmentioning

confidence: 99%

Posttraumatic Stress Disorder, Cardiovascular, and Metabolic Disease: A Review of the Evidence

et al. 2010

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Background Posttraumatic stress disorder (PTSD) is a significant risk factor for cardiovascular and metabolic disease. Purpose The purpose of the current review is to evaluate the evidence suggesting that PTSD increases cardiovascular and metabolic risk factors, and to identify possible biomarkers and psychosocial characteristics and behavioral variables that are associated with these outcomes. Methods A systematic literature search in the period of 2002–2009 for PTSD, cardiovascular disease, and metabolic disease was conducted. Results The literature search yielded 78 studies on PTSD and cardiovascular/metabolic disease and biomarkers. Conclusions Although the available literature suggests an association of PTSD with cardiovascular disease and biomarkers, further research must consider potential confounds, incorporate longitudinal designs, and conduct careful PTSD assessments in diverse samples to address gaps in the research literature. Research on metabolic disease and biomarkers suggests an association with PTSD, but has not progressed as far as the cardiovascular research.

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Baseline level of platelet-leukocyte aggregates, platelet CD63 expression, and soluble P-selectin concentration in patientswith posttraumatic stress disorder: A pilot study

Cited by 15 publications

References 36 publications

Post-traumatic stress disorder and cardiovascular disease

Post-traumatic stress disorder and cardiovascular disease

Stress and Hemostasis: An Update

Posttraumatic Stress Disorder, Cardiovascular, and Metabolic Disease: A Review of the Evidence

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