Skip to main content

Role of Complement in Myocardial Ischemia and Infarction

  • Chapter

Abstract

The complement system is involved in several aspects of the pathophysiology of myocardial ischemia and infarction. Initially a role for complement in ischemic heart disease was inferred from the deposition of complement components within the myocardium of experimental models of myocardial infarction. Further animal models demonstrated that depletion or inhibition of complement prior to myocardial ischemia/reperfusion (MI/R) can reduce complement-mediated tissue injury. Recently, in vivo examination of naturally occurring complement inhibitors and monoclonal antibodies directed at specific complement components has confirmed complement dependent injury following MI/R. Current research provides intriguing evidence on the initiating pathways and the possible methods of complement regulation in the management of MI/R injury. This chapter focuses on many of the studies demonstrating complement activation and deposition in MI/R, the functional consequences of complement activation following MI/R, the initial and recent anti-complement therapies used in vivo and the current insight of the mechanisms of complement activation following MI/R.

co-authorship

This is a preview of subscription content, log in via an institution.

Buying options

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD   219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD   219.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. American Heart Association. Heart Disease and Stroke Statistics-2003 Update. American Heart Association. 2002.

    Google Scholar 

  2. Ribichini F, Wijns W. Acute myocardial infarction: reperfusion treatment. Heart. 2002;88:298–305.

    Article  PubMed  Google Scholar 

  3. Braunwald E, Zipes DP, Libby P. Heart Disease. 6th. 2001.

    Google Scholar 

  4. Kloner RA. Does reperfusion injury exist in humans? J Am Coll Cardiol. 1993;21:537–545.

    CAS  PubMed  Google Scholar 

  5. Ganz W. Direct Demonstration in Dogs of the Absence of Lethal Reperfusion Injury. J Thromb Thrombolysis. 1997;4:105–107.

    Article  PubMed  Google Scholar 

  6. Farb A, Kolodgie FD, Jenkins M et al. Myocardial infarct extension during reperfusion after coronary artery occlusion: pathologic evidence. J Am Coll Cardiol. 1993;21:1245–1253.

    CAS  PubMed  Google Scholar 

  7. Matsumura K, Jeremy RW, Schaper J et al. Progression of myocardial necrosis during reperfusion of ischemic myocardium. Circulation. 1998;97:795–804.

    CAS  PubMed  Google Scholar 

  8. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res. 2002;53:31–47.

    Article  CAS  PubMed  Google Scholar 

  9. Shernan SK, Collard CD. Role of the complement system in ischaemic heart disease: potential for pharmacological intervention. BioDrugs. 2001;15:595–607.

    Article  CAS  PubMed  Google Scholar 

  10. Riedemann NC, Ward PA. Complement in ischemia reperfusion injury. Am J Pathol. 2003;162:363–367.

    PubMed  Google Scholar 

  11. Walport MJ. Complement. First of two parts. N Engl J Med. 2001;344:1058–1066.

    CAS  PubMed  Google Scholar 

  12. Hill JH, Ward PA. The phlogistic role of C3 leukotactic fragments in myocardial infarcts in rats. J Exp Med. 1971;133:885–900.

    Article  CAS  PubMed  Google Scholar 

  13. Schafer H, Mathey D, Hugo F et al. Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. J Immunol. 1986;137:1945–1949.

    CAS  PubMed  Google Scholar 

  14. Maroko PR, Carpenter CB, Chariello M. Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion. J Clin Invest. 1978;61:661–670.

    CAS  PubMed  Google Scholar 

  15. Weisman HF, Bartow T, Leppo MK et al. Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis. Science. 1990;249:146–151.

    CAS  PubMed  Google Scholar 

  16. Hill JH, Ward PA. C3 leukotactic factors produced by a tissue protease. J Exp Med. 1969;130:505–518.

    Article  CAS  PubMed  Google Scholar 

  17. Pinckard RN, Olson MS, Giclas PC et al. Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. J Clin Invest. 1975;56:740–750.

    CAS  PubMed  Google Scholar 

  18. Pinckard RN, Olson MS, Giclas PC et al. Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction. J Clin Invest. 1975;56:740–750.

    CAS  PubMed  Google Scholar 

  19. Giclas PC, Pinckard RN, Olson MS. In vitro activation of complement by isolated human heart subcellular membranes. J Immunol. 1979;122:146–151.

    CAS  PubMed  Google Scholar 

  20. Pinckard RN, O’Roarke RA, Crawford MH. Complement localization and mediation of ischemic injury in baboon myocardium. J Clin Invest. 1980;66:1050–1056.

    CAS  PubMed  Google Scholar 

  21. McManus LM, Kolb WP, Crawford MH et al. Complement localization in ischemic baboon myocardium. Lab Invest. 1983;48:436–447.

    CAS  PubMed  Google Scholar 

  22. Rossen RD, Swain JL, Michael LH. 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. Circ Res. 1985;57:119–130.

    CAS  PubMed  Google Scholar 

  23. Crawford MH, Grover FL, Kolb WP et al. Complement and neutrophil activation in the pathogenesis of ischemic myocardial injury. Circ Res. 1988;78:1449–1458.

    CAS  Google Scholar 

  24. Vakeva A, Laurila P, Meri S. Loss of expression of protectin (CD59) is associated with complement membrane attack complex deposition in myocardial infarction. Lab Invest. 1992;67:608–616.

    CAS  PubMed  Google Scholar 

  25. Väkevä A, Laurila P, Meri S. Co-deposition of clusterin with the complement membrane attack complex in myocardial infarction. Immunology. 1993;80:177–182.

    PubMed  Google Scholar 

  26. Vakeva A, Agah A, Rollins SA et al. Myocardial infarction and apoptosis after myocardial ischemia and reperfusion. Role of the terminal complement components and inhibition by anti-C5 therapy. Circulation. 1998;97:2259–2267.

    CAS  PubMed  Google Scholar 

  27. Buerke M, Prüfer D, Dahm M et al. Blocking of classical complement pathway inhibits endothelial adhesion molecule expression and preserves ischemic myocardium from reperfusion injury. Journal of Pharmacology and Experimental Therapeutics. 1998;286:429–438.

    CAS  PubMed  Google Scholar 

  28. Collard CD, Vakeva A, Morrissey MA et al. Complement activation after oxidative stress: role of the lectin complement pathway. Am J Pathol. 2000;156:1549–1556.

    CAS  PubMed  Google Scholar 

  29. Väkevä A, Morgan BP, Tikkanen I et al. Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium. Am J Pathol. 1994;144:1357–1368.

    PubMed  Google Scholar 

  30. Buerke M, Murohara T, Lefer AM. Cardioprotective effects of a C1 esterase inhibitor in myocardial ischemia and reperfusion. Circulation. 1995;91:393–402.

    CAS  PubMed  Google Scholar 

  31. Yasojima K, Schwab C, McGeer EG et al. Human heart generates complement proteins that are upregulated and activated after myocardial infarction. Circ Res. 1998;83:860–869.

    CAS  PubMed  Google Scholar 

  32. Kilgore KS, Friedrichs GS, Homeister JW et al. The complement system in myocardial ischaemia/reperfusion injury. Cardiovasc Res. 1994;28:437–444.

    CAS  PubMed  Google Scholar 

  33. Gardinali M, Conciato L, Cafaro C et al. Complement system in coronary heart disease: A review. Immunopharmacology. 1995;30:105–117.

    Article  CAS  PubMed  Google Scholar 

  34. Dreyer WJ, Michael LH, Nguyen T et al. Kinetics of C5a release in cardiac lymph of dogs experiencing coronary artery ischemia-reperfusion injury. Circ Res. 1992;71:1518–1524.

    CAS  PubMed  Google Scholar 

  35. McManus LM, Kolb WP, Crawford MH et al. Complement localization in ischemic baboon myocardium. Lab Invest. 1983;48:436–447.

    CAS  PubMed  Google Scholar 

  36. Chenoweth DE. The properties of human C5a anaphylatoxin. The significance of C5a formation during hemodialysis. Contr Nephrol. 1987;59:51–71.

    CAS  Google Scholar 

  37. Daffern PJ, Pfeifer PH, Ember JA et al. C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation. J Exp Med. 1995;181:2119–2127.

    Article  CAS  PubMed  Google Scholar 

  38. Takafuji S, Tadokoro K, Ito K et al. Degranulation from human eosinophils stimulated with C3a and C5a. Int Arch Allergy Immunol. 1994;104 Suppl 1:27–29.

    CAS  PubMed  Google Scholar 

  39. Chakraborti T, Mandal A, Mandal M et al. Complement activation in heart diseases: Role of oxidants. Cell Signal. 2000;12:607–617.

    CAS  PubMed  Google Scholar 

  40. Ito BR, Roth DM, Engler RL. Thromboxane A2and peptidoleukotrienes contribute to the myocardial ischemia and contractile dysfunction in response to intracoronary infusion of complement C5a in pigs. Circ Res. 1990;66:596–607.

    CAS  PubMed  Google Scholar 

  41. Stahl GL, Amsterdam EA, Symons JD et al. Role of thromboxane A2 in the cardiovascular response to intracoronary C5a. Circ Res. 1990;66:1103–1111.

    CAS  PubMed  Google Scholar 

  42. Entman ML, Michael L, Rossen RD et al. Inflammation in the course of early myocardial ischemia. FASEB J. 1991;5:2529–2537.

    CAS  PubMed  Google Scholar 

  43. Dreyer WJ, Smith CW, Entman ML. Invited letter concerning: neutrophil activation during cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1991;102:318–320.

    CAS  PubMed  Google Scholar 

  44. Sacks T, Moldow CF, Craddock PR et al. Endothelial damage provoked by toxic oxygen radicals released from complement-triggered granulocytes. Prog Clin Biol Res. 1978;21:719–26.:719–726.

    CAS  PubMed  Google Scholar 

  45. Schindler R, Gelfand JA, Dinarello CA. Recombinant C5a stimulates transcription rather than translation of interleukin-1 (IL-1) and tumor necrosis factor: Translational signal provided by lipopolysaccharide or IL-1 itself. Blood. 1990;76:1631–1638.

    CAS  PubMed  Google Scholar 

  46. Scholz W, McClurg MR, Cardenas GJ et al. C5a-mediated release of interleukin 6 by human monocytes. Clin Immunol Immunopathol. 1990;57:297–307.

    Article  CAS  PubMed  Google Scholar 

  47. Cavaillon JM, Fitting C, Haeffner-Cavaillon N. Recombinant C5a enhances interleukin 1 and tumor necrosis factor release by lipopolysaccharide-stimulated monocytes and macrophages. Eur J Immunol. 1990;20:253–257.

    CAS  PubMed  Google Scholar 

  48. Moon R, Parikh AA, Szabo C et al. Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1beta and tumor necrosis factor alpha. Arch Surg. 1997;132:1289–1293.

    CAS  PubMed  Google Scholar 

  49. Buerke M, Prüfer D, Dahm M et al. Blocking of classical complement pathway inhibits endothelial adhesion molecule expression and preserves ischemic myocardium from reperfusion injury. Journal of Pharmacology and Experimental Therapeutics. 1998;286:429–438.

    CAS  PubMed  Google Scholar 

  50. Mathey D, Schofer J, Schafer H et al. Early accumulation of the terminal complement-complex in the ischemic myocardium after reperfusion. Eur Heart J. 1994; 15:418–423.

    CAS  PubMed  Google Scholar 

  51. Homeister JW, Satoh P, Lucchesi BR. Effects of complement activation in the isolated heart. Role of the terminal complement components. Circ Res. 1992;71:303–319.

    CAS  PubMed  Google Scholar 

  52. Kim SH, Carney DF, Hammer CH et al. Nucleated cell killing by complement: effects of C5b-9 channel size and extracellular Ca2+ on the lytic process. J Immunol. 1987;138:1530–1536.

    CAS  PubMed  Google Scholar 

  53. Nicholson-Weller A, Halperin JA. Membrane signaling by complement C5b-9, the membrane attack complex. Immunol Res. 1993; 12:244–257.

    CAS  PubMed  Google Scholar 

  54. Berger H-J, Taratuska A, Smith TW et al. Activated complement directly modifies the performance of isolated heart muscle cells from guinea pig and rat. Am J Physiol Heart Circ Physiol. 1993;265:H267–H272.

    CAS  Google Scholar 

  55. Becker LC, Ambrosio G. Myocardial consequences of reperfusion. Prog Cardiovasc Dis. 1987;30:23–44.

    CAS  PubMed  Google Scholar 

  56. Hoerter JA, Miceli MV, Renlund DG et al. A phosphorus-31 nuclear magnetic resonance study of the metabolic, contractile, and ionic consequences of induced calcium alterations in the isovolumic rat heart. Circ Res. 1986;58:539–551.

    CAS  PubMed  Google Scholar 

  57. Wiedmer T, Ando B, Sims PJ. Complement C5b-9-stimulated platelet secretion is associated with a Ca2+-initiated activation of cellular protein kinases. J Biol Chem. 1987;262:13674–13681.

    CAS  PubMed  Google Scholar 

  58. Saadi S, Holzknecht RA, Patte CP et al. Endothelial cell activation by pore-forming structures: pivotal role for interleukin-1 alpha. Circulation. 2000;101:1867–1873.

    CAS  PubMed  Google Scholar 

  59. Collard CD, Agah A, Reenstra W et al. Endothelial nuclear factor-kappaB translocation and vascular cell adhesion molecule-1 induction by complement: inhibition with anti-human C5 therapy or cGMP analogues. Arterioscler Thromb Vasc Biol. 1999;19:2623–2629.

    CAS  PubMed  Google Scholar 

  60. Kilgore KS, Schmid E, Shanley TP et al. Sublytic concentrations of the membrane attack complex of complement induce endothelial interleukin-8 and monocyte chemoattractant protein-1 through nuclear factor-kappaB activation. Am J Pathol. 1997;150:2019–2031.

    CAS  PubMed  Google Scholar 

  61. Entman ML, Youker K, Shoji T et al. Neutrophil induced oxidative injury of cardiac myocytes. A compartmented system requiring CD11b/CD18-ICAM-1 adherence. J Clin Invest. 1992;90:1335–1345.

    CAS  PubMed  Google Scholar 

  62. Kukielka GL, Hawkins HK, Michael L et al. Regulation of intercellular adhesion molecule-1 (ICAM-1) in ischemic and reperfused canine myocardium. J Clin Invest. 1993;92:1504–1516.

    CAS  PubMed  Google Scholar 

  63. Youker K, Smith CW, Anderson DC et al. Neutrophil adherence to isolated adult cardiac myocytes. Induction by cardiac lymph collected during ischemia and reperfusion. J Clin Invest. 1992;89:602–609.

    CAS  PubMed  Google Scholar 

  64. Zwaka TP, Manolov D, Ozdemir C et al. Complement and dilated cardiomyopathy: a role of sublytic terminal complement complex-induced tumor necrosis factor-alpha synthesis in cardiac myocytes. Am J Pathol. 2002;161:449–457.

    CAS  PubMed  Google Scholar 

  65. Meldrum DR, Dinarello CA, Shames BD et al. Ischemic preconditioning decreases postischemic myocardial tumor necrosis factor-alpha production. Potential ultimate effector mechanism of preconditioning. Circulation. 1998;98:II214–II218.

    CAS  PubMed  Google Scholar 

  66. Meldrum DR. Tumor necrosis factor in the heart. Am J Physiol. 1998;274: R577–R595.

    CAS  PubMed  Google Scholar 

  67. Ceconi C, Cargnoni A, Curello S et al. Recognized molecular mechanisms of heart failure: approaches to treatment. Rev Port Cardiol. 1998;17 Suppl 2:II79–II91.

    PubMed  Google Scholar 

  68. Meldrum DR, Dinarello CA, Shames BD et al. Ischemic preconditioning decreases postischemic myocardial tumor necrosis factor-alpha production. Potential ultimate effector mechanism of preconditioning. Circulation. 1998;98:II214–II218.

    CAS  PubMed  Google Scholar 

  69. Doyama K, Fujiwara H, Fukumoto M et al. Tumour necrosis factor is expressed in cardiac tissues of patients with heart failure. Int J Cardiol. 1996;54:217–225.

    Article  CAS  PubMed  Google Scholar 

  70. Stahl GL, Reenstra WR, Frendl G. Complement mediated loss of endothelium-dependent relaxation of porcine coronary arteries. Role of the terminal membrane attack complex. Circ Res. 1995;76:575–583.

    CAS  PubMed  Google Scholar 

  71. Lennon PF, Collard CD, Morrissey MA et al. Complement-induced endothelial dysfunction in rabbits: mechanisms, recovery, and gender differences. Am J Physiol Heart Circ Physiol. 1996;270:H1924–H1932.

    CAS  Google Scholar 

  72. Collard CD, Agah A, Reenstra W et al. Endothelial nuclear factor-kappaB translocation and vascular cell adhesion molecule-1 induction by complement: inhibition with anti-human C5 therapy or cGMP analogues. Arterioscler Thromb Vasc Biol. 1999;19: 2623–2629.

    CAS  PubMed  Google Scholar 

  73. Lucchesi BR, Kilgore KS. Complement inhibitors in myocardial ischemia/reperfusion injury. Immunopharmacology. 1997;38:27–42.

    Article  CAS  PubMed  Google Scholar 

  74. MacLean D, Fishbein MC, Braunwald E et al. Long-term preservation of ischemic myocardium after experimental coronary artery occlusion. J Clin Invest. 1978;61:541–551.

    CAS  PubMed  Google Scholar 

  75. Smith EF, III, Griswold DE, Egan JW et al. Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730). Eur J Pharmacol. 1993;236:477–481.

    Article  CAS  PubMed  Google Scholar 

  76. Zacharowski K, Otto M, Hafner G et al. Reduction of myocardial infarct size with sCR1sLe(x), an alternatively glycosylated form of human soluble complement receptor type 1 (sCR1), possessing sialyl Lewis x. Br J Pharmacol. 1999;128:945–952.

    Article  CAS  PubMed  Google Scholar 

  77. Foxall C, Watson SR, Dowbenko D et al. The three members of the selectin receptor family recognize a common carbohydrate epitope, the sialyl Lewis(x) oligosaccharide. J Cell Biol. 1992;117:895–902.

    Article  CAS  PubMed  Google Scholar 

  78. Zacharowski K, Otto M, Hafner G et al. Reduction of myocardial infarct size with sCR1sLe(x), an alternatively glycosylated form of human soluble complement receptor type 1 (sCR1), possessing sialyl Lewis x. Br J Pharmacol. 1999:128:945–952.

    Article  CAS  PubMed  Google Scholar 

  79. Zacharowski K, Otto M, Hafner G et al. Reduction of myocardial infarct size with sCR1sLe(x), an alternatively glycosylated form of human soluble complement receptor type 1 (sCR1), possessing sialyl Lewis x. Br J Pharmacol. 1999;128:945–952.

    Article  CAS  PubMed  Google Scholar 

  80. AVANT Pharmaceuticals. AVANT TP-10 clinical trial press release. 4-29-2003.

    Google Scholar 

  81. Sahul A, Lambris JD. Complement inhibitors: a resurgent concept in anti-inflammatory therapeutics. Immunopharmacology. 2000;49:133–148.

    Google Scholar 

  82. Matsushita M, Thiel S, Jensenius JC et al. Proteolytic activities of two types of mannose-binding lectin-associated serine protease. J Immunol. 2000;165:2637–2642.

    CAS  PubMed  Google Scholar 

  83. Buerke M, Prüfer D, Dahm M et al. Blocking of classical complement pathway inhibits endothelial adhesion molecule expression and preserves ischemic myocardium from reperfusion injury. Journal of Pharmacology and Experimental Therapeutics. 1998;286:429–438.

    CAS  PubMed  Google Scholar 

  84. Horstick G, Heimann A, Gotze O et al. Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and reperfusion. Circulation. 1997;95:701–708.

    CAS  PubMed  Google Scholar 

  85. Horstick G, Berg O, Heimann A et al. Application of C1-esterase inhibitor during reperfusion of ischemic myocardium: dose-related beneficial versus detrimental effects. Circulation. 2001;104:3125–3131.

    CAS  PubMed  Google Scholar 

  86. Horstick G. C1-esterase inhibitor in ischemia and reperfusion. Immunobiology. 2002;205:552–562.

    Article  CAS  PubMed  Google Scholar 

  87. de Zwaan C, Kleine AH, Diris JH et al. Continuous 48-h C1-inhibitor treatment, following reperfusion therapy, in patients with acute myocardial infarction. Eur Heart J. 2002;23:1670–1677.

    PubMed  Google Scholar 

  88. Horstick G, Berg O, Heimann A et al. Application of C1-esterase inhibitor during reperfusion of ischemic myocardium: dose-related beneficial versus detrimental effects. Circulation. 2001;104:3125–3131.

    CAS  PubMed  Google Scholar 

  89. Horstick G, Berg O, Heimann A et al. Application of C1-esterase inhibitor during reperfusion of ischemic myocardium: dose-related beneficial versus detrimental effects. Circulation. 2001;104:3125–3131.

    CAS  PubMed  Google Scholar 

  90. Horstick G, Berg O, Heimann A et al. Application of C1-esterase inhibitor during reperfusion of ischemic myocardium: dose-related beneficial versus detrimental effects. Circulation. 2001;104:3125–3131.

    CAS  PubMed  Google Scholar 

  91. Scesney SM, Makrides SC, Gosselin ML et al. A soluble deletion mutant of the human complement receptor type 1, which lacks the C4b binding site, is a selective inhibitor of the alternative complement pathway. Eur J Immunol. 1996;26:1729–1735.

    CAS  PubMed  Google Scholar 

  92. Buerke M, Schwertz H, Seitz W et al. Novel small molecule inhibitor of C1s exerts cardioprotective effects in ischemia-reperfusion injury in rabbits. J Immunol. 2001;167:5375–5380.

    CAS  PubMed  Google Scholar 

  93. Pellas TC, Boyar W, Van Oostrum J et al. Novel C5a receptor antagonists regulate neutrophil functions in vitro and in vivo. J Immunol. 1998;160:5616–5621.

    CAS  PubMed  Google Scholar 

  94. Murohara T, Guo JP, Delyani JA et al. Cardioprotective effects of selective inhibition of the two complement activation pathways in myocardial ischemia and reperfusion injury. Meth and Find Exptl Clin Pharmacol. 1995;17:499–507.

    CAS  Google Scholar 

  95. Buerke M, Schwertz H, Seitz W et al. Novel small molecule inhibitor of C1s exerts cardioprotective effects in ischemia-reperfusion injury in rabbits. J Immunol. 2001;167:5375–5380.

    CAS  PubMed  Google Scholar 

  96. Pellas TC, Boyar W, Van Oostrum J et al. Novel C5a receptor antagonists regulate neutrophil functions in vitro and in vivo. J Immunol. 1998;160:5616–5621.

    CAS  PubMed  Google Scholar 

  97. Riley RD, Sato H, Zhao ZQ et al. Recombinant human complement C5a receptor antagonist reduces infarct size after surgical revascularization. J Thorac Cardiovasc Surg. 2000;120:350–358.

    Article  CAS  PubMed  Google Scholar 

  98. Amsterdam EA, Stahl GL, Pan H-L et al. Limitation of reperfusion injury by a monoclonal antibody to C5a during myocardial infarction in pigs. Am J Physiol Heart Circ Physiol. 1995;268:H448–H457.

    CAS  Google Scholar 

  99. Fitch JCK, Rollins SA, Matis LA et al. Pharmacology and biological efficacy of a recombinant, humanized, single chain antibody, C5 complement inhibitor in patients undergoing coronary artery bypass graft surgery utilizing cardiopulmonary bypass. Circulation. 1999;100:2499–2509.

    CAS  PubMed  Google Scholar 

  100. American Heart Association. AHA Scientific Sessions 2002-COMMA and COMPLY. American Heart Association. 2002.

    Google Scholar 

  101. Giclas PC, Pinckard RN, Olson MS. In vitro activation of complement by isolated human heart subcellular membranes. J Immunol. 1979;122:146–151.

    CAS  PubMed  Google Scholar 

  102. Rossen RD, Michael LH, Kagiyama A 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. Circ Res. 1988;62:572–584.

    CAS  PubMed  Google Scholar 

  103. Collard CD, Vakeva A, Morrissey MA et al. Complement activation after oxidative stress: role of the lectin complement pathway. Am J Pathol. 2000;156:1549–1556.

    CAS  PubMed  Google Scholar 

  104. Collard CD, Montalto MC, Reenstra WR et al. Endothelial oxidative stress activates the lectin complement pathway: role of cytokeratin 1. Am J Pathol. 2001;159:1045–1054.

    CAS  PubMed  Google Scholar 

  105. Montalto MC, Collard CD, Buras JA et al. A keratin peptide inhibits mannose-binding lectin. J Immunol. 2001;166:4148–4153.

    CAS  PubMed  Google Scholar 

  106. Lekowski R, Collard CD, Reenstra WR et al. Ulex europaeus agglutinin II (UEA-II) is a novel, potent inhibitor of complement activation. Protein Sci. 2001;10:277–284.

    Article  CAS  PubMed  Google Scholar 

  107. Collard CD, Vakeva A, Morrissey MA et al. Complement activation after oxidative stress: role of the lectin complement pathway. Am J Pathol. 2000;156:1549–1556.

    CAS  PubMed  Google Scholar 

  108. Jordan JE, Montalto MC, Stahl GL. Inhibition of mannose-binding lectin reduces postischemic myocardial reperfusion injury. Circulation. 2001;104:1413–1418.

    CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2004 Springer Science + Business Media, Inc.

About this chapter

Cite this chapter

Walsh, M.C., Hart, M.L., Bourcier, T., Bhole, D., Takahashi, M., Stahl, G.L. (2004). Role of Complement in Myocardial Ischemia and Infarction. In: Szebeni, J. (eds) The Complement System. Springer, Boston, MA. https://doi.org/10.1007/1-4020-8056-5_19

Download citation

  • DOI: https://doi.org/10.1007/1-4020-8056-5_19

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4020-8055-5

  • Online ISBN: 978-1-4020-8056-2

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics