Available: 01/10/22, Expires: 05/01/29
In response to the growing prevalence of peripheral arterial disease (PAD), an estimated 200 million, largely due to worldwide changes in population dynamics, revascularization procedures are increasingly offered for lifestyle-limiting claudication. The total number of revascularization procedures nearly doubled over the prior decade. Yet despite this increase in operative interventions, limb loss remains high. Early bypass graft and/or stent thrombosis is frequent, ranging between 5-17%. Thrombosis is a leading cause of both amputation and mortality following revascularization, with up to 50% of patients dying within one year of amputation. Hypercoagulability is commonly implicated in graft and stent thrombosis. Thus, antithrombotic therapy is a pillar of postoperative maintenance of graft patency. Basic science research has well established the highly synchronized and dynamic interplay between platelet activation and the coagulation cascade. Thrombin is a platelet agonist through the cleavage of protease-activated receptors and fibrinogen bridges activated platelets to enhance clot strength. Activated platelets, on the other hand, enhance coagulation with their phospholipid surface upon which thrombin generation occurs. This is the basis for evolving antithrombotic strategies within PAD, with drugs directed at Factor Xa levels acting to inhibit thrombin-mediated platelet activation, and antiplatelet therapy acting to attenuate thrombin generation. Despite our understanding of the molecular biology, there is no specific level 1A evidence supporting the use of multimodal antithrombotic therapy for PAD. The majority of recommendations are derived from subgroup analysis of randomized trials for coronary and cerebrovascular disease patients. Prior trials examining the use of antithrombotic therapy after bypass surgery have lacked efficacy and found an unacceptable bleeding risk. This lack of consensus for medical management in postoperative PAD may largely be due to the myriad of factors involved in hypercoagulability within this patient population. Medication noncompliance is estimated to be up to 43% in cardiovascular patients. Comorbidities that increase the risk for hypercoagulability, such as diabetes or smoking status, are often categorized as binary variables and not stratified based on severity or chronicity, so subgroup analysis is often inaccurate and lacks nuance. Patients after surgery can have transient hypercoagulable states, due to factors such as blood transfusions, critical illness, and uremia, resulting in a transitory thrombotic risk. Additionally, non-sensitivity to antiplatelet agents is up to 60-65% in the cardiovascular population, resulting in significant variability of individual response to therapy unbeknownst to the surgeon. Current standards for the assessment of hypercoagulability do not match the complexity and interplay of these various factors. Prothrombin time (PT), international normalized ratio (INR) and activated partial thromboplastin time (aPTT) measure individual steps of the coagulation cascade in a non-physiologic setting and can poorly reflect in vivo coagulation. Additionally, these metrics do not measure for effectiveness of certain antithrombotic agents, such as direct-acting oral anticoagulants (DOACs) or antiplatelet therapies. Complete blood counts value platelet number but are limited in that they do not reflect platelet function, which may be affected by factors such as antiplatelet medications, uremia or alcohol. Viscoelastic assays, such as thromboelastography (TEG), measure the multi-pathway dynamics of clot formation, strengthening and breakdown. With time displayed on the X-axis, the measurements of initial fibrin clot formation (R time), thrombin “burst” and fibrin crosslinking (K time and a-angle), fibrin-platelet interactions resulting in maximal clot strength (MA) and clot disintegration at 30 seconds (Ly30) are the five standard Y-axis outputs. Platelet function is estimated to result in 80% of the MA, while the remaining 20% is derived from fibrin. Thromboelastography with platelet mapping (TEG-PM) not only measures the MA but also utilizes platelet activators, such as adenosine diphosphate and arachidonic acid, to provide a quantitative analysis of platelet aggregation and inhibition. In this way, TEG-PM can be used to understand platelet function, including those effects from antiplatelet medications. While the use of TEG has become well-established as the standard of care in states of hemorrhagic shock due to its efficacy in guiding resuscitation, its use in the prothrombotic space is only recently emerging. Promising data for the prediction of clinical outcomes in the cerebrovascular disease and venous thromboembolism populations has precluded the use of TEG in PAD despite the intricate relationship between vascular disease and coagulation. Currently there are no data examining the utilization of TEG-PM in postoperative PAD patients, nor has TEG-PM been studied in correlation to clinical outcomes in PAD. This prospective, observational study aimed to determine if TEG-PM could predict thrombosis following named vessel lower extremity revascularization.