Athlete-Specific Risk Factors for VTE
It is well established that strenuous endurance exercise, such as marathon running, activates the coagulatory system (clot formation) by immediately increasing markers of coagulation. In response, the fibrinolytic (clot breakdown) system activates in coordination with the coagulatory system following exercise, such that changes in coagulation are paralleled by an activation of fibrinolysis to preserve hemostatic balance. In other words, in healthy athletes, postexercise clot formation is approximately equal to clot breakdown. This phenomenon, by which both markers of coagulation and fibrinolysis are increased in the bloodstream, is termed “hemostatic activation” and is a normal response to exercise. While exercise-induced hemostatic activation is not detrimental for most individuals, factors incident to endurance exercise may disproportionately activate the coagulatory system, increasing the risk for VTE and contributing to reports of DVT, PE, or both—all of which have been reported after prolonged strenuous endurance events in otherwise healthy athletes.
Of the several published and anecdotal case reports detailing VTE in athletes, travel is a frequent commonality. Endurance events often require travel to and from the event, with long periods of immobilization or inactivity, juxtaposed with prolonged, strenuous exercise. It has been shown that travel by any mode (ie, car, bus, train, or plane) at least 4 hr in duration increases risk of DVT twofold. We were the first group to examine the effect of prolonged exercise and air travel on thrombotic risk factors. In 2010, we conducted a study at the Boston Marathon where we assessed markers of blood clot formation and breakdown in athletes who flew cross-country to and from the marathon versus local runners who drove a short distance to compete. Interestingly, the athletes who flew to the marathon showed dramatically elevated levels of clot formation relative to local, non-traveling athletes. In a subsequent analysis, we found that d-dimer, a clinical biomarker of DVT, was also significantly greater immediately after the marathon in the travel group of athletes. In fact, 6 of the travel subjects (versus no local controls) had d-dimer values that exceeded the clinical threshold for preliminary diagnosis of DVT.
Dehydration and inflammation post-competition also present as significant, but modifiable, risks. Extreme environmental conditions (i.e., temperature, altitude) can further exacerbate these risks. However, properly executed pre-race strategies such as heat acclimatization can reduce risk of dehydration and heat stress during an endurance event.
Injury and/or Vascular Damage
Sustained, prolonged exercise results in microtrauma to the lining of the blood vessel wall due to the increased blood flow and shear stress exerted upon the vascular wall. Prolonged shear stress induces platelet and pro-inflammatory marker release, which in turn activate the clotting cascade. We have previously shown that p-selectin (a marker of inflammation) nearly doubles after a marathon and that increasing age is associated with greater post-exercise levels of this thrombotic risk marker.
Bradycardia and Hypotension
Hypothetically, low circulatory blood flow at rest may increase risk of VTE, particularly in combination with long periods of tapering, low activity, and prolonged travel (i.e., venous stasis); though this has yet to be examined to the best of our knowledge
Summary of Risk Factors for VTE and Potential Countermeasures to Mitigate Risk