Inflammation And Percutaneous Coronary Intervention

The treatment of stable yet symptomatic coronary atherosclerosis and unstable coronary atherothrom-bosis has progressed from balloon angioplasty to the modern era of DES and will continue to evolve. Adjunctive medical therapy in the form of statins, glycoprotein inhibitors, and thienopyridines and antithrombin agents has also been a mainstay of treatment aimed at controlling risk factors and progression of disease, both at the time of intervention and afterward. The ultimate success or failure of PCI and management of coronary atherosclerosis varies among individuals. Beyond technical considerations, revascularization has been and will continue to be limited in efficacy by one major variable—inflammation. The focus of treatment must address inflammation to improve outcomes in PCI.

Many of the challenges faced by interventional cardiologists are rooted in problems related to inflammation, a process mediating the response to injury after insult to the endothelial integrity imparted by PCI. The resultant neointima formation has been noted to be a significant problem and occurs as a result of cell death and inflammation. Although DES have been able to temper this process, they are neither a definitive nor a perfect solution.39,40 Inflammation is a more prominent force, not only in the initiation and propagation of disease, such as in ACS, but also in response to injury after PCI.

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