In vivo 18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients.

[1]  Zahi A Fayad,et al.  Imaging atherosclerotic plaque inflammation , 2008, Nature Clinical Practice Cardiovascular Medicine.

[2]  Martin J Graves,et al.  Identification of Culprit Lesions After Transient Ischemic Attack by Combined 18F Fluorodeoxyglucose Positron-Emission Tomography and High-Resolution Magnetic Resonance Imaging , 2005, Stroke.

[3]  J. Egido,et al.  Intensive Treatment With Atorvastatin Reduces Inflammation in Mononuclear Cells and Human Atherosclerotic Lesions in One Month , 2005, Stroke.

[4]  Ahmed Tawakol,et al.  Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography , 2005, Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology.

[5]  C. Ruiz,et al.  High-sensitivity C-reactive protein in high-grade carotid stenosis: risk marker for unstable carotid plaque. , 2003, Journal of vascular surgery.

[6]  E. Topol,et al.  Prognostic value of myeloperoxidase in patients with chest pain. , 2003, The New England journal of medicine.

[7]  C. Heeschen,et al.  Myeloperoxidase Serum Levels Predict Risk in Patients With Acute Coronary Syndromes , 2003, Circulation.

[8]  Ose,et al.  Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events* , 2002 .

[9]  W S Kerwin,et al.  In Vivo Accuracy of Multispectral Magnetic Resonance Imaging for Identifying Lipid-Rich Necrotic Cores and Intraplaque Hemorrhage in Advanced Human Carotid Plaques , 2001, Circulation.

[10]  R. Wahl,et al.  Detection of atherosclerosis using a novel positron-sensitive probe and 18-fluorodeoxyglucose (FDG) , 2001, Nuclear medicine communications.

[11]  P. Shah,et al.  Pravastatin Treatment Increases Collagen Content and Decreases Lipid Content, Inflammation, Metalloproteinases, and Cell Death in Human Carotid Plaques: Implications for Plaque Stabilization , 2001, Circulation.

[12]  N. Alpert,et al.  Evidence of reduced resting blood flow in viable myocardial regions with chronic asynergy. , 2000, Journal of the American College of Cardiology.

[13]  P. Libby.  Coronary artery injury and the biology of atherosclerosis: inflammation, thrombosis, and stabilization. , 2000, The American journal of cardiology.

[14]  M. Béhé,et al.  Fever of unknown origin: prospective comparison of [18F]FDG imaging with a double-head coincidence camera and gallium-67 citrate SPET , 2000, European Journal of Nuclear Medicine.

[15]  J. Bogaert,et al.  Positron emission tomography scan in the diagnosis and follow-up of aortitis of the thoracic aorta. , 2000, Acta cardiologica.

[16]  R. Ross.  Atherosclerosis is an inflammatory disease , 1999 .

[17]  J. Nuyts,et al.  New arguments for a vasculitic nature of polymyalgia rheumatica using positron emission tomography. , 1999, Rheumatology.

[18]  P. Goodman,et al.  FDG-PET finding in early-phase Takayasu arteritis. , 1999, Journal of computer assisted tomography.

[19]  D. Sackett,et al.  Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. , 1998, The New England journal of medicine.

[20]  A. Gallino,et al.  Spiral computed tomography: a novel diagnostic approach for investigation of the extracranial cerebral arteries and its complementary role in duplex ultrasonography. , 1998, Circulation.

[21]  H. Steinmetz,et al.  Inflammation in high-grade carotid stenosis: a possible role for macrophages and T cells in plaque destabilization. , 1998, Stroke.

[22]  J. Slattery,et al.  Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST) , 1998, The Lancet.

[23]  J. Kirkpatrick,et al.  Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. , 1998, Journal of insurance medicine.

[24]  A. Davies,et al.  Carotid plaque characteristics and presenting symptom , 1997, The British journal of surgery.

[25]  C. Degueldre,et al.  Relation between contractile reserve and positron emission tomographic patterns of perfusion and glucose utilization in chronic ischemic left ventricular dysfunction: implications for identification of myocardial viability. , 1997, Journal of the American College of Cardiology.

[26]  R. Virmani,et al.  Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis. , 1997, Surgery.

[27]  R. Virmani,et al.  Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. , 1997, The New England journal of medicine.

[28]  A Bol,et al.  Myocardial blood flow, glucose uptake, and recruitment of inotropic reserve in chronic left ventricular ischemic dysfunction. Implications for the pathophysiology of chronic myocardial hibernation. , 1996, Circulation.

[29]  R. Virmani,et al.  Atherosclerotic plaque rupture in symptomatic carotid artery stenosis. , 1996, Journal of vascular surgery.

[30]  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.

[31]  A. Davies,et al.  Endarterectomy for asymptomatic carotid artery stenosis , 1995, BMJ.

[32]  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.

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