Title: Inflammation as a pathogenetic factor in unstable coronary artery disease
- Michał R. Żebrowski
- Review articles
- Polish Journal of Cardiology
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- Final page:
- unstable atherosclerotic plaque, rupture, cytokines, inflammation, endothelium
Atherosclerotic vascular disease is the most common cause of mortality in developed countries, and the importance of acute vascular syndromes is increasing. Acute myocardial ischemia generally results from acute occlusion of the atherosclerotic coronary artery by a thrombus. This occlusion may be transient and episodic, resulting in the syndrome of unstable angina or firm and permanent, resulting in cellular death. The platelet-rich thrombus formation occurs at the site of atherosclerotic plaque rupture or hemorrhage into the plaque with subsequent break in endothelial integrity. Histological studies have established specific structural features of unstable plaque. Plaque disruptions may vary greatly in extent from tiny fissures or erosions of the plaque surface to deep intimal tears, which extend into the soft lipid core of lesions. In all these instances at least some degree of thrombus formation occurs. Current evidence suggests that inflammation is involved in plaque rupture and the biology of thrombosis.This relationship between inflammation with atherosclerosis and myocardial ischemia is now an area of many investigations. The precise steps leading to atherosclerosis still remain enigmatic. Recruitment of circulating monocytes is an early event in atherosclerosis, and enhanced macrophage infiltration in the atherosclerotic plaque is correlated with acute clinical syndromes. Macrophages can be involved in the induction of plaque rupture through digestion of fibrous caps, and they express tissue factor that is thought to promote local thrombogenicity. Macrophages/foam cells and endothelium act as a source of growth factors and chemoattractants for smooth muscle cells. In this report the current understanding of inflammation in unstable coronary disease is reviewed.