The Role of Antiplatelet Therapy in Carotid Stenting for Ischemic Stroke Prevention

Abstract

Carotid angioplasty and stenting (CAS) is a minimally invasive revascularization procedure that has become a popular and acceptable treatment option in the United States for high surgical risk patients with internal carotid artery atherosclerosis. It is effective and has an acceptable risk profile, but ischemic complications caused by distal embolization and underlying atherothrombosis persist. Atherothrombosis is the pathological process that is frequently implicated as the underlying cause of stroke, transient ischemic attacks, and most other ischemic vascular disease. Critical steps in the development of occlusive episodes are the disruption of atherosclerotic plaque and subsequent formation of a platelet-rich mural thrombus. Vascular injury as a result of CAS or any other percutaneous intervention triggers platelet adhesion, activation, and aggregation, resulting in the formation of a mural thrombosis. This risk, in addition to the potential risk of embolization to distal sites, provides a rationale for early antiplatelet therapy with CAS. The risk of late stent (>30 days after stenting) thrombosis in some patients, particularly those receiving drug-eluting stents, provides a rationale for prolonged antiplatelet prophylaxis as well as for prophylaxis against late atherothrombotic events. Because of the systemic and progressive nature of atherothrombosis, protection against ischemic vascular events in other arterial beds expands the benefits of long-term antiplatelet therapy. As clinical experience with CAS increases, it is likely that it will be used more frequently for patients with occlusive carotid disease. In addition, adjunct antiplatelet therapy will play a key role in the continued development of CAS.