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A systematic review of the effects of acute psychological stress and physical activity on haemorheology, coagulation, fibrinolysis and platelet reactivity: Implications for the pathogenesis of acute coronary syndromes

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Abstract

Physical activity and psychological stress are two potential triggers for the onset of acute coronary syndromes (ACS). To examine the mechanisms underlying this association, we systematically reviewed the literature to determine the effects of acute psychological stress and physical activity on haemorheology and haemostasis. Studies examining the haemorheological and haemostatic response to an acute bout of physical activity (i.e. < 60 min) or laboratory psychological stress task were eligible for inclusion. The experimental evidence, although compromised by various methodological weaknesses, suggests that low and moderate intensity physical activity may be cardio-protective through beneficial effects on fibrinolytic system. High levels of physical activity, and psychological to a lesser extent, have been consistently associated with robust changes in haemorheology and haemostasis. Such findings imply that such activities may have the potential to trigger the onset of ACS, although in reality this may be limited sedentary individual and/or those with pre-existing vascular disease. In addition, the data also suggest that individuals may be at a greatest risk of stress-induced thrombogenesis in the period immediately following physical activity or psychological stress, rather than during the activity per se. In conclusion, psychological stress and physical activity may act as potential triggers for the onset of ACS via effects on haemostasis and haemorheology.

Introduction

Cardiovascular disease (CVD) remains the major cause of mortality and morbidity in the western world, with acute myocardial infarction (MI) accounting for a large percentage of that observed [1]. The aetiology of MI is usually a chronic and multi-factorial process, with several risk factors such as elevated serum cholesterol, hypertension and smoking, being well recognised. In addition to established risk factors, it has been suggested that lifestyle and daily activities, such as psychological stress and physical activity, may act as triggers for acute coronary syndromes (ACS).

The concept of ‘triggering’ emerged almost a century ago when Obraztsov and Strazhesko provided anecdotal evidence stating that ‘direct events’ (such as psychological stress or physical activity) could precipitate MI [2]. More robust evidence has subsequently emerged from self-report studies, demonstrating that in a population of patients who had experienced a MI nearly half (40–50%) reported one or more potential trigger, the most common being moderate/heavy physical activity, sudden change in position, and acute emotional upset [3], [4], [5].

Cannon and Mendenhall were the first to study the mechanisms through which psychological stress might influence the risk of development/progression of CVD [6]. In a series of experiments on cats, they found that emotional excitement could elicit a hypercoagulable state through alterations in blood-clotting time. Naturalistic studies added further support to such findings [7], demonstrating that stressful activities such as sitting an examination or giving blood had the potential to increase fibrinolytic activity or decrease blood-clotting time.

Research examining the effects of physical activity on haemostasis was initiated over 50 years ago, demonstrating that an acute bout of exercise had the potential to increase ‘mean fibrinolytic activity’ [8], with a ‘standard bout of muscular effort' having the potential to decrease blood-clotting time [9].

Section snippets

Haemorheology

In his seminal paper in 1854, Virchow recognised that blood flow plays an integral role in thrombogenesis [10]. The flow of blood and the subsequent sheer stress it exerts within the vessel is influenced by an array of factors such as blood viscosity, fibrinogen and low-density lipoprotein (LDL) cholesterol. Studies focusing on the haemorheological response to stressors have, in the main, focussed on haemoconcentration, determined by increases in haematocrit and/or decreases in plasma volume.

Results of our systematic review

The searches resulted in 1889 citations, of which 120 studies published between 1988 and 2005, met the inclusion criteria (see Supplementary Figure 1). The details of the included studies are summarised separately into studies examining the effect of psychological stress (see Table 1) [24], [25], [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41], studies examining the effect of acute physical activity (see Table 2a–c) [53], [54], [55], [56], [57],

Discussion

The notion that physical activity and psychological stress can trigger the onset of acute coronary syndromes (ACS) is intuitively appealing, and has inspired a considerable amount of research over the last 50 years. This review of the experimental findings suggests that acute physical activity, and to a lesser extent psychological stress, may contribute to the development of a prothrombotic state through alterations in blood rheology and haemostasis (see Table 1 and Table 2a–c). The biological

References (130)

  • F. Tomoda et al.

    Different platelet aggregability during mental stress in two stages of essential hypertension

    Am J Hypertens

    (1999)
  • M. Eriksson-Berg et al.

    Retained fibrinolytic response and no coagulation activation after acute physical exercise in middle-aged women with previous myocardial infarction

    Thromb Res

    (2002)
  • G. Ersoz et al.

    The effect of submaximal exercise on platelet aggregation during late follicular and midluteal phases in women

    Thromb Res

    (2002)
  • B. Dufaux et al.

    Can physical exercise induce an effective fibrinolysis?

    Thromb Res

    (1984)
  • M. Mockel et al.

    Exhaustive cycle exercise induces P-selectin expression, coagulation, and fibrinolysis activation in ultraendurance athletes

    Thromb Res

    (1999)
  • R. Otterstetter et al.

    Hemostatic responses to maximal exercise in oral contraceptive users

    Am J Obstet Gynecol

    (1999)
  • H.D. Kvernmo et al.

    The effect of physical conditioning suggests adaptation in procoagulant and fibrinolytic potential

    Thromb Res

    (1997)
  • S. Sakita et al.

    Acute vigorous exercise attenuates sensitivity of platelets to nitric oxide

    Thromb Res

    (1997)
  • KA. LaCroix et al.

    The effects of acute exercise and increased atmospheric pressure on the hemostatic mechanism and plasma catecholamine levels

    Thromb Res

    (1990)
  • N. Vene et al.

    Tissue-type plasminogen activator inhibitor-1 after exercise: comparison to venous occlusion and DDAVP

    Fibrinolysis

    (1990)
  • H.I. Chen et al.

    Effects of acute exercise on bleeding time, bleeding amount and blood cell counts: a comparative study

    Thromb Res

    (1989)
  • S. Lindemann et al.

    Increased platelet sensitivity toward platelet inhibitors during physical exercise in patients with coronary artery disease

    Thromb Res

    (1999)
  • H. Bounameaux et al.

    Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia

    Thromb Res

    (1992)
  • D. McGill et al.

    Platelet function and exercise-induced myocardial ischaemia in coronary heart disease patients

    Thromb Res

    (1989)
  • W. Speiser et al.

    Increased blood fibrinolytic activity after physical exercise: comparative study in individuals with different sporting activities and in patients after myocardial infarction taking part in a rehabilitation sports program

    Thromb Res

    (1988)
  • W.E. Strauss et al.

    Serial studies of platelet factor 4 and beta thromboglobulin during exercise in patients with coronary artery disease

    Am Heart J

    (1985)
  • C.M. Michaud et al.

    Burden of disease: implications for future research

    JAMA

    (2001)
  • V.P. Obraztsov et al.

    The symptomatology and diagnosis of coronary thrombosis

  • W.B. Cannon et al.

    Factors affecting the coagulatioin time of blood. IV. The hastening of coagulatioin with pain and emotional excitement

    Am J Physiol

    (1914)
  • R. von Kanel et al.

    Effects of psychological stress and psychiatric disorders on blood coagulation and fibrinolysis: a biobehavioral pathway to coronary artery disease?

    Psychosom Med

    (2001)
  • R.A. Schneider et al.

    Variations in clotting time, relative viscosity, and other physiochemical properties of blood accompanying physical and emotional stress in normotensive and hypertensive subjects

    Psychosomat Med

    (1951)
  • G.D. Lowe

    Virchow's triad revisited: abnormal flow

    Pathophysiol Haemost Thromb

    (2004)
  • E.H. Starling

    On the absorbtion of fluids from the connective tissue spaces

    J Physiol

    (1896)
  • E.M. Landis

    Micro-injection studies of capillary permeability. II. The relation between capillary pressure and the rate at which fluid passes through the walls of single capillaries

    Am J Physiol

    (1927)
  • S. Kamath et al.

    Platelet activation: assessment and quantification

    Eur Heart J

    (2001)
  • Veldhuijzen van Zanten JJ, Ring C, Carroll D, McIntyre D, Brown MD. Mental stress-induced hemoconcentration: mechanisms...
  • J.J. Veldhuijzen Van Zanten et al.

    The influence of hydration status on stress-induced hemoconcentration

    Psychophysiology

    (2005)
  • J.J. Veldhuijzen van Zanten et al.

    Mental stress-induced hemoconcentration: Sex differences and mechanisms

    Psychophysiology

    (2004)
  • A.E. Ross et al.

    Gender specific sympathetic and hemorrheological responses to mental stress in healthy young subjects

    Scand Cardiovasc J

    (2001)
  • S.M. Patterson et al.

    Acute hemoconcentration during psychological stress: assessment of hemorheological factors

    Intern J Behav Med

    (1995)
  • M.F. Muldoon et al.

    Effects of acute psychological stress on serum lipid levels, hemoconcentration, and blood viscosity

    Arch Intern Med

    (1995)
  • S.M. Patterson et al.

    Time course and mechanisms of decreased plasma volume during acute psychological stress and postural change in humans

    Psychophysiology

    (1995)
  • C. Jern et al.

    Haematological changes during acute mental stress

    Br J Haematol

    (1989)
  • R. von Kanel et al.

    The effect of natural habituation on coagulation responses to acute mental stress and recovery in men

    Thromb Haemost

    (2004)
  • A. Steptoe et al.

    Influence of socioeconomic status and job control on plasma fibrinogen responses to acute mental stress

    Psychosom Med

    (2003)
  • R. von Kanel et al.

    Acute procoagulant stress response as a dynamic measure of allostatic load in Alzheimer caregivers

    Ann Behav Med

    (2003)
  • S.M. Patterson et al.

    Prothrombotic effects of environmental stress: changes in platelet function, hematocrit, and total plasma protein

    Psychosom Med

    (1995)
  • C. Jern et al.

    In vivo release of tissue-type plasminogen activator across the human forearm during mental stress

    Thromb Haemost

    (1994)
  • S.B. Malkoff et al.

    Blood platelet responsivity to acute mental stress

    Psychosom Med

    (1993)
  • O. Naesh et al.

    Platelet activation in mental stress

    Clin Physiol

    (1993)
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