© 2002 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
The inflammatory response in myocardial infarction
aSection of Cardiovascular Sciences, Department of Medicine, Baylor College of Medicine and the DeBakey Heart Center, One Baylor Plaza M/S F-602, Houston, TX 77030, USA
bSection of Leukocyte Biology, Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
* Corresponding author. Tel.: +1-713-798-4188; fax: +1-713-796-0015 mentman{at}bcm.tmc.edu
One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial necrosis and optimizing cardiac repair following myocardial infarction. However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion. Myocardial necrosis induces complement activation and free radical generation, triggering a cytokine cascade initiated by Tumor Necrosis Factor (TNF)-
release. If reperfusion of the infarcted area is initiated, it is attended by an intense inflammatory reaction. Interleukin (IL)-8 synthesis and C5a activation have a crucial role in recruiting neutrophils in the ischemic and reperfused myocardium. Neutrophil infiltration is regulated through a complex sequence of molecular steps involving the selectins and the integrins, which mediate leukocyte rolling and adhesion to the endothelium. Marginated neutrophils exert potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. Despite this potential injury, substantial evidence suggests that reperfusion enhances cardiac repair improving patient survival; this effect may be in part related to the inflammatory response. Monocyte Chemoattractant Protein (MCP)-1 is also markedly upregulated in the infarcted myocardium inducing recruitment of mononuclear cells in the injured areas. Monocyte-derived macrophages and mast cells may produce cytokines and growth factors necessary for fibroblast proliferation and neovascularization, leading to effective repair and scar formation. At this stage expression of inhibitory cytokines such as IL-10 may have a role in suppressing the acute inflammatory response and in regulating extracellular matrix metabolism. Fibroblasts in the healing scar undergo phenotypic changes expressing smooth muscle cell markers. Our previous review in this journal focused almost exclusively on reduction of the inflammatory injury. The current update is prompted by the potential therapeutic opportunity that the open vessel offers. By promoting more effective tissue repair, it may be possible to reduce the deleterious remodeling, that is the leading cause of heart failure and death. Elucidating the complex interactions and regulatory mechanisms responsible for cardiac repair may allow us to design effective inflammation-related interventions for the treatment of myocardial infarction.
KEYWORDS -SMAc, -Smooth Muscle Actin; bFGF, basic Fibroblast Growth Factor; CSIF, Cytokine Synthesis Inhibitory Factor; DCFH, dichlorofluorescein; ICAM-1, Intercellular Adhesion Molecule-1; IL, interleukin; IP-10, Interferon 
-Inducible Protein-10; LFA-1, Leukocyte Function Antigen-1; LPS, lipopolysaccharide; LTB4, Leukotriene B4; LTC4, Leukotriene C4; MCP-1, Monocyte Chemoattractant Protein-1; M-CSF, Macrophage Colony-Stimulating Factor; MMP, matrix metalloproteinase; NADP, nicotineamide-adenine dinucleotide phosphate; NF-
B, Nuclear Factor-B; PAF, Platelet Activating Factor; PAF-AH, Platelet Activating Factor-Acetylhydrolase; PDGF, Platelet-Derived Growth Factor; PSGL-1, P-Selectin Glycoprotein Ligand-1; ROS, reactive oxygen species; SCF, Stem Cell Factor; sCR1, Soluble Complement Receptor Type 1; SMemb, embryonic isoform of smooth muscle myosin heavy chain; SOD, superoxide dismutase; TIMP-1, Tissue Inhibitor of Metalloproteinases-1; TGF-β, Transforming Growth Factor-β; TNF-, Tumor Necrosis Factor-; TNFR, Tumor Necrosis Factor Receptor; u-PA, Urokinase-type Plasminogen Activator; VEGF, Vascular Endothelial Growth Factor; VLA-5, Very Late Antigen-5
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J. T. Colston, S. D. de la Rosa, M. Koehler, K. Gonzales, R. Mestril, G. L. Freeman, S. R. Bailey, and B. Chandrasekar Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1839 - H1846. [Abstract] [Full Text] [PDF]
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V. Drobic, R. H. Cunnington, K. M. Bedosky, J. E. Raizman, V. V. Elimban, S. G. Rattan, and I. M. C. Dixon Differential and combined effects of cardiotrophin-1 and TGF-beta1 on cardiac myofibroblast proliferation and contraction Am J Physiol Heart Circ Physiol, August 1, 2007; 293(2): H1053 - H1064. [Abstract] [Full Text] [PDF]
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X. Liu, J. A. Simpson, K. R. Brunt, C. A. Ward, S. R. R. Hall, R. T. Kinobe, V. Barrette, M. Y. Tse, S. C. Pang, A. S. Pachori, et al. Preemptive heme oxygenase-1 gene delivery reveals reduced mortality and preservation of left ventricular function 1 yr after acute myocardial infarction Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H48 - H59. [Abstract] [Full Text] [PDF]
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M. L. Batista Jr., R. V. T. Santos, E. M. Oliveira, M. C. L. Seelaender, and L. F. B. P. Costa Rosa Endurance training restores peritoneal macrophage function in post-MI congestive heart failure rats J Appl Physiol, May 1, 2007; 102(5): 2033 - 2039. [Abstract] [Full Text] [PDF]
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P. Zymek, D.-Y. Nah, M. Bujak, G. Ren, A. Koerting, T. Leucker, P. Huebener, G. Taffet, M. Entman, and N. G. Frangogiannis Interleukin-10 is not a critical regulator of infarct healing and left ventricular remodeling Cardiovasc Res, May 1, 2007; 74(2): 313 - 322. [Abstract] [Full Text] [PDF]
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S. Fukushima, A. Varela-Carver, S. R. Coppen, K. Yamahara, L. E. Felkin, J. Lee, P. J.R. Barton, C. M.N. Terracciano, M. H. Yacoub, and K. Suzuki Direct Intramyocardial But Not Intracoronary Injection of Bone Marrow Cells Induces Ventricular Arrhythmias in a Rat Chronic Ischemic Heart Failure Model Circulation, May 1, 2007; 115(17): 2254 - 2261. [Abstract] [Full Text] [PDF]
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M. Nahrendorf, D. E. Sosnovik, P. Waterman, F. K. Swirski, A. N. Pande, E. Aikawa, J.-L. Figueiredo, M. J. Pittet, and R. Weissleder Dual Channel Optical Tomographic Imaging of Leukocyte Recruitment and Protease Activity in the Healing Myocardial Infarct Circ. Res., April 27, 2007; 100(8): 1218 - 1225. [Abstract] [Full Text] [PDF]
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D. E. Sosnovik, M. Nahrendorf, N. Deliolanis, M. Novikov, E. Aikawa, L. Josephson, A. Rosenzweig, R. Weissleder, and V. Ntziachristos Fluorescence Tomography and Magnetic Resonance Imaging of Myocardial Macrophage Infiltration in Infarcted Myocardium In Vivo Circulation, March 20, 2007; 115(11): 1384 - 1391. [Abstract] [Full Text] [PDF]
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P. Agostoni and C. Banfi Matrix metalloproteinase and heart failure: is it time to move from research to clinical laboratories? Eur. Heart J., March 8, 2007; (2007) ehl574v1. [Full Text] [PDF]
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D. Kelly, G. Cockerill, L. L. Ng, M. Thompson, S. Khan, N. J. Samani, and I. B. Squire Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study Eur. Heart J., March 5, 2007; (2007) ehm003v1. [Abstract] [Full Text] [PDF]
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H. Clements-Jewery, D. J. Hearse, and M. J. Curtis Neutrophil ablation with anti-serum does not protect against phase 2 ventricular arrhythmias in anaesthetised rats with myocardial infarction Cardiovasc Res, March 1, 2007; 73(4): 761 - 769. [Abstract] [Full Text] [PDF]
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H. Oren, A. R. Erbay, M. Balc, and S. Cehreli Role of Novel Mediators of Inflammation in Left Ventricular Remodeling in Patients With Acute Myocardial Infarction: Do They Affect the Outcome of Patients? Angiology, February 1, 2007; 58(1): 45 - 54. [Abstract] [PDF]
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S. Hazarika, M. R. Van Scott, and R. M. Lust Severity of myocardial injury following ischemia-reperfusion is increased in a mouse model of allergic asthma Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H572 - H579. [Abstract] [Full Text] [PDF]
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Y. Onai, J.-i. Suzuki, Y. Maejima, G. Haraguchi, S. Muto, A. Itai, and M. Isobe Inhibition of NF-{kappa}B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H530 - H538. [Abstract] [Full Text] [PDF]
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P. Zymek, M. Bujak, K. Chatila, A. Cieslak, G. Thakker, M. L. Entman, and N. G. Frangogiannis The Role of Platelet-Derived Growth Factor Signaling in Healing Myocardial Infarcts J. Am. Coll. Cardiol., December 5, 2006; 48(11): 2315 - 2323. [Abstract] [Full Text] [PDF]
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S. B. Haudek, Y. Xia, P. Huebener, J. M. Lee, S. Carlson, J. R. Crawford, D. Pilling, R. H. Gomer, J. Trial, N. G. Frangogiannis, et al. Bone marrow-derived fibroblast precursors mediate ischemic cardiomyopathy in mice PNAS, November 28, 2006; 103(48): 18284 - 18289. [Abstract] [Full Text] [PDF]
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G. D. Thakker, N. G. Frangogiannis, M. Bujak, P. Zymek, J. W. Gaubatz, A. K. Reddy, G. Taffet, L. H. Michael, M. L. Entman, and C. M. Ballantyne Effects of diet-induced obesity on inflammation and remodeling after myocardial infarction Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2504 - H2514. [Abstract] [Full Text] [PDF]
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H. Morimoto, M. Takahashi, A. Izawa, H. Ise, M. Hongo, P. E. Kolattukudy, and U. Ikeda Cardiac Overexpression of Monocyte Chemoattractant Protein-1 in Transgenic Mice Prevents Cardiac Dysfunction and Remodeling After Myocardial Infarction Circ. Res., October 13, 2006; 99(8): 891 - 899. [Abstract] [Full Text] [PDF]
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F. G. Spinale, G. P. Escobar, J. W. Hendrick, L. L. Clark, S. S. Camens, J. P. Mingoia, C. G. Squires, R. E. Stroud, and J. S. Ikonomidis Chronic Matrix Metalloproteinase Inhibition Following Myocardial Infarction in Mice: Differential Effects on Short and Long-Term Survival J. Pharmacol. Exp. Ther., September 1, 2006; 318(3): 966 - 973. [Abstract] [Full Text] [PDF]
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M. Takaoka, S. Uemura, H. Kawata, K.-i. Imagawa, Y. Takeda, K. Nakatani, N. Naya, M. Horii, S. Yamano, Y. Miyamoto, et al. Inflammatory Response to Acute Myocardial Infarction Augments Neointimal Hyperplasia After Vascular Injury in a Remote Artery Arterioscler Thromb Vasc Biol, September 1, 2006; 26(9): 2083 - 2089. [Abstract] [Full Text] [PDF]
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Q. Feng Beyond erythropoiesis: The anti-inflammatory effects of erythropoietin Cardiovasc Res, September 1, 2006; 71(4): 615 - 617. [Full Text] [PDF]
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Y. Kodama, Y. Kitta, T. Nakamura, H. Takano, K. Umetani, D. Fujioka, Y. Saito, K.-i. Kawabata, J.-e. Obata, A. Mende, et al. Atorvastatin Increases Plasma Soluble Fms-Like Tyrosine Kinase-1 and Decreases Vascular Endothelial Growth Factor and Placental Growth Factor in Association With Improvement of Ventricular Function in Acute Myocardial Infarction J. Am. Coll. Cardiol., July 4, 2006; 48(1): 43 - 50. [Abstract] [Full Text] [PDF]
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S. Fukushima, S. R. Coppen, A. Varela-Carver, K. Yamahara, P. Sarathchandra, R. T. Smolenski, M. H. Yacoub, and K. Suzuki A Novel Strategy for Myocardial Protection by Combined Antibody Therapy Inhibiting Both P-Selectin and Intercellular Adhesion Molecule-1 Via Retrograde Intracoronary Route Circulation, July 4, 2006; 114(1_suppl): I-251 - I-256. [Abstract] [Full Text] [PDF]
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