A Review of Pharmacological Prevention of Peri-and Post-Procedural Myocardial Injury after Percutaneous Coronary Intervention
Commenced in January 2007
Frequency: Monthly
Edition: International
Paper Count: 32794
A Review of Pharmacological Prevention of Peri-and Post-Procedural Myocardial Injury after Percutaneous Coronary Intervention

Authors: Syed Dawood Md. Taimur, Md. Hasanur Rahman, Syeda Fahmida Afrin, Farzana Islam

Abstract:

The concept of myocardial injury, although first recognized from animal studies, is now recognized as a clinical phenomenon that may result in microvascular damage, no-reflow phenomenon, myocardial stunning, myocardial hibernation and ischemic preconditioning. The final consequence of this event is left ventricular (LV) systolic dysfunction leading to increased morbidity and mortality. The typical clinical case of reperfusion injury occurs in acute myocardial infarction (MI) with ST segment elevation in which an occlusion of a major epicardial coronary artery is followed by recanalization of the artery. This may occur spontaneously or by means of thrombolysis and/or by primary percutaneous coronary intervention (PCI) with efficient platelet inhibition by aspirin (acetylsalicylic acid), clopidogrel and glycoprotein IIb/IIIa inhibitors. In recent years, percutaneous coronary intervention (PCI) has become a well-established technique for the treatment of coronary artery disease. PCI improves symptoms in patients with coronary artery disease and it has been increasing safety of procedures. However, peri- and post-procedural myocardial injury, including angiographical slow coronary flow, microvascular embolization, and elevated levels of cardiac enzyme, such as creatine kinase and troponin-T and -I, has also been reported even in elective cases. Furthermore, myocardial reperfusion injury at the beginning of myocardial reperfusion, which causes tissue damage and cardiac dysfunction, may occur in cases of acute coronary syndrome. Because patients with myocardial injury is related to larger myocardial infarction and have a worse long-term prognosis than those without myocardial injury, it is important to prevent myocardial injury during and/or after PCI in patients with coronary artery disease. To date, many studies have demonstrated that adjunctive pharmacological treatment suppresses myocardial injury and increases coronary blood flow during PCI procedures. In this review, we highlight the usefulness of pharmacological treatment in combination with PCI in attenuating myocardial injury in patients with coronary artery disease.

Keywords: Coronary artery disease, Percutaneous coronary intervention, Myocardial injury, Pharmacology.

Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1336014

Procedia APA BibTeX Chicago EndNote Harvard JSON MLA RIS XML ISO 690 PDF Downloads 2261

References:


[1] Ravkilde J, Nissen H, Mickley H, Andersen PE, Thayssen P, Horder M. Cardiac troponin T and CK-MB mass release after visually successful percutaneous transluminal coronary angioplasty in stable angina pectoris. Am Heart J. 1994;127:13–20.
[2] Califf RM, Abdelmeguid AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol. 1998;31:241–251.
[3] Kugelmass AD, Cohen DJ, Moscucci M, et al. Elevation of the creatine kinase myocardial isoform following otherwise successful directional coronary atherectomy and stenting. Am J Cardiol. 1994;74:748–754.
[4] Tardiff BE, Califf RM, Tcheng JE, et al. Clinical outcomes after detection of elevated enzymes in patients undergoing percutaneous intervention. J Am Coll Cardiol. 1999;33:88–96.
[5] Simoons ML, van den Brand M, Lincoff M, et al. Minimal myocardial damage during coronary intervention is associated with impaired outcome. Eur Heart J. 1999;20:1112–1119.
[6] Ramírez-Moreno A, Cardenal R, Pera C, et al. Predictors and prognostic value of myocardial injury following stent implantation. Int J Cardiol. 2004;97:193–198.
[7] Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial wall damage and wall shear rate on platelet deposition: Ex vivo study in a swine model. Arteriosclerosis. 1986;6:312–320.
[8] Wilentz JR, Sanborn TA, Haudenschild CC, Valeri CR, Ryan TJ, Faxon DP. Platelet accumulation in experimental angioplasty: Time course in relation to cardiovascular injury. Circulation. 1987;75:636–642.
[9] Serruys PW, de Jaegere P, Kiemeneij F, et al. A comparison of balloon expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994;331:489–495.
[10] Fischman DL, Leon MB, Baim DS, et al. A randomized comparison of coronary stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331:496–501.
[11] Gawaz M, Neumann FJ, Ott I, May A, Rudiger S, Schomig A. Changes in membrane glycoproteins of circulating platelets after coronary stent implantation. Heart. 1996;76:166–172.
[12] Gawaz M, Neumann FJ, Ott I, May A, Schomig A. Platelet activation and coronary stent implantation. Effect of antitrombotic therapy. Circulation. 1996;94:279–285.
[13] van’t Hof AWJ, Liem A, de Boer MJ, Zijlstra F. For the Zwolle Myocardial Infarction Study Group. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Lancet. 1997;350:615–619.
[14] Claeys MJ, Bosmans J, Veenstra L, Jorens P, Raedt HD, Vrints CJ. Determinants and prognostic of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction. Circulation. 1999;99:1972–1977.
[15] Phillips DR, Charo IF, Parise LV, Fitzgerald LA. The platelet membrane glycoprotein IIb-IIIa complex. Blood. 1988;71:831–843.
[16] Coller BS. Platelets and thrombolytic therapy. N Engl J Med. 1990;322:33–42.
[17] Gawaz M, Neumann FJ, Ott I, Schiessler A, Schömig A. Platelet function in acute myocardial infarction treated with direct angioplasty. Circulation. 1996;93:229–237.
[18] The EPIC Investigators. Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty. N Engl J Med. 1994;330:956–961.
[19] EPILOG Investigators. Effect of the platelet glycoprotein IIb/IIIa receptor inhibitor abciximab with lowere heparin dosages on ischemic complications of the percutaneous coronary revascularization. N Engl J Med. 1997;336:1689–696.
[20] The EPISTENT Investigators. Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-IIb/IIIa blockade. Lancet. 1998;352:87–92.
[21] Islam MA, Blankenship JC, Balog C, et al. Effect of abciximab on angiographic complications during percutaneous coronary stenting in the Evaluation of Platelet IIb/IIIa Inhibition in Stenting trial (EPISTENT) Am J Cardiol. 2002;90:916–921.
[22] Montalescot G, Barragan P, Wittenberg O, et al. Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction. N Eng J Med. 2001;344:1895–1903.
[23] Montalescot G, Borentain M, Payot L, Collet JP, Thomas D. Early vs late administration of glycoprotein IIb/IIIa inhibitors in primary percutaneous coronary intervention of acute ST-segment elevation myocardial infarction. JAMA. 2004;292:362–366.
[24] Ebrahimi R, Lincoff AM, Bittl JA, et al. Bivalirudin vs heparin in percutaneous coronary intervention: a pooled analysis. J Cardiovasc Pharmacol Ther. 2005;10:209–216.
[25] Feldman DN, Wong SC, Gade CL, Gidseg DS, Bergman G, Minutello RM. Impact of bivalirudin on outcomes after percutaneous coronary revascularization with drug-eluting stents. Am Heart J. 2007;154:695–701.
[26] Schömig A, Neumann FJ, Kastrati A, et al. A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronary-artery stent. N Engl J Med. 1996;334:1084–1089.
[27] Berg JM, Kelder JC, Suttorp MJ, et al. Effect of coumarins started before coronary angioplasty on acute complications and long-term follow-up, a randomized trial. Circulation. 2000;102:386–391.
[28] Steinhubl SR, Lauer MS, Mukherjee DP, et al. The duration of pretreatment with ticlopidine prior to stenting is associated with the risk of procedure-related non-Q-wave myocardial infarctions. J Am Coll Cardiol. 1998;32:1366–1370.
[29] van der Heijden DJ, Westendorp ICD, Riezebos RK, et al. Lack of efficacy of clopidogrel pre-treatment in the prevention of myocardial damage after elective stent implantation. J Am Coll Cardiol. 2004;44:20–24.
[30] Laskey WK. Beneficial impact of preconditioning during PTCA on creatine kinase release. Circulation. 1999;99:2085–2089.
[31] Nakagawa Y, Ito H, Kitakaze M, et al. Effect of angina pectoris on myocardial protection in patients with reperfused anterior wall myocardial infarction: retrospective clinical evidence of "preconditioning” J Am Coll Cardiol. 1995;25:1076–1083.
[32] Liu GS, Thornton J, Van Winkle DM, Stanley AW, Olsson RA, Downey JM. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart. Circulation. 1991;84:350–356.
[33] Desmet WJR, Dens J, Coussement P, van de Werf F. Does adenosine prevent myocardial micronecrosis following percutaneous coronary intervention? The ADELINE pilot trial. Heart. 2002;88:293–295.
[34] Hanna GP, Yhip P, Fujise K, et al. Intracoronary adenosine administrated during rotational atherectomy of complex lesions in native coronary arteries reduces the incidence of no-reflow phenomenon. Catheter Cardiovasc Interv. 1999;48:275–278.
[35] Ellis SG, Popma JJ, Buchbinder M, et al. Relation of clinical presentation, stenosis morphology, and operator technique to the procedural results of rotational atherectomy and rotational atherectomy-facilitated angioplasty. Circulation. 1994;89:882–892.
[36] Marzilli M, Orsini E, Marraccini P, Testa R. Beneficial effects of intracoronary adenosine as an adjunct to primary angioplasty in acute myocardial infarction. Circulation. 2000;101:2154–2159.
[37] Fallen EL, Nahmias C, Scheffel A, Coates G, Beanlands R, Garnett ES. Redistribution of myocardial blood flow with topical nitroglycerin in patients with coronary artery disease. Circulation. 1995;91:1381–1388.
[38] Kurz DJ, Naegeli B, Bertel O. A double-blind, randomized study of the effect of immediate intravenous nitroglycerin on the incidence of postprocedural chest pain and minor myocardial necrosis after elective coronary stenting. Am Heart J. 2000;139:35–43.
[39] Amit G, Cafri C, Yaroslavtsev S, et al. Intracoronary nitroprusside for the prevention of the no-reflow phenomenon after primary percutaneous coronary intervention in acute myocardial infarction. A randomized, double-blind, placebo-controlled clinical trial. Am Heart J. 2006;152:887 e9–e14.
[40] Akai K, Wang Y, Sato K, et al. Vasodilatory effect of nicorandil on coronary arterial microvessels: its dependency on vessel size and the involvement of the ATP-sensitive potassium channels. J Cardiovasc Pharmacol. 1995;26:541–547.
[41] The IONA Study Group. Effect of nicorandil on coronary events in patients with stable angina: the Impact Of Nicorandil in Angina (IONA) randomised trial. Lancet. 2002;359:1269–1275.
[42] Kasama S, Toyama T, Hatori T, et al. Comparative effects of nicorandil with isosorbide mononitrate on cardiac sympathetic nerve activity and left ventricular function in patients with ischemic cardiomyopathy. Am Heart J. 2005;150:477 e1–e8.
[43] Murakami M, Iwasaki K, Kusachi S, et al. Nicorandil reduces the incidence of minor cardiac marker elevation after coronary stenting. Int J Cardiol. 2006;107:48–53.
[44] Kuwabara Y, Watanabe S, Nakaya J, et al. Postrevascularization recovery of fatty acid utilization in ischemic myocardium: a randomized clinical trial of potassium channel opener. J Nucl Cardiol. 2000;7:320–327.
[45] Iwasaki K, Samukawa M, Furukawa H. Comparison of the effects of nicorandil versus verapamil on the incidence of slow flow/no reflow during rotational atherectomy. Am J Cardiol. 2006;98:1354–1356.
[46] Ito H, Taniyama Y, Iwakura K, et al. Intravenous nicorandil can preserve microvascular integrity and myocardial viability in patients with reperfused anterior wall myocardial infarction. J Am Coll Cardiol. 1999;33:654–660.
[47] Ishii H, Ichimiya S, Kanashiro M, et al. Impact of a single intravenous administration of nicorandil before reperfusion in patients with ST-segment elevation myocardial infarction. Circulation. 2005;112:1284–1288.
[48] Kato K. Haemodynamic and clinical effects of an intravenous potassium channel opener—a review. Eur Heart J. 1993;14(Suppl. B):40–47
[49] Kojima S, Ishikawa S, Ohsawa K, Mori H. Determination of effective and safe dose for intracoronary administration of nicorandil in dogs. Cardiovasc Res. 1990;24:727–732.
[50] Reimer KA, Rasmussen MM, Jennings RB. Reduction by propranolol of myocardial necrosis following temporary coronary occlusion in dogs. Circ Res. 1973;33:353–363.
[51] Sharma SK, Kini A, Marmur JD, Fuster V. Cardioprotective effect of prior β-blocker therapy in reducing creatine kinase-MB elevation afte rcoronary intervention: benefit is extended to improvement in intermediate-term survival. Circulation. 2000;102:166–172.
[52] Ellis SG, Brener SJ, Lincoff M, et al. β-blockers before percutaneous coronary intervention do not attenuate postprocedural creatine kinase isoenzyme rise. Circulation. 2001;104:2685–2688.
[53] Wang FW, Osman A, Otero J, et al. Distal myocardial protection during percutaneous coronary intervention with an intracoronary β-blocker. Circulation. 2003;107:2914–2919.
[54] Brown NJ, Agirbasli MA, Williams GH, Litchfield WR, Vaughan DE. Effect of activation and inhibition of the rennin angiotensin system on plasma PAI-1 in humans. Hypertension. 1998;32:965–971.
[55] Schulz R, Post H, Vahlhaus C, Heusch G. Ischemic preconditioning in pigs: a graded phenomenon: its relation to adenosine and bradykinin. Circulation. 1998;98:1022–1029.
[56] Leesar MA, Jneid H, Tang XL, Bolli R. Pretreatment with intracoronary enalaprilat protects human myocardium during percutaneous coronary angioplasty. J Am Coll Cardiol. 2007;49:1607–1610.
[57] Serruys PW, de Feyter P, Macaya C, et al. Fluvastatin for prevention of cardiac events following successful first percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002;287:3215–3122.
[58] Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712–1719.
[59] Herrmann J, Lerman A, Baumgart D, et al. Preprocedural statin medication reduces the extent of periprocedural non-Q-wave myocardial infarction. Circulation. 2002;106:2180–2183.
[60] Pasceri V, Patti G, Nusca A, Pristipino C, Richichi G, Di Sciascio G. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of Myocardial Damage during Angioplasty) study. Circulation. 2004;110:674–678.
[61] Briguori C, Colombo A, Airoldi F, et al. Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction. Eur Heart J. 2004;25:1822–828.
[62] Ishii H, Ichimiya S, Kanashiro M, et al. Effects of receipt of chronic statin therapy before the onset of acute myocardial infarction: a retrospective study in patients undergoing primary percutaneous coronary intervention. Clin Ther. 2006;28:1812–819.
[63] Iwakura K, Ito H, Kawano S, et al. Chronic pre-treatment of statins is associated with the reduction of the no-reflow phenomenon in the patients with reperfused acute myocardial infarction. Eur Heart J. 2006;27:534–539.
[64] www.Health-beliefnet.com. Coronary Stenting (Copy right by Nucleus Medical Art, Inc. 2008) Last reviewed November 2007 by J.Peter Oettgen MD.
[65] Janet M. Torpy MD, Cassio Lynm MA et al. Percutenous Coronary Intervention.JAMA.Feb11, 2004;291(6):778.