Interpretive Limitations Associated With Plasma Volume Shifts in the Clinical Assessment of Hemostasis

Fall, Lewis; Bailey, Damian Miles

doi:10.1097/psy.0b013e318286f799

Cited by 2 publications

(1 citation statement)

References 11 publications

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“…52 Acute stressinduced changes in plasma volume only explain between 4 and 10% of the variance in changes of FVII:C, FVIII:C, and FXII: C. 49 The most accurate methods to investigate the relative contribution of stress-hemoconcentration to the acute prothrombotic stress response are of current debate. [53][54][55] Arithmetic adjustment for stress-hemoconcentration has differing effects on fibrinogen, FVII:C, FVIII:C, FXII:C, VWF:Ag, PT%, and aPTT. 31,56 Saline reconstitution of contracted plasma suggested that stress-induced elevations of most measures was due to hemoconcentration, with the notable exception of FVIII:C. 31 In fact, no correction technique removed the effects for FVIII:C, suggesting that the intrinsic pathway is genuinely activated during acute stress.…”

Section: Underlying Physiological Mechanisms With Acute Stressmentioning

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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Section: Underlying Physiological Mechanisms With Acute Stressmentioning

confidence: 99%

Stress and Hemostasis: An Update

Austin

Wissmann

Känel

2013

Semin Thromb Hemost

116

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Simulated Hypergravity Activates Hemostasis in Healthy Volunteers

Limper

Ahnert

Maegele

et al. 2020

JAHA

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Background Hypergravity may promote human hemostasis thereby increasing thrombotic risk. Future touristic suborbital spaceflight will expose older individuals with chronic medical conditions, who are at much higher thromboembolic risk compared with professional astronauts, to hypergravity. Therefore, we tested the impact of hypergravity on hemostasis in healthy volunteers undergoing centrifugation. Methods and Results We studied 20 healthy seated men before and after 15 minutes under 3 Gz hypergravity on a long‐arm centrifuge. We obtained blood samples for hemostasis testing before, immediately after, and 30 minutes after centrifugation. Tests included viscoelastic thromboelastometry, platelet impedance aggregometry, endothelial activation markers, blood rheology testing, microparticle analyses, and clotting factor analysis. Exposure to hypergravity reduced plasma volume by 12.5% ( P =0.002) and increased the red blood cell aggregation index ( P <0.05). With hypergravity, thrombelastographic clotting time of native blood shortened from 719±117 seconds to 628±89 seconds ( P =0.038) and platetet reactivity increased ( P =0.045). Hypergravity shortened partial thromboplastin time from 28 (26–29) seconds to 25 (24–28) seconds ( P <0.001) and increased the activity of coagulation factors (eg, factor VIII 117 [93–134] versus 151 [133–175] %, P <0.001). Tissue factor concentration was 188±95 pg/mL before and 298±136 pg/mL after hypergravity exposure ( P =0.023). Antithrombin ( P =0.005), thrombin‐antithrombin complex ( P <0.001), plasmin‐alpha2‐antiplasmin complex (0.002), tissue‐plasminogen activatior ( P <0.001), and plasminogen activator inhibitor‐1 ( P =0.002) increased with centrifugation. Statistical adjustment for plasma volume attenuated changes in coagulation. Conclusions Hypergravity triggers low‐level hemostasis activation through endothelial cell activation, increased viscoelasticity, and augmented platelet reactivity, albeit partly counteracted through endogenous coagulation inhibitors release. Hemoconcentration may contribute to the response.

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Interpretive Limitations Associated With Plasma Volume Shifts in the Clinical Assessment of Hemostasis

Cited by 2 publications

References 11 publications

Stress and Hemostasis: An Update

Stress and Hemostasis: An Update

Simulated Hypergravity Activates Hemostasis in Healthy Volunteers

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