RESUMEN
Intimal hyperplasia is a feature of the normal adaptive response of vessels to hemodynamic stresses, as well as being a characteristic of vessel injuries that are healing. Intimal hyperplasia in the region of endarterectomy, balloon angioplasty and vascular bypass graft anastomosis is a major cause of the long-term failure of vascular reconstruction. The underlying causes of intimal hyperplasia are proliferation and migration of vascular smooth muscle cells, and this is all provoked by injury, inflammation and mechanical stretch. This review discusses both the final common pathways that lead to smooth muscle cell migration and proliferation and their patho-physiological triggers. In this review, we have critically evaluated and summarized the literature to understand and interlink the numerous established and emerging factors that play key roles in the development of intimal hyperplasia.
Asunto(s)
Angioplastia de Balón , Endarterectomía , Glicosaminoglicanos , Hemodinámica , Hiperplasia , Inflamación , Metaloproteasas , Músculo Liso Vascular , Miocitos del Músculo Liso , TrasplantesRESUMEN
Objective To study the platelet activity changes in patients before and after percutaneous coronary cutting balloon angioplasty (CBA) and plain old balloon angioplasty (POBA) as well as its clinical significance.Methods Blood was obtained from the coronary sinus. Bioassay method used for assessment of PDGF. The plasma 6-keto-PGF 1a level was determined using ELISA.Results The amount of PDGF and 6-keto-PGF 1a were significantly different after PTCA between CBA group and POBA group (P