Acquired and Genetic Thrombotic Risk Factors in the Athlete

Abstract

While athletes are often considered the epitome of health due to their physique and lowered potential for metabolic and cardiovascular diseases, they may also be at risk for the onset and development of venous thromboembolism (VTE). In an attempt to achieve and remain competitive, athletes are frequently exposed to numerous athlete-specific risk factors, which may predispose them to VTE through the disruption of factors associated with Virchow's triad (i.e., hypercoagulability, venous stasis, and vessel wall injury). Indeed, hypercoagulability within an athletic population has been well documented to occur due to a combination of multiple factors including exercise, dehydration, and polycythemia. Furthermore, venous stasis within an athletic population may occur as a direct result of prolonged periods of immobilization experienced when undertaking long-distance travels for training and competition, recovery from injury, and overdevelopment of musculature. While all components of Virchow's triad are disrupted, injury to the vessel wall has emerged as the most important factor contributing to thrombosis formation within an athletic population, due to its ability to influence multiple hemostatic mechanisms. Vessel wall injury within an athletic population is often related to repetitive microtrauma to the venous and arterial walls as a direct result of sport-dependent trauma, in addition to high metabolic rates and repetitive blood monitoring. Although disturbances to Virchow's triad may not be detrimental to most individuals, approximately 1 in 1,000 athletes will experience a potentially fatal post-exercise thrombotic incidence. When acquired factors are considered in conjunction with genetic predispositions to hypercoagulability present in some athletes, an overall increased risk for VTE is present.

Unexpected Populations for Deep Vein Thrombosis: Presentation in an Endurance Athlete

“…Virchow's triad includes hypercoagulability, venous stasis, and vessel wall injury. Like Zadow et al mention, dehydration and subsequent polycythemia are one example of athletic hypercoagulability, travel to races and bedrest after injury are illustrative of venous stasis, and repetitive microtrauma to the venous and arterial vasculature in athletes demonstrates vessel wall injury [14]; this means that the population can reasonably have exposure to at least one but up to all three aspects of Virchow's triad. Interestingly, this same logic has been shown to apply to a phenomenon seen in the upper extremities.…”

Pre‐pregnancy participation and performance in world's largest cross‐country ski race as a proxy for physical exercise and fitness, and perinatal outcomes: Prospective registry‐based cohort study

“…General population studies show associations between exercise and lower VTE risk, but there are reports of higher risk after vigorous exercise 58 . Short‐term physiological effects such as dehydration and vessel wall injury could theoretically increase the VTE risk 59 . Although these results need further investigation, recommendations of pregnancy exercise should include compensating water loss.…”

“…58 Short-term physiological effects such as dehydration and vessel wall injury could theoretically increase the VTE risk. 59 Although these results need further investigation, recommendations of pregnancy exercise should include compensating water loss.…”

<p>Physical Activity and Thrombophilic Risk in a Short Series</p>

“…The impact of vigorous exercise on the coagulation cascade is not yet understood, and the combined effect of exercise and defects of the PC system, should be studied. 9,10 According to some studies, post-exercise hypercoagulability is counterbalanced by hyperfibrinolysis, whereas other investigators report that the increased level of fibrinolytic activity falls sharply during the recovery phase and that activation of coagulation persists. 11 Our results show that the maximal hypercoagulability develops not during exercise but progressively during the first 30 min of the subsequent recovery phase, peaking at 30 mins.…”