The complement system in the acute phase of myocardial infarction.

Although some studies suggest that complement activation is involved in the development of acute myocardial infarction, there has been little convincing evidence of a change in the complement system in patients suffering from myocardial infarction. In this study circulating levels of C3a, C3, C4 and the total hemolytic complement titer (CH50) were serially measured in 12 patients with acute myocardial infarction up to 10 days after an attack. The plasma C3a level was greatly elevated throughout the post-attack observation period. The C3, C4 and CH50 levels were significantly increased above those controls on days 8, 9 and 10 after infarction. These findings indicate that there is complement activation in patients with acute myocardial infarction, and suggest a pathogenetic role for complement activation in the development of myocardial damage after infarction.

[1]  M. Entman,et al.  Mechanism of Complement Activation After Coronary Artery Occlusion: Evidence That Myocardial Ischemia in Dogs Causes Release of Constituents of Myocardial Subcellular Origin That Complex With Human C1q In Vivo , 1988, Circulation research.

[2]  J. Kruskal,et al.  Fibrin and fibrinogen-related antigens in patients with stable and unstable coronary artery disease. , 1987, The New England journal of medicine.

[3]  R. Bolli,et al.  Activation of the complement system by recombinant tissue plasminogen activator. , 1987, Journal of the American College of Cardiology.

[4]  D. Mathey,et al.  Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. , 1986, Journal of immunology.

[5]  J. Bauman,et al.  Current concepts in clinical therapeutics: acute myocardial infarction. , 1986, Clinical pharmacy.

[6]  M. Entman,et al.  Selective Accumulation of the First Component of Complement and Leukocytes in Ischemic Canine Heart Muscle: A Possible Initiator of an Extra Myocardial Mechanism of Ischemic Injury , 1985, Circulation research.

[7]  J. Earis,et al.  Complement activation after myocardial infarction. , 1985, Chest.

[8]  P. Fenster,et al.  Significance of the Q wave in acute myocardial infarction , 1985, Clinical cardiology.

[9]  S. Takase,et al.  Serial changes of complement titers in the acute phase of myocardial infarction. , 1983, Japanese circulation journal.

[10]  Gerson Mc.  Myocardial imaging in myocardial infarction: technetium vs. thallium. , 1983 .

[11]  M. Chiariello,et al.  Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion. , 1978, The Journal of clinical investigation.

[12]  E. Braunwald,et al.  Long-term preservation of ischemic myocardium after experimental coronary artery occlusion. , 1978, The Journal of clinical investigation.

[13]  R. O'rourke,et al.  Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. , 1975, The Journal of clinical investigation.

[14]  P. Ward,et al.  THE PHLOGISTIC ROLE OF C3 LEUKOTACTIC FRAGMENTS IN MYOCARDIAL INFARCTS OF RATS , 1971, The Journal of experimental medicine.

[15]  O. Ratnoff,et al.  THE CONVERSION OF C'1S TO C'1 ESTERASE BY PLASMIN AND TRYPSIN , 1967, The Journal of experimental medicine.

[16]  J. Heremans,et al.  Immunochemical quantitation of antigens by single radial immunodiffusion. , 1965, Immunochemistry.

[17]  R. Jennings,et al.  A COMPARATIVE STUDY OF THE FINE STRUCTURE OF NORMAL AND ISCHEMIC DOG MYOCARDIUM WITH SPECIAL REFERENCE TO EARLY CHANGES FOLLOWING TEMPORARY OCCLUSION OF A CORONARY ARTERY. , 1965, The American journal of pathology.