Too much, too little, or just right: Tailoring postrevascularization antithrombotic therapy in PAD versus CAD when one size does not fit all

even after revascularization or with guideline-directed medical therapy. Traditionally, single antiplatelet therapy (SAPT) has reduced cardiovascular events; however, in patients with PAD, persistent vulnerability to limb-related and systemic ischemic events has been demonstrated repeatedly in various trials. 7,8 In contrast to patients with PAD, those with CAD exhibit more predictable event rates and a more reliable response to SAPT. The heterogeneity of ischemic pathways in PAD, including thrombosis by endothelial dysfunction, advanced intimal calcification, and chronic inflammation, highlight why sole extrapolation of CAD therapy to PAD risk reduction does not fully translate. Thus, the risk of thrombosis has spurred the development of DPI that combines low-dose anti-coagulation with antiplatelet therapy to suppress both thrombin-mediated clot propagation and platelet activation. 9 In the novel analysis of the ASPARAGUS study, Horie and colleagues 5 demonstrated that patients with PAD had higher Academic Research Consortium for High Bleeding Risk (ARC-HBR) 10 scores at baseline and a greater incidence of postrevascularization bleeding compared to patients with CAD. Although the phenotype of patients with PAD in this registry correlates with known risk factors for bleeding, such as older age, greater burden of frailty, diabetes, renal dysfunction,