Detection of the terminal complement complex in patient plasma following acute myocardial infarction.
The mechanisms of inflammation responsible for the myocardial tissue damage seen after an acute myocardial infarction (AMI) have not been clearly identified. Recent lines of evidence, demonstrating depressed sera levels of individual complement components in patients after myocardial infarction, have suggested involvement of the complement (C) system in micro- and macrovascular injury subsequent to AMI. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation including, the terminal complement complex (TCC) the cytolytic component of the complement system, C1rC1s-C1 inhibitor complex and C3bBbP complex, formed following activation of the classical and alternative pathway, respectively, and anaphylatoxins C3a and C5a in 41 patients following AMI. Plasma TCC and C1rC1s-C1 inhibitor complex concentrations increased up to 32-fold (P less than 0.001) and 8-fold (P less than 0.001), respectively, while the C3bBbP complex, C3a des-Arg and C5a des-Arg each increased over 2-fold (P less than 0.001) 16 h after AMI, and were only minimally detectable during non-inflammatory myocardial conditions. Furthermore, TCC concentrations increased over 150% (P less than 0.001) one day after patients reinfarcted, subsequent to hospitalization for a primary AMI. These results demonstrate activation of complement after AMI and suggest that inflammatory mediators of the complement system may contribute to myocardial tissue damage during the infarction process.
Langlois
P F
PF
Department of Immunology/Microbiology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.
Gawryl
M S
MS
D000328:Adult; D000368:Aged; D003167:Complement Activation; D003174:Complement C1 Inactivator Proteins / Q000032:analysis; D003176:Complement C3 / Q000031:analogs & derivatives / Q000032:analysis; D015926:Complement C3a / Q000031:analogs & derivatives*; D003179:Complement C3b / Q000032:analysis; D003182:Complement C5 / Q000031:analogs & derivatives / Q000032:analysis; D015937:Complement C5a, des-Arginine; D011415:Complement Factor B / Q000032:analysis; D015938:Complement Membrane Attack Complex; D003165:Complement System Proteins / Q000032:analysis*; D005260:Female; D006760:Hospitalization; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000276:immunology*; D012008:Recurrence
D003174:Complement C1 Inactivator Proteins; D003176:Complement C3; D003182:Complement C5; D015937:Complement C5a, des-Arginine; D015938:Complement Membrane Attack Complex; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D003179:Complement C3b; D003165:Complement System Proteins; D011415:Complement Factor B