Restenosis after percutaneous transluminal angioplasty: II. Possibilities for pharmacologic intervention
Review published in VASA (1996)
Abstract
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.
Resumen
Reocclusion after percutaneous transluminal angioplasty is a major mechanism contributing to morbidity of patients after catheterization.
Por qué esto importa para la hirudoterapia
Esta revisión explora enfoques farmacológicos para prevenir la reestenosis tras la angioplastia transluminal percutánea, discutiendo tanto los inhibidores de la agregación plaquetaria y la coagulación de fase temprana como los agentes antiproliferativos de fase tardía. El resumen identifica la hirudina como uno de varios inhibidores nuevos de la agregación plaquetaria y la coagulación introducidos para la fase temprana de la reoclusión trombótica, al tiempo que señala que muchas sustancias prometedoras han resultado ineficaces en los ensayos clínicos iniciales. El resumen no hace referencia a sanguijuelas, saliva de sanguijuela ni hirudoterapia. La hirudina aparece solo como un agente más dentro de un amplio estudio farmacológico, sin datos clínicos específicos aportados y sin conexión establecida con la terapia con sanguijuelas vivas ni con el ámbito de ASH.
Citación
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026