RESUMO
Background: There are limited number of studies in India which have looked at this clinical and angiographic characteristic of the disease. Thus, this study was conducted to assess the clinical and angiographic profile of symptomatic patients who underwent percutaneous transluminal coronary angioplasty (PTCA) and drug-eluting stent (DES) implantation.Methods: This was an observational study conducted at a tertiary-care center in India between November 2014 and November 2015. A total of 106 consecutive patients who received either Cypher/Xience/BioMime stent presented with anginal symptoms were included in the study. Based on the type of stent received, patients were divided into two groups: (A) Limus group; (B) Paclitaxel group. Coronary angiogram was done in all the patients. Angioplasty data were collected from patient records. Angiographic profiles of the two groups were compared and analysed.Results: Among the 106 patients, 54 patients were included in the Limus group and 52 patients were included in the Taxus stent. De novo lesions were found to be significantly higher in the Limus group (40(74%), p = 0.06) whereas the in-stent restenosis was found to be significantly higher in the paclitaxel group (22(42.3%), p = 0.08). At follow-up, the incidence of death was 0% and no patients suffered by myocardial infarction. One (1.8%), two (3.8%) patients from the Limus and Paclitaxel groups had target vessel revascularization, respectively.Conclusions: Development of lesions in new areas rather than in-stent restenosis is the cause for angina in the majority of patients who underwent angioplasty presenting with anginal symptoms.
RESUMO
"Percutaneous Transluminal Coronary Angioplasty (PTCA) remains limited by restenosis that occurs in 30 to 50% of patients with coronary artery disease. During the last decade, numerous agents have been used to prevent restenosis. Despite positive results in animal models, no pharmacological therapy has been found to significantly decrease the risk of restenosis in humans. These discrepancies between animal models and clinical situation were probably related to an incomplete understanding of the mechanism of restenosis. Neointimal thickening occurs in response to experimental arterial injury with a balloon catheter. Neointimal formation involves different steps: smooth muscle cell activation, proliferation and migration, and the production of extracellular matrix. The factors that control neointimal hyperplasia include growth factors, humoral factors and mechanical factors. Arterial remodeling also plays a major role in the restenosis process. Studies performed in animal and human subjects have established the potentials for "constrictive remodeling" to reduce the post-angioplasty vessel area, thereby indirectly narrowing the vessel lumen and thus contributing to restenosis. The reduction of restenosis rate in patients with intracoronary stent implantation has been attributed to the preventive effect of stent itself for this negative remodeling. In addition to these mechanisms for restenosis, intraluminal or intra-plaque thrombus formation, reendothelialization and apoptosis theories have been introduced and confirmed at least in part.