Biomarker analysis by fluorokine multianalyte profiling distinguishes patients requiring intervention from patients with long-term quiescent coronary artery disease: a potential approach to identify atherosclerotic disease progression.

[1]  K. Furie,et al.  Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. , 2007, Circulation.

[2]  J. Egido,et al.  Inflammatory biomarkers in stable atherosclerosis. , 2006, The American journal of cardiology.

[3]  Dan M. Roden,et al.  ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines , 2006 .

[4]  P. Barter,et al.  The rationale for using apoA‐I as a clinical marker of cardiovascular risk , 2006, Journal of internal medicine.

[5]  K. Shimada,et al.  Comparison of levels of serum matrix metalloproteinase-9 in patients with acute myocardial infarction versus unstable angina pectoris versus stable angina pectoris. , 2006, The American journal of cardiology.

[6]  G. Keren,et al.  Circulating matrix metalloproteinase-2 but not matrix metalloproteinase-3, matrix metalloproteinase-9, or tissue inhibitor of metalloproteinase-1 predicts outcome in patients with congestive heart failure. , 2005, American heart journal.

[7]  D. Brieger,et al.  Elevated circulating levels of matrix metalloproteinase‐9 and ‐2 in patients with symptomatic coronary artery disease , 2005, Internal medicine journal.

[8]  Leong L Ng,et al.  Plasma MMP-9 and MMP-2 following acute myocardial infarction in man: correlation with echocardiographic and neurohumoral parameters of left ventricular dysfunction. , 2004, Journal of cardiac failure.

[9]  Paul M. Ridker,et al.  Inflammation as a Cardiovascular Risk Factor , 2004, Circulation.

[10]  Antonio Colombo,et al.  From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. , 2003, Circulation.

[11]  E. Boerwinkle,et al.  From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. , 2003, Circulation.

[12]  F. Ceci,et al.  Serum Metalloproteinase 9 Levels in Patients with Coronary Artery Disease: A Novel Marker of Inflammation , 2003, Journal of Investigative Medicine.

[13]  D. Kereiakes.  The Emperor's clothes: in search of the vulnerable plaque. , 2003, Circulation.

[14]  V. Fuster,et al.  Pathogenetic concepts of acute coronary syndromes. , 2003, Journal of the American College of Cardiology.

[15]  P. Shah,et al.  Mechanisms of plaque vulnerability and rupture. , 2003, Journal of the American College of Cardiology.

[16]  A. Naylor,et al.  Matrix metalloproteinases and atherosclerotic plaque instability , 2002, The British journal of surgery.

[17]  Renu Virmani,et al.  Healed Plaque Ruptures and Sudden Coronary Death: Evidence That Subclinical Rupture Has a Role in Plaque Progression , 2001, Circulation.

[18]  D. Vignali.  Multiplexed particle-based flow cytometric assays. , 2000, Journal of immunological methods.

[19]  T. Ueno,et al.  Peripheral blood levels of matrix metalloproteases-2 and -9 are elevated in patients with acute coronary syndromes. , 1998, Journal of the American College of Cardiology.

[20]  G. Thompson.  Angiographic evidence for the role of triglyceride-rich lipoproteins in progression of coronary artery disease. , 1998, European heart journal.

[21]  C. Sing,et al.  Effects of polymorphisms in apolipoproteins E, A-IV, and H on quantitative traits related to risk for cardiovascular disease. , 1991, Arteriosclerosis and thrombosis : a journal of vascular biology.

[22]  J V Castell,et al.  Interleukin-6 and the acute phase response. , 1990, The Biochemical journal.