RSS-Feed abonnieren
DOI: 10.1160/TH08-12-0837
The inflammatory response as a target to reduce myocardial ischaemia and reperfusion injury
Publikationsverlauf
Received:
23. Dezember 2008
Accepted after minor revision:
17. Februar 2009
Publikationsdatum:
22. November 2017 (online)
Summary
Acute myocardial infarction is the leading cause of morbidity and mortality in the adult population of developed and developing nations. Although the prompt restoration of antegrade blood flow in the infarct-related coronary artery is the mean therapy for improving survival, reperfusion itself may cause damage to ischaemic myocardial tissue. This event is well known as “reperfusion injury”. Crucial mediators for cardiac damage in the reperfusion phases are oxidative stress, inflammation and leukocyte infiltration. Already approved and novel therapies might directly reduce these inflammatory processes. Treatments modulating chemokine secretion and activity should be considered as very promising approaches to reduce myocardial reperfusion injury.
* These authors contributed equally.
-
References
- 1 Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet 2003; 361: 13-20.
- 2 Cannon CP. Evolving management of ST-segment elevation myocardial infarction: update on recent data. Am J Cardiol 2006; 98: 10Q-21Q.
- 3 Hillis LD, Lange RA. Myocardial infarction and the open-artery hypothesis. N Engl J Med 2006; 355: 2475-2477.
- 4 Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med 2007; 357: 1121-1135.
- 5 Kilgore KS, Friedrichs GS, Homeister JW. et al. The complement system in myocardial ischaemia/reperfusion injury. Cardiovasc Res 1994; 28: 437-444.
- 6 Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction. Cardiovasc Res 2002; 53: 31-47.
- 7 Jolly SR, Kane WJ, Hook BG. et al. Reduction of myocardial infarct size by neutrophil depletion: effect of duration of occlusion. Am Heart J 1986; 112: 682-690.
- 8 Entman ML, Smith CW. Postreperfusion inflammation: a model for reaction to injury in cardiovascular disease. Cardiovasc Res 1994; 28: 1301-1311.
- 9 Birdsall HH, Green DM, Trial J. et al. Complement C5a, TGF-beta 1, and MCP-1, in sequence, induce migration of monocytes into ischaemic canine myocardium within the first one to five hours after reperfusion. Circulation 1997; 95: 684-692.
- 10 Dhalla NS, Elmoselhi AB, Hata T. et al. Status of myocardial antioxidants in ischaemia-reperfusion injury. Cardiovasc Res 2000; 47: 446-456.
- 11 Dewald O, Ren G, Duerr GD. et al. Of mice and dogs: species-specific differences in the inflammatory response following myocardial infarction. Am J Pathol 2004; 164: 665-677.
- 12 Hansen PR. Role of neutrophils in myocardial ischaemia and reperfusion. Circulation 1995; 91: 1872-1885.
- 13 Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischaemia-reperfusion injury. Cardiovasc Res 1999; 43: 860-878.
- 14 Frangogiannis NG. Chemokines in ischaemia and reperfusion. Thromb Haemost 2007; 97: 738-747.
- 15 Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res 2004; 61: 448-460.
- 16 Dewald O, Zymek P, Winkelmann K. et al. CCL2/Monocyte Chemoattractant Protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circ Res 2005; 96: 881-889.
- 17 Tao L, Gao E, Jiao X. et al. Adiponectin cardioprotection after myocardial ischaemia/reperfusion involves the reduction of oxidative/nitrative stress. Circulation 2007; 115: 1408-1416.
- 18 Charo IF, Ransohoff RM. The many roles of chemokines and chemokine receptors in inflammation. N Engl J Med 2006; 354: 610-621.
- 19 Kukielka GL, Smith CW, LaRosa GJ. et al. Interleukin-8 gene induction in the myocardium after ischaemia and reperfusion in vivo. J Clin Invest 1995; 95: 89-103.
- 20 Boyle Jr EM, Kovacich JC, Hebert CA. et al. Inhibition of interleukin-8 blocks myocardial ischaemiareperfusion injury. J Thorac Cardiovasc Surg 1998; 116: 114-121.
- 21 Vandervelde S, van Luyn MJ, Rozenbaum MH. et al. Stem cell-related cardiac gene expression early after murine myocardial infarction. Cardiovasc Res 2007; 73: 783-793.
- 22 Feng Y, Zhao H, Xu X. et al. Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischaemia-reperfusion in mice. Am J Physiol Heart Circ Physiol 2008; 295: H1311-1318.
- 23 Knuefermann P, Nemoto S, Misra A. et al. CD14-deficient mice are protected against lipopolysaccharide-induced cardiac inflammation and left ventricular dysfunction. Circulation 2002; 106: 2608-2615.
- 24 Frantz S, Kobzik L, Kim YD. et al. Toll4 (TLR4) expression in cardiac myocytes in normal and failing myocardium. J Clin Invest 1999; 104: 271-280.
- 25 Frantz S, Kelly RA, Bourcier T. Role of TLR-2 in the activation of nuclear factor kappa B by oxidative stress in cardiac myocytes. J Biol Chem 2001; 276: 5197-5203.
- 26 Oyama J, Blais Jr C, Liu X. et al. Reduced myocardial ischaemia-reperfusion injury in toll-like receptor 4-deficient mice. Circulation 2004; 109: 784-789.
- 27 Shishido T, Nozaki N, Yamaguchi S. et al. Toll-like receptor-2 modulates ventricular remodeling after myocardial infarction. Circulation 2003; 108: 2905-2910.
- 28 Kumada M, Kihara S, Sumitsuji S. et al. Association of hypoadiponectinemia with coronary artery disease in men. Arterioscler Thromb Vasc Biol 2003; 23: 85-89.
- 29 Pischon T, Girman CJ, Hotamisligil GS. et al. Plasma adiponectin levels and risk of myocardial infarction in men. J Am Med Assoc 2004; 291: 1730-1737.
- 30 Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease. Circ Res 2005; 96: 939-949.
- 31 Shibata R, Sato K, Pimentel DR. et al. Adiponectin protects against myocardial ischaemia-reperfusion injury through AMPK-and COX-2-dependent mechanisms. Nat Med 2005; 11: 1096-1103.
- 32 Ridker PM, Hennekens CH, Buring JE. et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342: 836-843.
- 33 Ridker PM, Rifai N, Rose L. et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 2002; 347: 1557-1565.
- 34 Boekholdt SM, Hack CE, Sandhu MS. et al. C-reactive protein levels and coronary artery disease incidence and mortality in apparently healthy men and women: the EPIC-Norfolk prospective population study 1993–2003. Atherosclerosis 2006; 187: 415-422.
- 35 Dibra A, Mehilli J, Schwaiger M. et al. Predictive value of basal C-reactive protein levels for myocardial salvage in patients with acute myocardial infarction is dependent on the type of reperfusion treatment. Eur Heart J 2003; 24: 1128-1133.
- 36 Blancke F, Claeys MJ, Jorens P. et al. Systemic inflammation and reperfusion injury in patients with acute myocardial infarction. Mediators Inflamm 2005; 2005: 385-389.
- 37 Hoffmann R, Suliman H, Haager P. et al. Association of C-reactive protein and myocardial perfusion in patients with ST-elevation acute myocardial infarction. Atherosclerosis 2006; 186: 177-183.
- 38 Valtchanova-Matchouganska A, Gondwe M, Nadar A. The role of C-reactive protein in ischaemia/reperfusion injury and preconditioning in a rat model of myocardial infarction. Life Sci 2004; 75: 901-910.
- 39 Banfi A, von Degenfeld G, Blau HM. Critical role of microenvironmental factors in angiogenesis. Curr Atheroscler Rep 2005; 07: 227-234.
- 40 Frangogiannis NG, Mendoza LH, Lewallen M. et al. Induction and suppression of interferon-inducible protein 10 in reperfused myocardial infarcts may regulate angiogenesis. FASEB J 2001; 15: 1428-1430.
- 41 Ozawa CR, Banfi A, Glazer NL. et al. Microenvironmental VEGF concentration, not total dose, determines a threshold between normal and aberrant angiogenesis. J Clin Invest 2004; 113: 516-527.
- 42 von Degenfeld G, Banfi A, Springer ML. et al. Microenvironmental VEGF distribution is critical for stable and functional vessel growth in ischaemia. FASEB J 2006; 20: 2657-2659.
- 43 Saxena A, Fish JE, White MD. et al. Stromal cellderived factor-1alpha is cardioprotective after myocardial infarction. Circulation 2008; 117: 2224-2231.
- 44 Abbott JD, Huang Y, Liu D. et al. Stromal cell-derived factor-1alpha plays a critical role in stem cell recruitment to the heart after myocardial infarction but is not sufficient to induce homing in the absence of injury. Circulation 2004; 110: 3300-3305.
- 45 Balsam LB, Wagers AJ, Christensen JL. et al. Haematopoietic stem cells adopt mature haematopoietic fates in ischaemic myocardium. Nature 2004; 428: 668-673.
- 46 Murry CE, Soonpaa MH, Reinecke H. et al. Haematopoietic stem cells do not transdifferentiate into cardiac myocytes in myocardial infarcts. Nature 2004; 428: 664-668.
- 47 Nygren JM, Jovinge S, Breitbach M. et al. Bone marrow-derived hematopoietic cells generate cardiomyocytes at a low frequency through cell fusion, but not transdifferentiation. Nat Med 2004; 10: 494-501.
- 48 Kaikita K, Hayasaki T, Okuma T. et al. Targeted deletion of CC chemokine receptor 2 attenuates left ventricular remodeling after experimental myocardial infarction. Am J Pathol 2004; 165: 439-447.
- 49 Nahrendorf M, Swirski FK, Aikawa E. et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J Exp Med 2007; 204: 3037-3047.
- 50 Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988; 02: 349-360.
- 51 Cigarroa RG, Lange RA, Hillis LD. Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow. Am J Cardiol 1989; 64: 155-160.
- 52 Pollack Jr CV, Braunwald E. 2007 update to the ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: implications for emergency department practice. Ann Emerg Med 2008; 51: 591-606.
- 53 Arumugam TV, Okun E, Tang SC. et al. Toll-Like Receptors in Ischaemia-Reperfusion Injury. Shock. 2008 e-pub ahead of print.
- 54 Zeidan AM, Kouides PA, Tara MA. et al. Platelet function testing: state of the art. Expert Rev Cardiovasc Ther 2007; 05: 955-967.
- 55 Chaer RA, Graham JA, Mureebe L. Platelet function and pharmacologic inhibition. Vasc Endovascular Surg 2006; 40: 261-267.
- 56 Almeda FQ, Schaer GL. Noncardiac applications of glycoprotein IIb/IIIa inhibitors. Catheter Cardiovasc Interv 2004; 62: 530-538.
- 57 Steinhubl SR. Platelets as mediators of inflammation. Hematol Oncol Clin North Am 2007; 21: 115-121.
- 58 Steinhubl SR, Badimon JJ, Bhatt DL. et al. Clinical evidence for anti-inflammatory effects of antiplatelet therapy in patients with atherothrombotic disease. Vasc Med 2007; 12: 113-122.
- 59 Qiu YH, Cheng C, Dai L. et al. Effect of endogenous catecholamines in lymphocytes on lymphocyte function. J Neuroimmunol 2005; 167: 45-52.
- 60 DeGraba TJ. Immunogenetic susceptibility of atherosclerotic stroke: implications on current and future treatment of vascular inflammation. Stroke 2004; 35: 2712-2719.
- 61 Kuroki K, Takahashi HK, Iwagaki H. et al. beta2-adrenergic receptor stimulation-induced immunosuppressive effects possibly through down-regulation of co-stimulatory molecules, ICAM-1, CD40 and CD14 on monocytes. J Int Med Res 2004; 32: 465-483.
- 62 Chen CY, Lee BC, Hsu HC. et al. A proteomic study of the effects of ramipril on post-infarction left ventricular remodelling in the rabbit. Eur J Heart Fail 2008; 10: 740-748.
- 63 Ciulla MM, Montelatici E, Ferrero S. et al. Potential advantages of cell administration on the inflammatory response compared to standard ACE inhibitor treatment in experimental myocardial infarction. J Transl Med 2008; 06: 30.
- 64 Abdulla J, Barlera S, Latini R. et al. A systematic review: effect of angiotensin converting enzyme inhibition on left ventricular volumes and ejection fraction in patients with a myocardial infarction and in patients with left ventricular dysfunction. Eur J Heart Fail 2007; 09: 129-135.
- 65 Gallagher PE, Ferrario CM, Tallant EA. Regulation of ACE2 in cardiac myocytes and fibroblasts. Am J Physiol Heart Circ Physiol 2008; 295: H2373-2379.
- 66 Xu J, Carretero OA, Lin CX. et al. Role of cardiac overexpression of ANG II in the regulation of cardiac function and remodeling postmyocardial infarction. Am J Physiol Heart Circ Physiol 2007; 293: H1900-1907.
- 67 Ledoux J, Gee DM, Leblanc N. Increased peripheral resistance in heart failure: new evidence suggests an alteration in vascular smooth muscle function. Br J Pharmacol 2003; 139: 1245-1248.
- 68 Nabah YN, Mateo T, Estelles R. et al. Angiotensin II induces neutrophil accumulation in vivo through generation and release of CXC chemokines. Circulation 2004; 110: 3581-3586.
- 69 Ellis SG, Lincoff AM, Whitlow PL. et al. Evidence that angiotensin-converting enzyme inhibitor use diminishes the need for coronary revascularization after stenting. Am J Cardiol 2002; 89: 937-940.
- 70 Westermann D, Schultheiss HP, Tschope C. New perspective on the tissue kallikrein-kinin system in myocardial infarction: role of angiogenesis and cardiac regeneration. Int Immunopharmacol 2008; 08: 148-154.
- 71 Lapointe N, Blais Jr C, Adam A. et al. Comparison of the effects of an angiotensin-converting enzyme inhibitor and a vasopeptidase inhibitor after myocardial infarction in the rat. J Am Coll Cardiol 2002; 39: 1692-1698.
- 72 Lijnen P, Petrov V. Antagonism of the renin-angiotensin system, hypertrophy and gene expression in cardiac myocytes. Methods Find Exp Clin Pharmacol 1999; 21: 363-374.
- 73 Youn TJ, Kim HS, Oh BH. Ventricular remodeling and transforming growth factor-beta 1 mRNA expression after nontransmural myocardial infarction in rats: effects of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor blockade. Basic Res Cardiol 1999; 94: 246-253.
- 74 Yu CM, Tipoe GL, Wing-Hon Lai K. et al. Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction. J Am Coll Cardiol 2001; 38: 1207-1215.
- 75 Ellmers LJ, Scott NJ, Medicherla S. et al. Transforming growth factor-beta blockade down-regulates the renin-angiotensin system and modifies cardiac remodeling after myocardial infarction. Endocrinology 2008; 149: 5828-5834.
- 76 Zhang RY, Wang LF, Zhang L. et al. Effects of angiotensin converting enzyme inhibitor, angiotensin II type I receptor blocker and their combination on postinfarcted ventricular remodeling in rats. Chin Med J (Engl) 2006; 119: 649-655.
- 77 Pokharel S, van Geel PP, Sharma UC. et al. Increased myocardial collagen content in transgenic rats overexpressing cardiac angiotensin-converting enzyme is related to enhanced breakdown of N-acetylSer-Asp-Lys-Pro and increased phosphorylation of Smad2/3. Circulation 2004; 110: 3129-3135.
- 78 Ferrieres J, Bataille V, Leclercq F. et al. Patterns of statin prescription in acute myocardial infarction The French registry of Acute ST-elevation or non-ST-elevation Myocardial Infarction (FAST-MI). Atherosclerosis. 2008 e-pub ahead of print..
- 79 Kjekshus J, Apetrei E, Barrios V. et al. Rosuvastatin in older patients with systolic heart failure. N Engl J Med 2007; 357: 2248-2261.
- 80 Arnaud C, Burger F, Steffens S. et al. Statins reduce interleukin-6-induced C-reactive protein in human hepatocytes: new evidence for direct antiinflammatory effects of statins. Arterioscler Thromb Vasc Biol 2005; 25: 1231-1236.
- 81 Ridker PM, Danielson E, Fonseca FA. et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008; 359: 2195-2207.
- 82 Marino F, Guasti L, Cosentino M. et al. Simvastatin treatment in subjects at high cardiovascular risk modulates AT1R expression on circulating monocytes and T lymphocytes. J Hypertens 2008; 26: 1147-1155.
- 83 Blank N, Schiller M, Krienke S. et al. Atorvastatin inhibits T cell activation through 3-hydroxy-3-methylglutaryl coenzyme A reductase without decreasing cholesterol synthesis. J Immunol 2007; 179: 3613-3621.
- 84 Abe Y, Izumi T, Urabe A. et al. Pravastatin prevents myocardium from ischaemia-induced fibrosis by protecting vascular endothelial cells exposed to oxidative stress. Cardiovasc Drugs Ther 2006; 20: 273-280.
- 85 Zhai Y, Gao X, Wu Q. et al. Fluvastatin decreases cardiac fibrosis possibly through regulation of TGFbeta(1)/Smad 7 expression in the spontaneously hypertensive rats. Eur J Pharmacol 2008; 587: 196-203.
- 86 Weinberg EO, Scherrer-Crosbie M, Picard MH. et al. Rosuvastatin reduces experimental left ventricular infarct size after ischaemia-reperfusion injury but not total coronary occlusion. Am J Physiol Heart Circ Physiol 2005; 288: H1802-1809.
- 87 Steffel J, Eberli FR, Luscher TF. et al. Drug-eluting stents - what should be improved?. Ann Med 2008; 40: 242-252.
- 88 Chatterjee S, Pandey A. Drug eluting stents: friend or foe? A review of cellular mechanisms behind the effects of Paclitaxel and sirolimus eluting stents. Curr Drug Metab 2008; 09: 554-566.
- 89 Ferrero V, Ribichini F, Pesarini G. et al. Glucocorticoids in the prevention of restenosis after coronary angioplasty: therapeutic potential. Drugs 2007; 67: 1243-1255.
- 90 Ferrero V, Ribichini F, Rognoni A. et al. Comparison of efficacy and safety of lower-dose to higher-dose oral prednisone after percutaneous coronary interventions (the IMPRESS-LD study). Am J Cardiol 2007; 99: 1082-1086.
- 91 Rodriguez AE, Fernandez-Pereira C. Systemic immunosuppressive therapy with oral Sirolimus after bare metal stent implantation: the missing alternative in the prevention of coronary restenosis after percutaneous coronary interventions. Recent Patents Cardiovasc Drug Discov 2008; 03: 201-208.
- 92 Asanuma H, Sanada S, Ogai A. et al. Methotrexate and MX-68, a new derivative of methotrexate, limit infarct size via adenosine-dependent mechanisms in canine hearts. J Cardiovasc Pharmacol 2004; 43: 574-579.
- 93 Piot C, Croisille P, Staat P. et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med 2008; 359: 473-481.
- 94 Madias JE, Hood Jr WB. Effects of methylprednisolone on the ischaemic damage in patients with acute myocardial infarction. Circulation 1982; 65: 1106-1113.
- 95 Osher J, Lang TW, Meerbaum S. et al. Methylprednisolone treatment in acute myocardial infarction. Effect on regional and global myocardial function. Am J Cardiol 1976; 37: 564-571.
- 96 Peters RW, Norman A, Parmley WW. et al. Effect of therapy with methylprednisolone on the size of myocardial infarcts in man. Chest 1978; 73: 483-488.
- 97 Methylprednisolone as an intervention following myocardial infarction. The Solu-Medrol Sterile Powder AMI Studies Group. J Int Med Res 1986; 14 (Suppl. 01) 1-10.
- 98 Stubbs DF. Post-acute myocardial infarction symptomatic pericarditis (PAMISP): report on a large series and the effect of methylprednisolone therapy. J Int Med Res 1986; 14 (Suppl. 01) 25-29.
- 99 Armstrong PW, Granger CB, Adams PX. et al. Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention: a randomized controlled trial. J Am Med Assoc 2007; 297: 43-51.
- 100 Testa L, Van Gaal WJ, Bhindi R. et al. Pexelizumab in ischaemic heart disease: a systematic review and meta-analysis on 15,196 patients. J Thorac Cardiovasc Surg 2008; 136: 884-893.
- 101 Hoshida S, Yamashita N, Otsu K. et al. FR167653, a cytokine-suppressive agent, reduces myocardial ischaemia-reperfusion injury in rats. Cytokines Cell Mol Ther 2000; 06: 165-170.
- 102 de Lemos JA, Morrow DA, Blazing MA. et al. Serial measurement of monocyte chemoattractant protein-1 after acute coronary syndromes: results from the A to Z trial. J Am Coll Cardiol 2007; 50: 2117-2124.
- 103 Keeley EC, Mehrad B, Strieter RM. Chemokines as mediators of neovascularization. Arterioscler Thromb Vasc Biol 2008; 28: 1928-1936.
- 104 Marino AP, da Silva A, dos Santos P. et al. Regulated on activation, normal T cell expressed and secreted (RANTES) antagonist (Met-RANTES) controls the early phase of Trypanosoma cruzi-elicited myocarditis. Circulation 2004; 110: 1443-1449.
- 105 Abbate A, Salloum FN, Vecile E. et al. Anakinra, a recombinant human interleukin-1 receptor antagonist, inhibits apoptosis in experimental acute myocardial infarction. Circulation 2008; 117: 2670-2683.
- 106 Sun Y, Weber KT. Infarct scar: a dynamic tissue. Cardiovasc Res 2000; 46: 250-256.
- 107 Schuh A, Liehn EA, Sasse A. et al. Improved left ventricular function after transplantation of microspheres and fibroblasts in a rat model of myocardial infarction. Basic Res Cardiol. 2009 e-pub ahead of print.
- 108 Assmus B, Schachinger V, Teupe C. et al. Transplantation of Progenitor Cells and Regeneration Enhancement in Acute Myocardial Infarction (TOPCARE-AMI). Circulation 2002; 106: 3009-3017.
- 109 Chen SL, Fang WW, Ye F. et al. Effect on left ventricular function of intracoronary transplantation of autologous bone marrow mesenchymal stem cell in patients with acute myocardial infarction. Am J Cardiol 2004; 94: 92-95.
- 110 Fernandez-Aviles F, San Roman JA, Garcia-Frade J. et al. Experimental and clinical regenerative capability of human bone marrow cells after myocardial infarction. Circ Res 2004; 95: 742-748.
- 111 Schachinger V, Assmus B, Britten MB. et al. Transplantation of progenitor cells and regeneration enhancement in acute myocardial infarction: final oneyear results of the TOPCARE-AMI Trial. J Am Coll Cardiol 2004; 44: 1690-1699.
- 112 Strauer BE, Brehm M, Zeus T. et al. Repair of infarcted myocardium by autologous intracoronary mononuclear bone marrow cell transplantation in humans. Circulation 2002; 106: 1913-1918.
- 113 Erbs S, Linke A, Schachinger V. et al. Restoration of microvascular function in the infarct-related artery by intracoronary transplantation of bone marrow progenitor cells in patients with acute myocardial infarction: the Doppler Substudy of the Reinfusion of Enriched Progenitor Cells and Infarct Remodeling in Acute Myocardial Infarction (REPAIR-AMI) trial. Circulation 2007; 116: 366-374.
- 114 Wollert KC, Meyer GP, Lotz J. et al. Intracoronary autologous bone-marrow cell transfer after myocardial infarction: the BOOST randomised controlled clinical trial. Lancet 2004; 364: 141-148.
- 115 Janssens S, Dubois C, Bogaert J. et al. Autologous bone marrow-derived stem-cell transfer in patients with ST-segment elevation myocardial infarction: double-blind, randomised controlled trial. Lancet 2006; 367: 113-121.
- 116 Lunde K, Solheim S, Aakhus S. et al. Autologous stem cell transplantation in acute myocardial infarction: The ASTAMI randomized controlled trial. Intracoronary transplantation of autologous mononuclear bone marrow cells, study design and safety aspects. Scand Cardiovasc J 2005; 39: 150-158.
- 117 Srinivas G, Anversa P, Frishman WH. Cytokines and myocardial regeneration: a novel treatment option for acute myocardial infarction. Cardiol Rev 2009; 17: 1-9.