title: Acute coronary syndromes as auto-inflammatory disorders.
abstract: From the onset to the healing stage of acute coronary syndromes, an endless inflammation has been presented with complex, multiple cross-talk mechanisms at the molecular, cellular, and organ levels. Even though the early reperfusion treatment either by thrombolysis or percutaneous coronary intervention provides the excellent clinical benefits in patients with acute coronary syndromes, ischemia/ reperfusion injury may somewhat offset those great advantages. Inflammation, although potentially protective, has been deeply associated with those detrimental conditions. The hexagonal vascular inflammatory network which is composed of activated various leukocytes, vascular endothelial cells, vascular smooth muscle cells, platelets, excess reactive oxygen species, and cholesterol may contribute these vicious circles. To address these complex syndromes with more benefits regarding the prevention and treatment, this review comprehensively updates the pathogenesis of acute coronary syndromes from the view points of vascular inflammation.
authors.affiliation: Section of Cardiology, Department of Community Emergency Medicine, Ehime University Graduate School of Medicine, Toon, Japan. suzuki-m@m.ehime-u.or.jp
authors.forename: Makoto
authors.initials: M
authors.lastname: Suzuki
mesh_terms: D054058:Acute Coronary Syndrome / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy; D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy; D007962:Leukocytes / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D002784:Cholesterol