Atherosclerosis is currently thought to be an inflammatory condition. Inflammation has been shown to play a role in both the beginning and course of the disease. Coronary artery disease is the world's biggest cause of death. Percutaneous coronary intervention, which is still the subject of intense study and development, has revolutionised the treatment of coronary artery disease. Percutaneous coronary intervention causes a large inflammatory response in the wounded artery wall, which might lead to neointimal thickening and restenosis. Balloon coronary angioplasty or stent placement is linked to considerable platelet activation, which enhances leukocyte migration to the damaged artery wall and has also been linked to an inflammatory response. Through neointimal proliferation, inflammation plays a key role in defining stent restenosis. This inflammatory process has been linked to a number of acute-phase reactants, cytokines, and soluble cellular adhesion molecules. Furthermore, atherosclerotic disorders such as unstable angina pectoris, acute myocardial infarction, and angiographically confirmed coronary heart disease have been linked to higher inflammatory protein levels in the peripheral blood. As a result, large levels of acute phase reactants are linked to a poor prognosis.
Conclusion: Percutaneous coronary intervention causes a large inflammatory response in the wounded artery wall, which leads to 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. Anti-inflammatory treatments may be useful in reducing in-stent restenosis since the inflammatory response has an equal role in neointimal development following coronary stenting as arterial damage.Author(S) Details
Najah R. Hadi
Faculty of Medicine, University of Kufa, Iraq.
Bashaer M. Muhammad-Baqir
Faculty of Pharmacy, University of Kufa, Iraq.
Mustafa H. Ahmed
Al-Sader Teaching Hospital, The Specialist Centre for Nephrology and Kidney Transplantation, Iraq.
View Book:- https://stm.bookpi.org/IRPCI/article/view/4998
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