Abstract
Several evidences, ranging from in vitro experiments, pathologic analysis and epidemiologic studies, show that atherosclerosis is intrinsically an inflammatory disease. The plasma concentrations of interleukin-6 (IL-6) and its hepatic by-product, C-Reactive Protein (CRP), appear to reflect the intensity of occult plaque inflammation and by inference may determine the vulnerability of plaque rupture. The monocyte chemoattractant protein-1 (MCP-1) plays a crucial role in initiating coronary artery disease by recruiting monocytes/macrophages to the vessel wall. This leads to the formation of atherosclerotic lesions and also increases the vulnerability of the plaque. Indeed, circulating IL-6 and MCP-1 levels are elevated in patients with acute myocardial infarction, and also in patients with unstable angina, but not in those with stable angina. The plasma IL-6 and MCP-1 concentrations are also increased after percutaneous coronary intervention (PCI), and late restenosis is correlated with an increase in IL-6 or MCP-1 concentrations after the procedure. This finding suggests that the expression of IL-6 and MCP-1 may not only be related to the instability of atheromatous plaques, but also to the formation of restenotic lesions after PCI. The development of drugs specifically targeted against IL-6 and MCP-1 may be useful in the prevention of plaque formation, myocardial infarction and restenosis.
Keywords: myocardial infarction, angina pectoris, cytokine, crp, statin
Current Vascular Pharmacology
Title: Inflammation and Coronary Artery Disease
Volume: 1 Issue: 1
Author(s): Uichi Ikeda
Affiliation:
Keywords: myocardial infarction, angina pectoris, cytokine, crp, statin
Abstract: Several evidences, ranging from in vitro experiments, pathologic analysis and epidemiologic studies, show that atherosclerosis is intrinsically an inflammatory disease. The plasma concentrations of interleukin-6 (IL-6) and its hepatic by-product, C-Reactive Protein (CRP), appear to reflect the intensity of occult plaque inflammation and by inference may determine the vulnerability of plaque rupture. The monocyte chemoattractant protein-1 (MCP-1) plays a crucial role in initiating coronary artery disease by recruiting monocytes/macrophages to the vessel wall. This leads to the formation of atherosclerotic lesions and also increases the vulnerability of the plaque. Indeed, circulating IL-6 and MCP-1 levels are elevated in patients with acute myocardial infarction, and also in patients with unstable angina, but not in those with stable angina. The plasma IL-6 and MCP-1 concentrations are also increased after percutaneous coronary intervention (PCI), and late restenosis is correlated with an increase in IL-6 or MCP-1 concentrations after the procedure. This finding suggests that the expression of IL-6 and MCP-1 may not only be related to the instability of atheromatous plaques, but also to the formation of restenotic lesions after PCI. The development of drugs specifically targeted against IL-6 and MCP-1 may be useful in the prevention of plaque formation, myocardial infarction and restenosis.
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Cite this article as:
Ikeda Uichi, Inflammation and Coronary Artery Disease, Current Vascular Pharmacology 2003; 1 (1) . https://dx.doi.org/10.2174/1570161033386727
DOI https://dx.doi.org/10.2174/1570161033386727 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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Cardiovascular disease still remains the leading cause of death in Chronic and End Stage Kidney Disease, accounting for more than half of all deaths in dialysis patients. During the past decade, research has been focused on novel therapeutic agents that might delay or even reverse cardiovascular disease and vascular calcification, ...read more
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