Restenosis after percutaneous transluminal angioplasty: II. Possibilities for pharmacologic intervention

Reocclusion after percutaneous transluminal angioplasty is a major mechanism contributing to morbidity of patients after catheterization. Until now, pharmacological approaches to the prevention of restenosis were mostly disappointing, as only the early phase of thrombotic reocclusion, in which platelet activation is a major patho-physiological mechanism, could be treated with inhibitors of platelet aggregation and coagulation. Recently, several new approaches to the pharmacotherapy of restenosis have been introduced, for example thromboxane receptor antagonists or synthase inhibitors, GPIIb/IIa antagonists and hirudin as new inhibitors of platelet aggregation and coagulation, PDGF antagonists as inhibitors of intimal proliferation, and modulators of endothelial cell function, some of which may be effective in the late phase of myointimal proliferation. However, many substances that had been promising in experimental restenosis have proven ineffective in the first clinical trials. More recently, molecular biological techniques are increasingly used in experimental angioplasty. The role of these different approaches for the prevention of restenosis still has to be proven in clinical trials.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Reocclusion after percutaneous transluminal angioplasty is a major mechanism contributing to morbidity of patients after catheterization.

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