Abstract

The development of new and effective therapies for the prevention of intimal hyperplasia or restenosis and other vascular diseases has relied largely on the use of experimental animal models of vascular injury. The development and use of certain experimental models have been invaluable in the development of new pharmaceuticals in areas such as thrombosis and thrombolysis. The results generated from studies in models of restenosis have suggested that numerous compounds from a wide variety of pharmacological classes appear to be efficacious in inhibiting the proliferative response following acute vascular injury, such as that which occurs during percutaneous coronary interventions. While great strides in elucidating the hematologic, cellular, and molecular response to vascular injury have come from this body of work, no universally accepted pharmacologic treatment or intervention has yet been demonstrated to significantly and reproducibly reduce the incidence of restenosis after acute vascular injury (as caused by balloon angioplasty and/or stent placement) in humans.

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