Antiplatelet therapy in the treatment of takayasu arteritis

Abstract

Takayasu arteritis (TA) is a chronic idiopathic inflammatory disease that affects large vessels, mainly the aorta and its major branches, including the coronary, carotid, pulmonary and renal arteries.1 Vessel inflammation and subsequent intimal proliferation of the arterial wall may lead to lumen stenosis and occlusion, while aneurysms may result from an inflammatory process involving the elastic lamina of the arteries.2 First-line medical treatment for TA is the use of corticosteroids as anti-inflammatory agents. There is evidence that long-term corticosteroid therapy contributes to improvement of angiographic features.3 Immunosuppres-sive drugs are used only as a supplementary therapy because of their adverse effects. Adjunctive antiplatelet or anti-hypertensive agents are recommended as second-line medical treatment in patients with TA. Studies support the use of anti-platelet agents in TA. Numano et al reported that levels of plasma thromboxaneB2 (TXB2) and platelet P-selectin were significantly higher, especially during the active phase, and plasma cyclic adenosine monophosphate levels were significantly lower in patients with TA than healthy subjects.4,5 They also showed that mean plasma levels of TXB2 and 3 μmol/L ADP-induced platelet aggregation from the affected side were significantly higher than in samples from the non-affected side, respectively. Administration of 80 mg of aspirin led to significant decreases in platelet aggregation and plasma levels of TXB2 compared with a 40-mg regimen.6 Furthermore, Akazawa et al demonstrated that platelet and coagulation activities are significantly increased in patients with TA even during the inactive stages.7 These findings suggest that long-term treatment with aspirin is effective in preventing thrombus formation in surface-damaged blood vessels. No previous study, however, has demonstrated the clinical efficacy of long-term antiplatelet therapy in patients with TA.