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.

Atherosclerosis, the underlying cause for most cardiovascular disease is a process that starts early in life and progresses slowly and silently for decades, usually becoming manifest in the form of angina, myocardial infarction, stroke, or sudden death. Although several established risk factors are involved in this process, inflammation is now considered to play an important role. Treatment of cardio vascular disease aims to minimize symptoms and improve the prognosis, which could be achieved by lifestyle changes, medical treatment, and myocardial revascularization which includes percutaneous coronary intervention. The subspecialty of interventional cardiology has made significant progress in the management of coronary artery disease over the past three decades with the development of percutaneous coronary intervention.

Cardiovascular disease is the leading cause of death in the all world. One of its most important forms is coronary heart disease due to atherosclerosis. There is increasing evidence that inflammatory system has a role in the pathogenesis of cardiovascular disease and its complications. Inflammatory mechanisms also appear to determine clinical presentation and disease outcome. Plasma levels of several markers of inflammation has been associated with coronary artery disease and various studies have shown increased levels during chronic stable angina, acute myocardial infarction, and percutaneous coronary intervention and have been found to be associated with future cardiovascular risk in a variety of clinical settings.

Each year, millions of patients with coronary heart disease worldwide are treated by means of percutaneous coronary intervention which induces a significant inflammatory reaction in the injured vessel wall that leads to the development of neointimal thickening and restenosis. The systemic inflammatory response after technique that can be measured in the plasma by the inflammatory markers and can be detected by the concentration of  these markers after the procedure and its related to a greater risk of adverse clinical outcomes. There was a strong correlation between the extent of inflammatory reaction and the amount of neointimal formation within the stents and both inflammatory changes and the arterial injury can cause a neointimal reaction independently, even in the absence of the other.

The inflammatory response to percutaneous coronary intervention is largely driven by direct mechanical trauma induced by balloon inflation and/or stent deployment. The role of inflammation in the development of restenosis after percutaneous coronary interventions has been investigated in several studies. There is an interaction of inflammatory activation and vascular wall response to injury leading to intimal hyperplasia. In the clinical setting there are several methods for the recognition of the inflammatory activation and the treatment of inflammation before, after percutaneous coronary interventions.