The importance of platelets in the pathophysiology of cardiovascular and cerebrovascular disorders has been demonstrated by numerous clinical and pathological studies. Conventional antiplatelet agents are effective in both the primary and secondary prevention of vascular disorders, but suffer for the combined shortcomings of lack of selectivity and relative potency. Many new antiplatelet agents have been developed to overcome these differences, including serotonin receptor antagonists, prostanoid derivatives and antagonists, fibrinogen receptor antagonists, and selective thrombin inhibitors. In this review we consider the mechanisms by which these novel antiplatelet agents impair platelet function and their potential clinical utility.