Inflammatory Response to Percutaneous Coronary Intervention

Atherosclerosis is now considered an inflammatory disease. Inflammation has been demonstrated to contribute to its initiation as well as its progression. Coronary artery disease is a leading cause of death worldwide. The treatment of coronary artery disease has been transformed by the introduction of percutaneous coronary intervention, which remains the focus of intensive research and development. Percutaneous coronary intervention produces a significant inflammatory reaction in the injured vessel wall, that may lead to the development of neointimal thickening and restenosis. Balloon coronary angioplasty or stent deployment is associated with significant platelet activation, which promotes leukocyte recruitment to the injured vessel wall and it has also been shown to induce an inflammatory response. Inflammation plays a major role in determining stent restenosis via neointimal proliferation. Several acute-phase reactants, cytokines, and soluble cellular adhesion molecules have been implicated in this inflammatory process. Moreover, increased inflammatory protein levels in peripheral blood have been found in atherosclerotic diseases, such as unstable angina pectoris, acute myocardial infarction and angiographically documented coronary heart disease. Thus, high levels of acute phase reactants correlate with a worse prognosis. Conclusion: Percutaneous coronary intervention induces a significant inflammatory reaction in the injured vessel wall that leads to the development of neointimal thickening and restenosis. Post procedural inflammatory response in patients undergoing coronary intervention reveal a wide range of mechanisms, including mechanical disruption of atherosclerotic plaque, arterial wall injury, myocardial necrosis due to distal embolization and endothelial dysfunction, and release of inflammatory factors followed by leukocytes and platelet activation along with the ischaemiareperfusion injury. The inflammatory reaction plays an equally important role as arterial injury in neointimal formation after coronary stenting, and that anti-inflammatory approaches may be of value to reduce in-stent restenosis.