ATIS

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• 作者：Makiko Ueda (1)
  
• 刊名：Drugs
• 出版年：2010
• 出版时间：January 2010
• 年：2010
• 卷：70
• 期：1-supp
• 页码：3-8
• 全文大小：548KB
• 参考文献：1. Ogami M, Ikura Y, Ohsawa M, et al. Telomere shortening in human coronary artery diseases Arterioscler Thromb Vasc Biol 2004; 24: 546-0 CrossRef
  2. Naruko T, Ueda M, Haze K, et al. Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation 2002; 106: 2894-00 CrossRef
  3. Yunoki K, Naruko T, Komatsu R, et al. Enhanced expression of haemoglobin scavenger receptor in accumulated macrophages of culprit lesions in acute coron syndromes. Eur Heart J 2009; 30: 1844-2 CrossRef
  4. Komatsu R, Ueda M, Naruko T, et al. Neointimal tissue response at sites of coronary stenting in humans: macroscopic, histological, and immnunohistochemical analyses. Circulation 1998; 98: 224-3. CrossRef
  5. Naruko T, Itoh A, Haze K, et al. C-Type natriuretic peptide and natriuretic peptide receptors are expressed by smooth muscle cells in the neointima after percutaneous coronary intervention. Atherosclerosis. 2005; 181: 241-0 CrossRef
  6. Shirai N, Naruko T, Ohsawa M, et al. Expression of endothelin- converting enzyme, endothelin-1 and endothelin receptors at the site of percutaneous coronary intervention in humans. J Hypertens. 2006; 24: 711-1 CrossRef
  7. Naruko T, Ueda M, Ehara S, et al. Persistent high levels of plasma oxidized low-density lipoprotein after acute myocardial infarction predict stent restenosis. Arterioscler Thromb Vasc Biol. 2006; 26: 877-3 CrossRef
  
• 作者单位：Makiko Ueda (1)
  
  1. Department of Pathology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi Abeno-ku, Osaka, 545-8585, Japan
  

文摘

Once atherosclerosis develops, stenosis (or occlusion) may occur in the lumen of various arteries of the living body. This can lead to a range of conditions, including myocardial infarction, cerebral infarction, aortic aneurysm and peripheral artery disease. The acronym ‘ATIS-(AtheroThrombosIS) is a collective term for diseases characterized by a common course of development based on atherosclerosis. This article reviews pathological findings in atherothrombotic lesions of human coronary, carotid, and vertebrobasilar arteries as well as leg arteries and veins. Histologically, atheromatous plaques of coronary arteries can broadly be typed as fibrous and lipid-rich (atheromatous). Macroscopically, fibrous plaque has a whitish appearance and is composed of smooth muscle cells and collagen fibres. Lipid-rich (atheromatous) plaque, on the other hand, appears yellow macroscopically, with the superficial layer (closer to the lumen) having a white fibrous cap which covers the atheroma. This fibrous cap is quite thin and is likely to rupture. Typical pathological features of such atherothrombosis are narrowing of the vascular lumen due to lipid-rich (atheromatous) plaque, and thrombus formation due to a broken fibrous cap. Such plaque rupture is the underlying cause of acute myocardial infarction in about 70% of patients, while acute myocardial infarction in the remaining patients (30%) results from plaque erosion. In cases of plaque erosion, atheroma is seldom seen, and atherosclerosis manifests in a full-circumferential manner, resulting in thrombus formation due to endothelial cell injury and eventually leading to obstructive thrombi. Thus, thrombus formation associated with myocardial infarction is attributable to plaque rupture if the lesion contains a lipid-rich (atheromatous) plaque. In cases where plaques cause particularly intense injury of endothelial cells, plaque erosion is likely to occur, resulting in formation of obstructive thrombi within the vascular lumen. Primary factors involved in the evolution of ATIS are injury of vascular endothelial cells, inflammation of a vulnerable plaque and intra-plaque haemorrhage. ATIS in other vascular systems has similar pathological features. The continued increase in the aged population and the morbidity of lifestyle-related diseases will make more cases of ATIS intractable. It will be of paramount importance to prevent intractable ATIS in the future.