Drug Eluting Balloon

Since the first percutaneous transluminal coronary angioplasty (PTCA) performed by Andreas Gruntzig in 1977 the technology has evolved significantly. Progress of PTCA has seen the development of many devices, some of which are still in use and many others that have fallen in disuse. The main limitation of the plain old balloon angioplasty (POBA) was the problem of elastic vascular recoil causing abrupt vessel closure and restenosis. The patho-mechanism of restenosis that occurs following balloon angioplasty involves negative vascular remodeling, elastic recoil and thrombosis at the site of injury {Moreno, 1999}. While the thrombus formation can be reduced by use of antiplatelet drugs, the restenosis threat remains. Early restenosis occurred in as many as 30% of angioplasty cases. This led to the development of the metal stent to exert radial force on the vessel wall and thus prevent elastic recoil. Although stents reduced restenosis, their use led to the realisation of a different and new challenge of in stent restenois (ISR). This occurs mainly due to neointima formation {Mach, 2000,Mudra et al, 1997, Hoffman et al, 1996, Kearney et al, 1997} that is principally composed of proliferating smooth muscle cells (SMC) and extra cellular matrix {Geary et al, 2003, Grewe et al, 1999}. By the late 1990s, it was acknowledged that although the incidence of ISR was lower than that of restenosis following balloon angioplasty {Serruys et al, 1991}, it occurred in 15–30% of patients, and possibly more frequently in certain subgroups {Holmes et al, 2002}.