Past, present, and future of anti-platelet therapy

Anti-platelet drugs are useful in preventing unwanted clots, but the complexities of platelet activation and clot formation are challenging.

Platelets can be activated by a variety of agents, including natural biomolecules, foreign materials, and drugs. Calcium mediates a number of the intracellular processs Once activated, platelets release factors that act on other circulating cells and vascular endothelial cells to promote formation of a clot. The original anti-platelet drug, aspirin, inhibits cyclooxegenase, interfering with a crucial step in the biochemical cascade. Aspirin is cost-effective but limited in its application. Newer drugs, ticlopidine and clopidogrel, act on the activation pathway at different points, so they can supplement aspirin. NEW DIRECTIONS: Abciximab represents a new generation of antiplatelet drug, being an antibody that binds to platelet surface receptors, thus inhibiting growth of thrombus. Other potential sites for antibody intervention are extracellular matrix and endothelial surface components. As new drugs are developed it becomes more imperative to find assays of platelet function that are sensitive and cost-effective.

Although much progress has been made in anagement of clotting significant opportunities and challenges remain, both in treatment and in measurement of treatment effectiveness.