Regular ArticleA 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
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
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