Comparison of C-reactive protein and terminal complement complex in patients with unstable angina pectoris versus stable angina pectoris.

[1]  G. Hansson.  Immune mechanisms in atherosclerosis. , 1989, Arteriosclerosis, thrombosis, and vascular biology.

[2]  A. Baumbach,et al.  Fibrin specificity and procoagulant effect related to the kallikrein-contact phase system and to plasmin generation with double-bolus reteplase and front-loaded alteplase thrombolysis in acute myocardial infarction. , 2000, The American journal of cardiology.

[3]  M. Pepys,et al.  C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction , 1999, The Journal of experimental medicine.

[4]  H. Wendel,et al.  Thrombolytic therapy in acute myocardial infarction: comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the kallikrein system and plasmin. , 1998, Circulation.

[5]  W. Koenig,et al.  C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[6]  J. Rotter,et al.  Association between serum amyloid A proteins and coronary artery disease: evidence from two distinct arteriosclerotic processes. , 1997, Circulation.

[7]  V. Hombach,et al.  Immunohistochemical colocalization of the terminal complex of human complement and smooth muscle cell alpha-actin in early atherosclerotic lesions. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[8]  I. T. Ten Berge,et al.  CRP-mediated activation of complement in vivo: assessment by measuring circulating complement-C-reactive protein complexes. , 1996, Journal of immunology.

[9]  H. Wendel,et al.  Alterations of coagulation and fibrinolytic and kallikrein-kinin systems in the acute and postacute phases in patients with unstable angina pectoris. , 1995, Circulation.

[10]  A. Rebuzzi,et al.  The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. , 1994, The New England journal of medicine.

[11]  E. Peerschke,et al.  Platelet activation by C1q results in the induction of alpha IIb/beta 3 integrins (GPIIb-IIIa) and the expression of P-selectin and procoagulant activity , 1993, The Journal of experimental medicine.

[12]  A. Remppis,et al.  Development and in vitro characterization of a new immunoassay of cardiac troponin T. , 1992, Clinical chemistry.

[13]  J. Tebo,et al.  Characterization and isolation of a C-reactive protein receptor from the human monocytic cell line U-937. , 1990, Journal of immunology.

[14]  I. Toda,et al.  The complement system in ischemic heart disease. , 1990, Circulation.

[15]  E. Braunwald,et al.  Unstable angina. A classification. , 1989, Circulation.

[16]  G. Hansson,et al.  Prelesional complement activation in experimental atherosclerosis. Terminal C5b-9 complement deposition coincides with cholesterol accumulation in the aortic intima of hypercholesterolemic rabbits. , 1989, Laboratory investigation; a journal of technical methods and pathology.

[17]  P. Sims,et al.  Complement proteins C5b-9 initiate secretion of platelet storage granules without increased binding of fibrinogen or von Willebrand factor to newly expressed cell surface GPIIb-IIIa. , 1988, The Journal of biological chemistry.

[18]  B. Sobel,et al.  Interactions of tissue-type plasminogen activator with plasma inhibitors and their pharmacologic implications. , 1988, Circulation.

[19]  M. Pontet,et al.  Binding of C‐reactive protein to human neutrophils , 1987, FEBS letters.

[20]  M. Mayer.  Complement. Historical perspectives and some current issues. , 1984, Complement.

[21]  J. Volanakis.  COMPLEMENT ACTIVATION BY C‐REACTIVE PROTEIN COMPLEXES * , 1982, Annals of the New York Academy of Sciences.