Angiogenic Processes in the Pathogenesis of Human Coronary Atherosclerosis

Sueishi, Katsuo; Kumamoto, Masaya; Sakuda, Hitoshi; Tanaka, Kenichiro

doi:10.1007/978-3-642-76849-1_2

Cited by 14 publications

(8 citation statements)

References 18 publications

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“…One of the important causes of the onset of acute coronary syndrome, based on the pathology images of autopsy cases 13,14 or coronary angiograms, [15][16][17] is thrombogenesis accompanied by atheroma rupture. We have previously observed by light microscopy the coronary arterial thrombi that were extracted using thrombectomy, and we investigated pathologically the components of those coronary artery thrombi.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of the Pathological Images of Coronary Artery Thrombi According to the Infarct-Related Coronary Artery in Acute Myocardial Infarction

Nagata

Usuda

Uchiyama

et al. 2004

Circ J

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ercutaneous coronary intervention (PCI) is an effective treatment in the early phase of acute myocardial infarction (AMI), 1-3 but the unstable plaque and coronary arterial thrombi that are involved in the onset of AMI sometimes induce the no-reflow phenomenon after PCI whereby there is insufficient reperfusion. 4 There is reportedly a high incidence of the no-reflow phenomenon or slow flow in AMI in which the right coronary artery (RCA) is the culprit lesion. [4][5][6] The greater susceptibility of the RCA to developing large thrombi makes successful reperfusion more difficult to achieve. It is possible that the state of the thrombi affects the onset of complications related to PCI, but there have not been any reports investigating the differences in the images of pathological thrombi according to the infarct-related coronary artery.It is now possible to aspirate coronary arterial thrombi using coronary arterial thrombectomy, 7-9 and to evaluate the pathological images in vivo. 10,11 So we investigated the characteristics of the pathological images of coronary arterial thrombi according to the infarct-related coronary artery. Methods SubjectsSubjects were 231 patients with AMI who had sought treatment at Toyama Prefectural Central Hospital during a 30-months period from September 2000 to February 2003 and who had undergone emergency coronary angiography. AMI was diagnosed when chest pain persisted for at least 30 min and the 12-lead ECG confirmed ST elevation of at least 2 mm in at least 2 leads in succession, and there was confirmation by initial coronary angiography of occlusion or sub-occlusion of the infarct-related artery. Of the 199 patients indicated for PCI, 129 underwent thrombectomy. Patients who were scheduled for coronary bypass surgery (multivessel disease and left main trunk lesion), patients who could not undergo coronary arterial thrombectomy because of serious complications (fatal arrhythmia, cardiogenic shock, and pulmonary edema), and patients who had undergone thrombolytic therapy before emergency coronary angiography were excluded from the study. Of the 129 patients who underwent coronary arterial thrombectomy, there were 77 cases in which the coronary artery thrombi could be extracted for study within 24 h of the onset of AMI. Cardiac Catheterization and Coronary InterventionWritten informed consent was obtained from all patients, after the patients and their families were informed of the Background Unstable plaque and coronary arterial thrombi sometimes induce a no-reflow phenomenon after intervention whereby there is sufficient reperfusion. The greater susceptibility of the right coronary artery to development of large thrombi makes successful reperfusion more difficult, therefore the characteristics of the pathological images of coronary arterial thrombi according to the infarct-related coronary artery were investigated. Methods and ResultsCoronary arterial thrombi were extracted from 77 patients with acute myocardial infarction (AMI) using a thrombectomy catheter. The 36 patients had a...

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Section: Discussionmentioning

confidence: 99%

Characteristics of the Pathological Images of Coronary Artery Thrombi According to the Infarct-Related Coronary Artery in Acute Myocardial Infarction

Nagata

Usuda

Uchiyama

et al. 2004

Circ J

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“…In atherosclerotic lesions, neovascularization is frequently observed 41,42 and possibly contributes to progression of atherosclerosis by providing nutrient influx and cell recruitment. 43,44 In this regard, the interaction of VEGF and ET-1 may increase neovascularization and promote the progression of atherosclerosis, constituting a vicious circle.…”

Section: Discussionmentioning

confidence: 99%

Stimulatory Interaction Between Vascular Endothelial Growth Factor and Endothelin-1 on Each Gene Expression

et al. 1998

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Abstract-The precise regulation of cell growth in the vascular wall maintains vascular integrity, and its disruption leads to cardiovascular disorders including atherosclerosis and restenosis. Vascular endothelial growth factor (VEGF) is a specific mitogen for endothelial cells, and endothelin-1 (ET-1) is known to stimulate the proliferation of smooth muscle cells. The aim of this study was to explore a potential interaction between VEGF and ET-1 on each expression in vascular cells. VEGF enhanced preproET-1 mRNA expression and ET-1 secretion in bovine aortic endothelial cells (BAECs

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“…Intimal microvessels were noticed as early as 1876 [78], and reports and hypotheses about neovascularization of atherosclerotic lesions have surfaced at regular intervals in the literature [8]. A flurry of recent papers that describe neovascularizations arising from vasa vasorum in atherosclerosis lesions and their association with different elements of these lesions [50,112,157,177] has renewed the debate on the potential role of angiogenesis in atherosclerosis. Growth of neovascularizations into ischemic zones of atherosclerotic lesions could possibly contribute to lesional growth because of the influx of nutrients [177] and recruitment of cells [112].…”

Section: Angiogenesis In Atherosclerotic Lesions and Transplant Assocmentioning

confidence: 99%

Angiogenesis: mechanistic insights, neovascular diseases, and therapeutic prospects

1995

J Mol Med

497

285

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This review of angiogenesis aims to describe (a) stimuli that either elicit or antagonize angiogenesis, (b) the response of the vasculature to angiogenic or anti-angiogenic stimuli, i.e., processes required for the formation of new vessels, (c) aspects of angiogenesis relating to tissue remodeling and disease, and (d) the potential of angiogenic or antiangiogenic therapeutic measures. Angiogenesis, the formation of new vessels from existing microvessels, is important in embryogenesis, wound healing, diabetic retinopathy, tumor growth, and other diseases. Hypoxia and other as yet ill-defined stimuli drive tumor, inflammatory, and connective tissue cells to generate angiogenic molecules such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), transforming growth factor-beta (TGF-beta), platelet-derived growth factor (PDGF), and others. Natural and synthetic angiogenesis inhibitors such as angiostatin and thalidomide can repress angiogenesis. Angiogenic and antiangiogenic molecules control the formation of new vessels via different mechanisms. VEGF and FGF elicit their effects mainly via direct action on relevant endothelial cells. TGF-beta and PDGF can attract inflammatory or connective tissue cells which in turn control angiogenesis. Additionally, PDGF may act differently on specific phenotypes of endothelial cells that are engaged in angiogenesis or that are of microvascular origin. Thus phenotypic traits of endothelial cells committed to angiogenesis may determine their cellular responses to given stimuli. Processes necessary for new vessel formation and regulated by angiogenic/antiangiogenic molecules include the migration and proliferation of endothelial cells from the microvasculature, the controlled expression of proteolytic enzymes, the breakdown and reassembly of extracellular matrix, and the morphogenic process of endothelial tube formation. In animal models some angiogenesis-dependent diseases can be controlled via induction or inhibition of new vessel formation. Life-threatening infantile hemangiomas are a first established indication for antiangiogenic therapy in humans. Treatment of other diseases by modulation of angiogenesis are currently tested in clinical trials. Thus the manipulation of new vessel formation in angiogenesis-dependent conditions such as wound healing, inflammatory diseases, ischemic heart and peripheral vascular disease, myocardial infarction, diabetic retinopathy, and cancer is likely to create new therapeutic options.

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Angiogenic Processes in the Pathogenesis of Human Coronary Atherosclerosis

Cited by 14 publications

References 18 publications

Characteristics of the Pathological Images of Coronary Artery Thrombi According to the Infarct-Related Coronary Artery in Acute Myocardial Infarction

Characteristics of the Pathological Images of Coronary Artery Thrombi According to the Infarct-Related Coronary Artery in Acute Myocardial Infarction

Stimulatory Interaction Between Vascular Endothelial Growth Factor and Endothelin-1 on Each Gene Expression

Angiogenesis: mechanistic insights, neovascular diseases, and therapeutic prospects

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