Abstract

Cilostazol inhibits phosphodiesterase III (PDE III), which is predominantly distributed to and regulates physiologic responses in platelets, cardiac muscle cells, vascular smooth muscle cells, and adipose cells. Clinically, it is well known as an antiplatelet agent that inhibits the platelet aggregation normally induced by collagen, 5’-adenosine diphosphase (ADP), epinephrine, and arachidonic acid. It also has pleotropic effects, including the prevention of restenosis after angioplasty and the promotion of peripheral vascular flow in patients with peripheral vascular diseases. In the drug-eluting stent era, it has emerged as an effective post-intervention anti-atherothrombotic agent and a useful agent for therapy in diabetic patients. The aim of this study was to review the mechanisms of action and clinical trial results associated with cilostazol in cardiovascular disease patients. (Korean Circ J 2008;38:441-445)

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