Atherosclerotic Plaque Rupture: an Overview

[1]  P. Libby,et al.  Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. , 1994, The Journal of clinical investigation.

[2]  B Hillen,et al.  Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. , 1998, Journal of the American College of Cardiology.

[3]  M J Davies,et al.  Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. , 1984, The New England journal of medicine.

[4]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (1). , 1992, The New England journal of medicine.

[5]  P. Libby,et al.  Evidence for apoptosis in advanced human atheroma. Colocalization with interleukin-1 beta-converting enzyme. , 1995, The American journal of pathology.

[6]  P. Libby,et al.  The smooth muscle cell: sinner or saint in restenosis and the acute coronary syndromes? , 1998, Journal of the American College of Cardiology.

[7]  J. Reekers,et al.  Remodeling of De Novo atherosclerotic lesions in femoral arteries: impact on mechanism of balloon angioplasty. , 1995, Journal of the American College of Cardiology.

[8]  C. Wong.  Atherosclerotic arterial remodeling in the superficial femoral artery: individual variation in local compensatory enlargement response. , 1997, Circulation.

[9]  V. Fuster,et al.  Macrophage Infiltration in Acute Coronary Syndromes: Implications for Plaque Rupture , 1994, Circulation.

[10]  E. Bramucci,et al.  Tissue-factor antigen and activity in human coronary atherosclerotic plaques , 1997, The Lancet.

[11]  J. Hermiller,et al.  In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. , 1993, The American journal of cardiology.

[12]  V. Fuster,et al.  Atherosclerosis: imaging techniques and the evolving role of nuclear medicine. , 1997, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[13]  P. Ridker.  Inflammation, infection, and cardiovascular risk: how good is the clinical evidence? , 1998, Circulation.

[14]  V. Fuster,et al.  Tissue factor modulates the thrombogenicity of human atherosclerotic plaques. , 1997, Circulation.

[15]  P. Libby,et al.  Regulation of matrix metalloproteinase expression in human vascular smooth muscle cells by T lymphocytes: a role for CD40 signaling in plaque rupture? , 1997, Circulation research.

[16]  W. Roberts,et al.  Morphometric analysis of the composition of coronary arterial plaques in isolated unstable angina pectoris with pain at rest. , 1990, The American journal of cardiology.

[17]  Kathleen M. Smith,et al.  Localization of tissue factor in the normal vessel wall and in the atherosclerotic plaque. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[18]  V. Fuster,et al.  Coronary plaque disruption. , 1995, Circulation.

[19]  B Hillen,et al.  Paradoxical arterial wall shrinkage may contribute to luminal narrowing of human atherosclerotic femoral arteries. , 1995, Circulation.

[20]  J. Melrose,et al.  Increased synthesis of matrix metalloproteinases by aortic smooth muscle cells is implicated in the etiopathogenesis of abdominal aortic aneurysms. , 1996, Journal of vascular surgery.

[21]  P. Constantinides.  Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. , 1995, Circulation.

[22]  P. Libby.  Molecular bases of the acute coronary syndromes. , 1995, Circulation.

[23]  W. Santamore,et al.  Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? , 1988, Circulation.

[24]  J. Isner,et al.  Focal compensatory enlargement of human arteries in response to progressive atherosclerosis. In vivo documentation using intravascular ultrasound. , 1994, Circulation.

[25]  J. Guyton,et al.  The lipid-rich core region of human atherosclerotic fibrous plaques. Prevalence of small lipid droplets and vesicles by electron microscopy. , 1989, The American journal of pathology.

[26]  M. Marcus,et al.  Structural and Hemodynamic Responses of Peripheral Arteries of Macaque Monkeys to Atherogenic Diet , 1985, Arteriosclerosis.

[27]  W. Roberts,et al.  Hemodynamic shear force in rupture of coronary arterial atherosclerotic plaques. , 1990, The American journal of cardiology.

[28]  G. V. R. Born,et al.  INFLUENCE OF PLAQUE CONFIGURATION AND STRESS DISTRIBUTION ON FISSURING OF CORONARY ATHEROSCLEROTIC PLAQUES , 1989, The Lancet.

[29]  M. Davies.  Reactive oxygen species, metalloproteinases, and plaque stability. , 1998, Circulation.

[30]  E. Falk,et al.  Coronary thrombosis: pathogenesis and clinical manifestations. , 1991, The American journal of cardiology.

[31]  M. Davies,et al.  Vulnerable plaque. Relation of characteristics to degree of stenosis in human coronary arteries. , 1996, Circulation.

[32]  T. Wight,et al.  Cell biology of arterial proteoglycans. , 1989, Arteriosclerosis.

[33]  F J Schoen,et al.  Circumferential stress and matrix metalloproteinase 1 in human coronary atherosclerosis. Implications for plaque rupture. , 1996, Arteriosclerosis, thrombosis, and vascular biology.

[34]  M. S. Hamid,et al.  Effects of cyclic flexion of coronary arteries on progression of atherosclerosis. , 1994, The American journal of cardiology.

[35]  J. Powell,et al.  Inflammation and matrix metalloproteinases in the enlarging abdominal aortic aneurysm. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[36]  A. Angelini,et al.  Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. , 1989, European heart journal.

[37]  V. Fuster,et al.  Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.

[38]  G. Bearman,et al.  Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis , 1996, The Lancet.

[39]  J. Coucher,et al.  Expression of intercellular adhesion molecule-1 in atherosclerotic plaques. , 1992, The American journal of pathology.

[40]  P. Libby,et al.  The mechanisms by which infectious agents may contribute to atherosclerosis and its clinical manifestations. , 1998, Trends in cardiovascular medicine.

[41]  M. Davies,et al.  Atherosclerotic plaque caps are locally weakened when macrophages density is increased. , 1991, Atherosclerosis.

[42]  J. Guyton,et al.  Development of the atherosclerotic core region. Chemical and ultrastructural analysis of microdissected atherosclerotic lesions from human aorta. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[43]  P. Libby,et al.  Macrophage foam cells from experimental atheroma constitutively produce matrix-degrading proteinases. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[44]  C. Kim,et al.  Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: an in vivo intravascular ultrasound study. , 1996, Journal of the American College of Cardiology.

[45]  T. Els,et al.  Compensatory carotid artery dilatation in early atherosclerosis. , 1994, Circulation.

[46]  D. Small,et al.  George Lyman Duff memorial lecture. Progression and regression of atherosclerotic lesions. Insights from lipid physical biochemistry. , 1988, Arteriosclerosis.

[47]  R D Kamm,et al.  Mechanical properties of model atherosclerotic lesion lipid pools. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[48]  G Pasterkamp,et al.  Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[49]  V. Fuster,et al.  Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. , 1994, Journal of the American College of Cardiology.

[50]  Samin K. Sharma,et al.  Macrophages, smooth muscle cells, and tissue factor in unstable angina. Implications for cell-mediated thrombogenicity in acute coronary syndromes. , 1996, Circulation.

[51]  A. Becker,et al.  Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. , 1994, Circulation.

[52]  A. Maseri,et al.  Vasoreactivity of the Culprit Lesion in Unstable Angina , 1994, Circulation.

[53]  M. Kendall,et al.  The oxidation hypothesis of atherosclerosis , 1994, The Lancet.

[54]  T. B. Clarkson,et al.  A study of atherosclerosis regression in Macaca mulatta: III. Chemical changes in arteries from animals with atherosclerosis induced for 19 months and regressed for 48 months at plasma cholesterol concentrations of 300 or 200 mg/dl. , 1980, The American journal of pathology.

[55]  M. Davies,et al.  Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. , 1993, British heart journal.

[56]  A. Camm,et al.  Elevated Chlamydia pneumoniae antibodies, cardiovascular events, and azithromycin in male survivors of myocardial infarction. , 1998, Circulation.

[57]  R D Kamm,et al.  Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. , 1992, Circulation research.

[58]  Z. Galis,et al.  N-acetyl-cysteine decreases the matrix-degrading capacity of macrophage-derived foam cells: new target for antioxidant therapy? , 1998, Circulation.

[59]  C. Zarins,et al.  Compensatory enlargement of human atherosclerotic coronary arteries. , 1987, The New England journal of medicine.

[60]  E. Gurfinkel,et al.  Randomised trial of roxithromycin in non-Q-wave coronary syndromes: ROXIS pilot study , 1997, The Lancet.

[61]  J. Ferguson.  Meeting highlights: 47th Annual Scientific Sessions of the American College of Cardiology. , 1998, Circulation.

[62]  W. Roberts,et al.  Morphometric analysis of the composition of atherosclerotic plaques in the four major epicardial coronary arteries in acute myocardial infarction and in sudden coronary death. , 1989, Circulation.

[63]  R. Detrano,et al.  The dynamics of progression of coronary atherosclerosis studied in 168 medically treated patients who underwent coronary arteriography three times. , 1989, American heart journal.

[64]  P. Kovanen,et al.  Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture. , 1994, Circulation.

[65]  J. Skepper,et al.  Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma. , 1995, Atherosclerosis.

[66]  J. Zamorano,et al.  Coronary artery remodeling in atherosclerotic disease: An intravascular ultrasonic study in vivo , 1993, Coronary artery disease.

[67]  R. Kerber,et al.  Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis. , 1991, Journal of the American College of Cardiology.

[68]  M. Davies,et al.  Morphological characteristics of clinically significant coronary artery stenosis in stable angina. , 1986, British heart journal.

[69]  R. Virmani,et al.  Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. , 1996, Circulation.

[70]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.

[71]  B Hillen,et al.  The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely within the arterial system. A postmortem study. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[72]  E. Falk.  Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. , 1983, British heart journal.

[73]  R. Kamm,et al.  Distribution of Circumferential Stress in Ruptured and Stable Atherosclerotic Lesions A Structural Analysis With Histopathological Correlation , 1993, Circulation.

[74]  M L Woods,et al.  Increased incidence of Chlamydia species within the coronary arteries of patients with symptomatic atherosclerotic versus other forms of cardiovascular disease. , 1996, Journal of the American College of Cardiology.