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Renu Virmani - One of the best experts on this subject based on the ideXlab platform.
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imaging Atherosclerotic Plaque inflammation by fluorodeoxyglucose with positron emission tomography ready for prime time
Journal of the American College of Cardiology, 2010Co-Authors: James H.f. Rudd, Valentin Fuster, Renu Virmani, Jagat Narula, William H Strauss, Josef Machac, Mike Klimas, Nobuhiro Tahara, Elizabeth A Warburton, Zahi A. FayadAbstract:Inflammation is a determinant of Atherosclerotic Plaque rupture, the event leading to most myocardial infarctions and strokes. Although conventional imaging techniques identify the site and severity of luminal stenosis, the inflammatory status of the Plaque is not addressed. Positron emission tomography imaging of atherosclerosis using the metabolic marker fluorodeoxyglucose allows quantification of arterial inflammation across multiple vessels. This review sets out the background and current and potential future applications of this emerging biomarker of cardiovascular risk, along with its limitations.
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:Abstract Purpose: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. Methods: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. Results: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients ( p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques ( p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). Conclusions: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque. (J Vasc Surg 1996;23:755-66.)
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:PURPOSE: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). CONCLUSIONS: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque.
Sandra C Carr - One of the best experts on this subject based on the ideXlab platform.
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:Abstract Purpose: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. Methods: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. Results: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients ( p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques ( p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). Conclusions: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque. (J Vasc Surg 1996;23:755-66.)
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:PURPOSE: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). CONCLUSIONS: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque.
Andrew Farb - One of the best experts on this subject based on the ideXlab platform.
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:Abstract Purpose: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. Methods: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. Results: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients ( p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques ( p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). Conclusions: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque. (J Vasc Surg 1996;23:755-66.)
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:PURPOSE: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). CONCLUSIONS: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque.
William H Pearce - One of the best experts on this subject based on the ideXlab platform.
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:Abstract Purpose: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. Methods: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. Results: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients ( p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques ( p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). Conclusions: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque. (J Vasc Surg 1996;23:755-66.)
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Atherosclerotic Plaque rupture in symptomatic carotid artery stenosis
Journal of Vascular Surgery, 1996Co-Authors: Sandra C Carr, Andrew Farb, William H Pearce, Renu VirmaniAbstract:PURPOSE: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid Plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid Plaques and to determine which characteristics are more commonly associated with Plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS: Patients with symptomatic carotid artery disease were found to have more frequent Plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic Plaques and in only 32% of Plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic Plaques and in 48% of asymptomatic Plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic Plaques (84% vs 44% of asymptomatic Plaques; p = 0.006). In addition, intraPlaque fibrin was more common in symptomatic Plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to Plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and Plaque type (fibrous, necrotic, or calcified). CONCLUSIONS: As in the coronary artery system, rupture of the Atherosclerotic Plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the Atherosclerotic Plaque.
Valentin Fuster - One of the best experts on this subject based on the ideXlab platform.
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Effects of Colchicine on Atherosclerotic Plaque Stabilization: a Multimodality Imaging Study in an Animal Model
Journal of Cardiovascular Translational Research, 2020Co-Authors: Alberto Cecconi, Jean Paul Vilchez-tschischke, Jesus Mateo, Javier Sanchez-gonzalez, Samuel España, Rodrigo Fernandez-jimenez, Beatriz Lopez-melgar, Leticia Fernández Friera, Gonzalo J López-martín, Valentin FusterAbstract:Colchicine demonstrated clinical benefits in the treatment of stable coronary artery disease. Our aim was to evaluate the effects of colchicine on Atherosclerotic Plaque stabilization. Atherosclerosis was induced in the abdominal aorta of 20 rabbits with high-cholesterol diet and balloon endothelial denudation. Rabbits were randomized to receive either colchicine or placebo. All animals underwent MRI, ^18F-FDG PET/CT, optical coherence tomography (OCT), and histology. Similar progression of Atherosclerotic burden was observed in the two groups as relative increase of normalized wall index (NWI). Maximum ^18F-FDG standardized uptake value (meanSUVmax) decreased after colchicine treatment, while it increased in the placebo group with a trend toward significance. Animals with higher levels of cholesterol showed significant differences in favor to colchicine group, both as NWI at the end of the protocol and as relative increase in meanSUVmax. Colchicine may stabilize Atherosclerotic Plaque by reducing inflammatory activity and Plaque burden, without altering macrophage infiltration or Plaque typology.
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imaging Atherosclerotic Plaque inflammation by fluorodeoxyglucose with positron emission tomography ready for prime time
Journal of the American College of Cardiology, 2010Co-Authors: James H.f. Rudd, Valentin Fuster, Renu Virmani, Jagat Narula, William H Strauss, Josef Machac, Mike Klimas, Nobuhiro Tahara, Elizabeth A Warburton, Zahi A. FayadAbstract:Inflammation is a determinant of Atherosclerotic Plaque rupture, the event leading to most myocardial infarctions and strokes. Although conventional imaging techniques identify the site and severity of luminal stenosis, the inflammatory status of the Plaque is not addressed. Positron emission tomography imaging of atherosclerosis using the metabolic marker fluorodeoxyglucose allows quantification of arterial inflammation across multiple vessels. This review sets out the background and current and potential future applications of this emerging biomarker of cardiovascular risk, along with its limitations.
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multimodality imaging of Atherosclerotic Plaque activity and composition using fdg pet ct and mri in carotid and femoral arteries
Atherosclerosis, 2009Co-Authors: Stephane Silvera, Valentin Fuster, James H.f. Rudd, Hamza El Aidi, Venkatesh Mani, Lingde Yang, Michael E Farkouh, Zahi A. FayadAbstract:Purpose To evaluate the relationship between Atherosclerotic Plaque inflammation, as assessed by FDG-Positron Emission Tomography/Computed Tomography (FDG-PET/CT), and Plaque morphology and composition, as assessed by magnetic resonance imaging (MRI), in the carotid and femoral arteries.
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the diagnostic accuracy of ex vivo mri for human Atherosclerotic Plaque characterization
Arteriosclerosis Thrombosis and Vascular Biology, 1999Co-Authors: Meir Shinnar, Zahi A. Fayad, John T Fallon, Suzanne Wehrli, Michael G Levin, Dolcine Dalmacy, Juan J Badimon, Martin Harrington, Elizabeth O Harrington, Valentin FusterAbstract:Abstract —Recent evidence indicates that the type of Atherosclerotic Plaque, rather than the degree of obstruction to flow, is an important determinant of the risk of cardiovascular complications. In previous work, the feasibility of using MRI for the characterization of Plaque components was shown. This study extends the previous work to all the Plaque components and shows the accuracy of this method. Twenty-two human carotid endarterectomy specimens underwent ex vivo MRI and histopathological examination. Sixty-six cross sections were matched between MRI and histopathology. In each cross section, the presence or absence of Plaque components were prospectively identified on the MRI images. The overall sensitivity and specificity for each tissue component were very high. Calcification and fibrocellular tissue were readily identified. Lipid core was also identifiable. However, thrombus was the Plaque component for which MRI had the lowest sensitivity. A semiautomated algorithm was created to identify all major Atherosclerotic Plaque components. MRI can characterize carotid artery Plaques with a high level of sensitivity and specificity. Application of these results in the clinical setting may be feasible in the near future.
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Pathophysiology and clinical significance of Atherosclerotic Plaque rupture
Cardiovascular Research, 1999Co-Authors: David E. Gutstein, Valentin FusterAbstract:Atherosclerotic Plaque rupture and resulting intracoronary thrombosis are thought to account for most acute coronary syndromes. These syndromes include unstable angina, non-Q-wave myocardial infarction (MI) and Q-wave MI. In addition, many cases of sudden cardiac death may be attributable to Atherosclerotic Plaque disruption and its immediate complications. Our understanding of the Atherosclerotic process and the pathophysiology of Plaque disruption has advanced remarkably. Despite these advances, event rates after acute coronary syndromes remain unacceptably high. This review will focus on the pathophysiology underlying Atherosclerotic Plaque development, the sequellae of coronary Plaque rupture, and current therapies designed to treat the acute coronary syndromes. It is hoped that as our understanding of the Atherosclerotic Plaque improves, treatment strategies for the acute coronary syndromes will advance.
