Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects

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Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/51117803 Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects Article in Annals of Behavioral Medicine · May 2011 DOI: 10.1007/s12160-011-9274-0 · Source: PubMed CITATIONS READS 31 264 3 authors: Anthony W Austin Stephen M Patterson Stockton University Ohio University 17 PUBLICATIONS 128 CITATIONS 41 PUBLICATIONS 1,007 CITATIONS SEE PROFILE SEE PROFILE Roland von Känel University Hospital Zurich 462 PUBLICATIONS 8,630 CITATIONS SEE PROFILE Some of the authors of this publication are also working on these related projects: Guilt feelings, dysfunctional thoughts and cultural values: longitudinal and intervention study View project Leadership, work stress and workforce health View project All content following this page was uploaded by Anthony W Austin on 22 May 2014. The user has requested enhancement of the downloaded file. ann. behav. med. (2011) 42:153–173 DOI 10.1007/s12160-011-9274-0 ORIGINAL ARTICLE Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects Anthony W. Austin, M.A. & Stephen M. Patterson, Ph.D. & Roland von Känel, M.D. Published online: 12 May 2011 # The Society of Behavioral Medicine 2011 Abstract Introduction Background Acute psychological stress can produce sig- nificant hemoconcentration as well as prothrombotic Cardiovascular disease is the underlying cause of 36% of changes in blood, both of which may have potentially all deaths in the USA, making it the nation’s number one harmful effects on the cardiovascular system. It is unclear killer, with coronary heart disease (CHD) being the primary whether these effects are independent or have influence on cause of death [1]. Several risk factors have been identified each other. for CHD, but five have been recognized as conferring the Purpose This review discusses research investigating the most risk: high blood pressure, elevated serum cholesterol, effects of acute psychological stress on hemoconcentration body mass index, diabetes, and smoking [2]. However, and hemostasis and explores future directions for psycho- these traditional risk factors do not fully explain CHD risk hematology research. Physiology, associations with cardio- [3]. Psychological stress is one factor purported to explain vascular disease, and relationships between acute additional CHD risk. For example, in the INTERHEART psychological stress are discussed independently for hemo- study [4], individuals with myocardial infarction reported concentration and hemostasis, followed by an examination more financial stress, more stress at home and at work, and of the effects of stress-hemoconcentration on hemostasis. a greater number of major life events in the previous year Conclusions Traditional methods of adjusting for stress- compared to controls. However, physiological mechanisms hemoconcentration effects (e.g., calculated plasma volume linking stress to CHD have yet to be delineated fully. One or hematocrit level corrections) may not be appropriate possible mechanism through which stress may be linked to when examining stress-induced changes in hemostasis. The CHD is through adverse effects on hemostasis, which is the effects of acute stress on hemostasis should be examined in arrest of bleeding by the physiological properties of conjunction with hemoconcentration. vasoconstriction and coagulation or the interruption of blood flow through any vessel or to any anatomical area, Keywords Hemostasis . Hemoconcentration . and hemostatic processes such as platelet function [5, 6], Cardiovascular disease . Psychological stress hemorheology [7–9], and coagulation [10, 11]. In fact, elevations in several factors involved in hemostasis, such as Electronic supplementary material The online version of this article fibrinogen, D-dimer, von Willebrand factor, and factor VII (doi:10.1007/s12160-011-9274-0) contains supplementary material, which is available to authorized users. (FVII), FVIII, FIX, FXI, and FXII, have been reported as heightened risk markers for CHD [12, 13]. * : A. W. Austin ( ) S. M. Patterson The initiation of acute coronary syndromes (especially Department of Psychology, Ohio University, Athens, OH, USA myocardial infarction) and acute atherothrombotic events in e-mail: [email protected] the coronary tree has been linked to acute psychosocial stress that can result from negative emotions, taxing social R. von Känel situations, and traumatic events [11]. Several pathophysio- Department of General Internal Medicine, Inselspital (University Hospital Berne), logical mechanisms have been suggested, including hemo- Berne, Switzerland concentration (i.e., when the ratio of blood cells to plasma 154 ann. behav. med. (2011) 42:153–173 increases), alterations in blood rheology [7], vascular hemostasis, blood coagulation, and cardiovascular disease. endothelial dysfunction coupled with vasoconstriction, Given that the focus of this review is on acute stress, articles proinflammatory cytokine release, autonomic imbalance were then examined to exclude those focusing on naturalistic (e.g., alterations in heart rate variability), and activation of stressors (e.g., earthquakes), chronic stress, vital exhaustion, or the coagulation cascade as well as indirectly through related concepts. Additionally, a wide variation in methodol- changes in health behaviors [14–16]. The disruption of the ogy existed among acute stress studies, making a systematic hemostatic balance (i.e., balance between clot formation and review difficult. Therefore, the review is narrative in nature. clot dissolution) is a critical factor in atherosclerotic develop- ment and initiation of acute coronary syndromes. After plaque rupture, a vessel occlusion is more likely if the ratio of Hemoconcentration prothrombotic activity (i.e., promoting clot formation) to fibrinolytic activity (i.e., promoting clot dissolution) is high. Hemoconcentration refers to conditions in which the ratio During acute psychological stress, both prothrombotic and of cellular components (principally red blood cells) of the fibrinolytic activities increase, but with the former to a greater blood to the plasma volume increases [7]. Hemoconcentra- extent than the latter [10]. In a healthy person, such a tion mainly occurs in two ways. First, plasma volume can response is physiologically normal. However, this type of remain constant while the number of red blood cells response could have life-threatening effects in a patient with increases. This condition is seen in polycythemia vera, a CHD because stress-hypercoagulability seems to be exag- rare tumorous condition in which red blood cells are gerated in these patients [17] and could add to hypercoag- produced to a greater extent than normal [20] and in ulability initiated after plaque rupture. Therefore, risk secondary polycythemia which is associated with altitude increases for the formation of a clot large enough to critically sickness [21]. Second, and more commonly, hemoconcen- occlude the coronary artery. The ensuing net hypercoagula- tration occurs when the number of red blood cells remains bility resulting from acute psychological stress may put an constant while plasma volume decreases. This condition individual at a greater risk for coronary thrombosis after has been variously referred to as ‘stress’ polycythemia, plaque disruption and thus contribute to acute coronary relative polycythemia, pseudopolycythemia, spurious poly- syndromes [10, 11]. Other crucial factors suggested to cythemia, or stress-hemoconcentration [7, 22, 23]. Figure 1 accompany hypercoagulation are stress-induced hemocon- depicts stress-hemoconcentration that occurs when plasma centration [18] and increased blood viscosity [9, 19], both of moves or shifts from the vascular compartment into which exacerbate the shear stresses imposed by atheroscle- interstitial spaces during acute psychological stress pro- rotic plaques and plaque ruptures [7]. Elucidation of how duced by various laboratory stressors (e.g., mental arith- these mechanisms occur is central to understanding the metic, Stroop color–word recognition test, cold pressor test, relationship between stress and CHD. and public speaking). Early studies of plasma volume shifts The purpose of this review is to provide an update on the demonstrated this phenomenon during various psycholog- state of the research investigating the effects of acute ical states such as emotional stress [24] and anxiety [25]. psychological stress on hemoconcentration and hemostasis Additionally, acute psychological stress reliably elicits and to explore future directions for psychohematology research. plasma volume losses from the vasculature [26]. This review has two main sections: “Hemoconcentration” and “Hemostasis”. The first section provides an overview of Hemoconcentration Assessments hemoconcentration with a discussion of physiology, association with cardiovascular disease, and relationships between hemo- Plasma Proteins concentration and acute psychological stress. The second section is organized similarly, providing an overview of One indicator of stress-hemoconcentration is an increase in hemostasis with a discussion of physiology, association with the concentration of plasma proteins, such as serum cardiovascular disease, and relationships between hemostasis albumin. Plasma passes easily into interstitial spaces and acute psychological stress, with particular emphasis on through minute openings or
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