ACC/AHA 2008 statement on performance measurement and reperfusion therapy: a report of the ACC/AHA Task Force on Performance Measures (Work Group to address the challenges of Performance Measurement and Reperfusion Therapy). Circulation. 2008;118:2649 61. 20. Wang TY, Nallamothu BK, Krumholz HM, et al. Association of door-in to door-out time with reperfusion delays and outcomes among patients transferred for primary percutaneous coronary intervention. JAMA. 2011;305:2540 7. 21. Dauerman HL, Bates ER, Kontos MC, et al. Nationwide analysis of patients with ST-segment-elevation myocardial infarction transferred for primary percutaneous intervention: findings from the American Heart Association Mission: Lifeline Program. Circ Cardiovasc Interv. 2015;8:e002450. 22. Jneid H. Cardiac rehabilitation after myocardial infarction: unmet needs and future directions. JAMA Cardiol. 2016;1:978 9. 23. Aragam KG, Dai D, Neely ML, et al. Gaps in referral to cardiac reha- bilitation of patients undergoing percutaneous coronary intervention in the United States. J Am Coll Cardiol. 2015;65:2079 88. 11 24. Bangalore S, Fonarow GC, Peterson ED, et al. Age and gender differences in quality of care and outcomes for patients with ST-segment elevation myocardial infarction. Am J Med. 2012;125:1000 9. 25. Li S, Fonarow GC, Mukamal KJ, et al. Sex and race/ethnicity-related dis- parities in care and outcomes after hospitalization for coronary artery dis- ease among older adults. Circ Cardiovasc Qual Outcomes. 2016;9:S36 44. 26. Normand SL, McNeil BJ, Peterson LE, et al. Eliciting expert opinion us- ing the Delphi technique: identifying performance indicators for cardio- vascular disease. Int J Qual Health Care. 1998;10:247 60. 27. Physician Consortium for Performance Improvement. Tobacco Use: Screening and Cessation Intervention. Available at: https://www.thep- cpi.org/pcpi/media/PCPI-Maintained-Measures/Preventive-Care-and- Screening-Updated-June-2016.pdf. Accessed June 2, 2017. 28. Thomas RJ, King M, Lui K, et al. AACVPR/ACCF/AHA 2010 Update: Performance Measures on Cardiac Rehabilitation for Referral to Cardiac Rehabilitation/Secondary Prevention Services. Circulation. 2010;122:1342 50. 29. Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial in- farction. N Engl J Med. 2003;348:1309 21. 30 ISIS-2 (Second International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988;2:349 60. 31. Xian Y, Wang TY, McCoy LA, et al. Association of discharge aspirin dose with outcomes after acute myocardial infarction: insights from the Treatment with ADP Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events after Acute Coronary Syndrome (TRANSLATE-ACS) study. Circulation. 2015;132:174 81. 32. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocar- dial infarction, and stroke in high risk patients. BMJ. 2002;324:71 86. 33. Mehta SR, Bassand JP, Chrolavicius S, et al. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. N Engl J Med. 2010;363:930 42. 34. Grosser T, Fries S, Lawson JA, et al. Drug resistance and pseudoresis- tance: an unintended consequence of enteric coating aspirin. Circulation. 2013;127:377 85. 35. Barnathan ES, Schwartz JS, Taylor L, et al. Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angio- plasty. Circulation. 1987;76:125 34. 36. Jolly SS, Pogue J, Haladyn K, et al. Effects of aspirin dose on ischaemic events and bleeding after percutaneous coronary intervention: insights from the PCI-CURE study. Eur Heart J. 2009;30:900 7. 37. Chen ZM, Jiang LX, Chen YP, et al. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo- controlled trial. Lancet. 2005;366:1607 21. 38. Sabatine MS, Cannon CP, Gibson CM, et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005;352:1179 89. 39. Baigent C, Blackwell L, Collins R, et al. Aspirin in the primary and sec- ondary prevention of vascular disease: collaborative meta-analysis of indi- vidual participant data from randomised trials. Lancet. 2009;373:1849 60. 40. Mahaffey KW, Wojdyla DM, Carroll K, et al. Ticagrelor compared with clopidogrel by geographic region in the Platelet Inhibition and Patient Outcomes (PLATO) trial. Circulation. 2011;124:544 54. 41. Mehta SR, Tanguay JF, Eikelboom JW, et al. Double-dose versus stan- dard-dose clopidogrel and high-dose versus low-dose aspirin in individu- als undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. Lancet. 2010;376:1233 43. 42. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment el- evation. N Engl J Med. 2001;345:494 502. 43. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/ SCAI guideline for percutaneous coronary intervention: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation. 2011;124:e574 651. 44. Popma JJ, Berger P, Ohman EM, et al. Antithrombotic therapy during percutaneous coronary intervention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:576S 99S. 45. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet. 1996;348:1329 39. 46. Deleted in proof. 47. Schomig A, Neumann FJ, Kastrati A, et al. A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronary- artery stents. N Engl J Med. 1996;334:1084 9. 48. Freemantle N, Cleland J, Young P, et al. Beta blockade after myocar- dial infarction: systematic review and meta regression analysis. BMJ. 1999;318:1730 7. 49. BHAT Study Investigators. A randomized trial of propranolol in pa- tients with acute myocardial infarction. I. Mortality results. JAMA. 1982;247:1707 14. 50 Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383 9. 51. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coro- nary events after myocardial infarction in patients with average choles- terol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med. 1996;335:1001 9. 52. Wilt TJ, Bloomfield HE, MacDonald R, et al. Effectiveness of statin therapy in adults with coronary heart disease. Arch Intern Med. 2004;164:1427 36. 53. Baigent C, Blackwell L, Emberson J, et al. Efficacy and safety of more in- tensive lowering of LDL cholesterol: a meta-analysis of data from 170000 participants in 26 randomised trials. Lancet. 2010;376:1670 81. 54. Larsson H, Areskog M, Areskog NH, et al. Should the exercise test (ET) be performed at discharge or one month later after an episode of unsta- ble angina or non-Q-wave myocardial infarction? Int J Card Imaging. 1991;7:7 14. 55. Mahmarian JJ, Shaw LJ, Filipchuk NG, et al. A multinational study to establish the value of early adenosine technetium-99m sestamibi myo- cardial perfusion imaging in identifying a low-risk group for early hos- pital discharge after acute myocardial infarction. J Am Coll Cardiol. 2006;48:2448 57. 56. Nyman I, Larsson H, Areskog M, et al. The predictive value of silent isch- emia at an exercise test before discharge after an episode of unstable coro- nary artery disease. RISC Study Group. Am Heart J. 1992;123:324 31. 57. Starling MR, Crawford MH, Kennedy GT, et al. Treadmill exercise tests predischarge and six weeks post-myocardial infarction to detect abnor- malities of known prognostic value. Ann Intern Med. 1981;94:721 7. 58. Marwick TH, Anderson T, Williams MJ, et al. Exercise echocardiography is an accurate and cost-efficient technique for detection of coronary artery disease in women. J Am Coll Cardiol. 1995;26:335 41. 59. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocar- dial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med. 1992;327:669 77. 60. Torp-Pedersen C, Kober L. Effect of ACE inhibitor trandolapril on life expectancy of patients with reduced left-ventricular function after acute myocardial infarction. TRACE Study Group. Trandolapril Cardiac Evaluation. Lancet. 1999;354:9 12. 61. ACE inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100000 patients in random- ized trials. ACE Inhibitor Myocardial Infarction Collaborative Group. Circulation. 1998;97:2202 12. 62. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003;349:1893 906. 63. Ball SG, Hall AS, Murray GD. ACE inhibition, atherosclerosis and myo- cardial infarction the AIRE Study in practice. Acute Infarction Ramipril Efficacy Study. Eur Heart J15 suppl B199420 5. 26 30. 64. Kober L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the an- giotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Engl J Med. 1995;333:1670 6. 65. Pfeffer MA, Greaves SC, Arnold JM, et al. Early versus delayed angio- tensin-converting enzyme inhibition therapy in acute myocardial infarc- tion: the healing and early afterload reducing therapy trial. Circulation. 1997;95:2643 51. 66. Maggioni AP, Fabbri G. VALIANT (VALsartan In Acute myocardial iN- farcTion) trial. Expert Opin Pharmacother. 2005;6:507 12. 67. Garg R,Yusuf S. Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials. JAMA. 1995;273:1450 6. 68. Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting- enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. 12 The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000;342:145 53. 69. Yusuf S, Teo KK, Pogue J, et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med. 2008;358:1547 59. 70. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collabora- tive overview of early mortality and major morbidity results from all ran- domised trials of more than 1000 patients. Lancet. 1994;343:311 22. 71. Boersma E, Maas AC, Deckers JW, et al. Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. Lancet. 1996;348:771 5. 72. Goldberg RJ, Mooradd M, Gurwitz JH, et al. Impact of time to treatment with tissue plasminogen activator on morbidity and mortality following acute myocardial infarction (The second National Registry of Myocardial Infarction). Am J Cardiol. 1998;82:259 64. 73. Milavetz JJ, Giebel DW, Christian TF, et al. Time to therapy and salvage in myocardial infarction. J Am Coll Cardiol. 1998;31:1246 51. 74. Nallamothu BK, Bates ER. Percutaneous coronary intervention versus fibrinolytic therapy in acute myocardial infarction: is timing (almost) everything? Am J Cardiol. 2003;92:824 6. 75. Pinto DS, Kirtane AJ, Nallamothu BK, et al. Hospital delays in reperfu- sion for ST-elevation myocardial infarction: implications when selecting a reperfusion strategy. Circulation. 2006;114:2019 25. 76. Chareonthaitawee P, Gibbons RJ, Roberts RS, et al. The impact of time to thrombolytic treatment on outcome in patients with acute myocardial infarction. For the CORE investigators (Collaborative Organisation for RheothRx Evaluation). Heart. 2000;84:142 8. 77. McNamara RL, Herrin J, Wang Y, et al. Impact of delay in door-to-needle time on mortality in patients with ST-segment elevation myocardial infarc- tion. Am J Cardiol. 2007;100:1227 32. 78. Newby LK, Rutsch WR, Califf RM, et al. Time from symptom on- set to treatment and outcomes after thrombolytic therapy. GUSTO-1 Investigators. J Am Coll Cardiol. 1996;27:1646 55. 79. The ISAM Study Group. A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days. N Engl J Med. 1986;314:1465 71. 80. Rossi P, Bolognese L. Comparison of intravenous urokinase plus hepa- rin versus heparin alone in acute myocardial infarction. Urochinasi per via Sistemica nell'Infarto Miocardico (USIM) Collaborative Group. Am J Cardiol. 1991;68:585 92. 81. AIMS Trial Study Group. Effect of intravenous APSAC on mortality after acute myocardial infarction: preliminary report of a placebo-controlled clinical trial. Lancet. 1988;1:545 9. 82. LATE Study Group. Late Assessment of Thrombolytic Efficacy (LATE) study with alteplase 6-24 hours after onset of acute myocardial infarction. Lancet. 1993;342:759 66. 83. EMERAS (Estudio Multicentrico Estreptoquinasa Republicas de America del Sur) Collaborative Group. Randomised trial of late throm- bolysis in patients with suspected acute myocardial infarction. Lancet. 1993;342:767 72. 84 Early effects of tissue-type plasminogen activator added to conventional therapy on the culprit coronary lesion in patients presenting with ischemic cardiac pain at rest. Results of the Thrombolysis in Myocardial Ischemia (TIMI IIIA) Trial. Circulation. 1993;87:38 52. 85. Barrabes JA, Figueras J, Moure C, et al. Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation. 2003;108:814 19. 86. de Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proxi- mal LAD occlusion. N Engl J Med. 2008;359:2071 3. 87. Jong GP, Ma T, Chou P, et al. Reciprocal changes in 12-lead electrocardi- ography can predict left main coronary artery lesion in patients with acute myocardial infarction. Int Heart J. 2006;47:13 20. 88. French JK, Feldman HA, Assmann SF, et al. Influence of thrombo- lytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial. Am Heart J. 2003;146:804 10. 89. Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clini- cal score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation. 2000;102:2031 7. 90. The Global Use of Strategies to Open Occluded CoronaryArteries inAcute Coronary Syndromes (GUSTO IIb) Angioplasty Substudy Investigators. A clinical trial comparing primary coronary angioplasty with tissue plas- minogen activator for acute myocardial infarction: GUSTO IIb. N Engl J Med. 1997;336:1621 8. 91. Zijlstra F, Hoorntje JC, de Boer MJ, et al. Long-term benefit of primary angioplasty as compared with thrombolytic therapy for acute myocardial infarction. N Engl J Med. 1999;341:1413 19. 92. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intrave- nous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13 20. 93. Andersen HR, Nielsen TT, Vesterlund T, et al. Danish multicenter ran- domized study on fibrinolytic therapy versus acute coronary angioplas- ty in acute myocardial infarction: rationale and design of the DANish trial in Acute Myocardial Infarction-2 (DANAMI-2). Am Heart J. 2003;146:234 41. 94. Dalby M, Bouzamondo A, Lechat P, et al. Transfer for primary angio- plasty versus immediate thrombolysis in acute myocardial infarction: a meta-analysis. Circulation. 2003;108:1809 14. 95. Le May MR, So DY, Dionne R, et al. A citywide protocol for prima- ry PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2008;358:231 40. 96. Rokos IC, French WJ, Koenig WJ, et al. Integration of pre-hospital elec- trocardiograms and ST-elevation myocardial infarction receiving center (SRC) networks: impact on Door-to-Balloon times across 10 indepen- dent regions. JACC Cardiovasc Interv. 2009;2:339 46. 97. Sorensen JT, Terkelsen CJ, Norgaard BL, et al. Urban and rural imple- mentation of pre-hospital diagnosis and direct referral for primary per- cutaneous coronary intervention in patients with acute ST-elevation myocardial infarction. Eur Heart J. 2011;32:430 6. 98. Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coro- nary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med. 2003;349:733 42. 99. Nielsen PH, Terkelsen CJ, Nielsen TT, et al. System Delay and Timing of Intervention in Acute Myocardial Infarction (from the Danish Acute Myocardial Infarction-2 [DANAMI-2] Trial). Am J Cardiol. 2011;108:776 81. 100. Grzybowski M, Clements EA, Parsons L, et al. Mortality benefit of im- mediate revascularization of acute ST-segment elevation myocardial infarction in patients with contraindications to thrombolytic therapy: a propensity analysis. JAMA. 2003;290:1891 8. 101. Zahn R, Schuster S, Schiele R, et al. Comparison of primary angioplasty with conservative therapy in patients with acute myocardial infarction and contraindications for thrombolytic therapy. Maximal Individual Therapy inAcute Myocardial Infarction (MITRA) Study Group. Catheter Cardiovasc Interv. 1999;46:127 33. 102. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should we emergently revascularize occluded coronaries for cardiogenic shock. N Engl J Med. 1999;341:625 34. 103. Hochman JS, Lamas GA, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. 2006;355:2395 407. 104. Thune JJ, Hoefsten DE, Lindholm MG, et al. Simple risk stratification at admission to identify patients with reduced mortality from primary angioplasty. Circulation. 2005;112:2017 21. 105. Wu AH, Parsons L, Every NR, et al. Hospital outcomes in patients pre- senting with congestive heart failure complicating acute myocardial infarction: a report from the Second National Registry of Myocardial Infarction (NRMI-2). J Am Coll Cardiol. 2002;40:1389 94. 106. Glickman SW, Lytle BL, Ou FS, et al. Care processes associated with quicker door-in-door-out times for patients with ST-elevation-myocardial infarction requiring transfer: results from a statewide regionalization pro- gram. Circ Cardiovasc Qual Outcomes. 2011;4:382 8. 107. Hochman JS, Sleeper LA, White HD, et al. One-year survival following early revascularization for cardiogenic shock. JAMA. 2001;285:190 2. 108. Eagle KA, Guyton RA, Davidoff R, et al. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: summary article. A re- port of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery). Circulation. 2004;110:1168 76. 109. Antman EM, Hand M, Armstrong PW, et al. 2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2008;117:296 329. 110. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-Elevation myocardial infarction: a report of the American College of Cardiology/ 13 American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction). Developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons. Circulation. 2007;116:e148 304. 111. Fraker TD Jr, Fihn SD, Gibbons RJ, et al. 2007 chronic angina fo- cused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Group to Develop the Focused Update of the 2002 Guidelines for the Management of Patients With Chronic Stable Angina). Circulation. 2007;116:2762 72. 112. Hunt SA. ACC/AHA 2005 guideline update for the diagnosis and man- agement of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). Circulation. 2005;112:e154 235. 113. Mosca L, Banka CL, Benjamin EJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update. Circulation. 2007;115:1481 501. 114. King SB III, Smith SC Jr, Hirshfeld JW Jr, et al. 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2008;117:261 95. 115. Montalescot G, Wiviott SD, Braunwald E, et al. Prasugrel compared with clopidogrel in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (TRITON-TIMI 38): double- blind, randomised controlled trial. Lancet. 2009;373:723 31. 116. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopi- dogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357:2001 15. 117. Steg PG, James S, Harrington RA, et al. Ticagrelor versus clopidogrel in patients with ST-elevation acute coronary syndromes intended for re- perfusion with primary percutaneous coronary intervention: A Platelet Inhibition and Patient Outcomes (PLATO) trial subgroup analysis. Circulation. 2010;122:2131 41. 118. James SK, Storey RF, Khurmi NS, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes and a history of stroke or tran- sient ischemic attack. Circulation. 2012;125:2914 21. 119. Shishehbor MH, Topol EJ, Mukherjee D, et al. Outcome of multivessel coronary intervention in the contemporary percutaneous revasculariza- tion era. Am J Cardiol. 2006;97:1585 90. 120. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopi- dogrel and aspirin followed by long-term therapy in patients undergo- ing percutaneous coronary intervention: the PCI-CURE study. Lancet. 2001;358:527 33. 121. Steinhubl SR, Bhatt DL, Brennan DM, et al. Aspirin to prevent cardio- vascular disease: the association of aspirin dose and clopidogrel with thrombosis and bleeding. Ann Intern Med. 2009;150:379 86. 122. Bendz B, Eritsland J, Nakstad AR, et al. Long-term prognosis after out- of-hospital cardiac arrest and primary percutaneous coronary interven- tion. Resuscitation. 2004;63:49 53. 123. Borger van der Burg AE, Bax JJ, Boersma E, et al. Impact of percuta- neous coronary intervention or coronary artery bypass grafting on out- come after nonfatal cardiac arrest outside the hospital. Am J Cardiol. 2003;91:785 9. 124. Bulut S, Aengevaeren WR, Luijten HJ, et al. Successful out-of-hospital cardiopulmonary resuscitation: what is the optimal in-hospital treatment strategy? Resuscitation. 2000;47:155 61. 125. Garot P, Lefevre T, Eltchaninoff H, et al. Six-month outcome of emergen- cy percutaneous coronary intervention in resuscitated patients after car- diac arrest complicating ST-elevation myocardial infarction. Circulation. 2007;115:1354 62. 126. Gorjup V, Radsel P, Kocjancic ST, et al. Acute ST-elevation myocardial infarction after successful cardiopulmonary resuscitation. Resuscitation. 2007;72:379 85. 127. Hosmane VR, Mustafa NG, Reddy VK, et al. Survival and neurologic recovery in patients with ST-segment elevation myocardial infarction re- suscitated from cardiac arrest. J Am Coll Cardiol. 2009;53:409 15. 128. Kahn JK, Glazier S, Swor R, et al. Primary coronary angioplasty for acute myocardial infarction complicated by out-of-hospital cardiac ar- rest. Am J Cardiol. 1995;75:1069 70. 129. Keelan PC, Bunch TJ, White RD, et al. Early direct coronary angio- plasty in survivors of out-of-hospital cardiac arrest. Am J Cardiol. 2003;91:1461 3, A6. 130. Kern KB, Rahman O. Emergent percutaneous coronary intervention for resuscitated victims of out-of-hospital cardiac arrest. Catheter Cardiovasc Interv. 2010;75:616 24. 131. Marcusohn E, Roguin A, Sebbag A, et al. Primary percutaneous coronary intervention after out-of-hospital cardiac arrest: patients and outcomes. Isr Med Assoc J. 2007;9:257 9. 132. Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of- hospitalcardiacarrestincidenceandoutcome.JAMA.2008;300:1423 31. 133. Pleskot M, Babu A, Hazukova R, et al. Out-of-hospital cardiac ar- rests in patients with acute ST elevation myocardial infarctions in the East Bohemian region over the period 2002-2004. Cardiology. 2008;109:41 51. 134. Quintero-Moran B, Moreno R, Villarreal S, et al. Percutaneous coronary intervention for cardiac arrest secondary to ST-elevation acute myocar- dial infarction. Influence of immediate paramedical/medical assistance on clinical outcome. J Invasive Cardiol. 2006;18:269 72. 135. Richling N, Herkner H, Holzer M, et al. Thrombolytic therapy vs prima- ry percutaneous intervention after ventricular fibrillation cardiac arrest due to acute ST-segment elevation myocardial infarction and its effect on outcome. Am J Emerg Med. 2007;25:545 50. 136. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary an- giography in survivors of out-of-hospital cardiac arrest. N Engl J Med. 1997;336:1629 33. 137. Werling M, Thoren AB, Axelsson C, et al. Treatment and outcome in post-resuscitation care after out-of-hospital cardiac arrest when a modern therapeutic approach was introduced. Resuscitation. 2007;73:40 5. 138. Leppo JA, O'Brien J, Rothendler JA, et al. Dipyridamole-thallium-201 scintigraphy in the prediction of future cardiac events after acute myo- cardial infarction. N Engl J Med. 1984;310:1014 18. 139. Marwick TH, Nakatani S, Haluska B, et al. Provocation of latent left ventricular outflow tract gradients with amyl nitrite and exercise in hy- pertrophic cardiomyopathy. Am J Cardiol. 1995;75:805 9. 140. Theroux P, Waters DD, Halphen C, et al. Prognostic value of exercise testing soon after myocardial infarction. N Engl J Med. 1979;301:341 5. 141. Villella A, Maggioni AP, Villella M, et al. Prognostic significance of maximal exercise testing after myocardial infarction treated with throm- bolytic agents: the GISSI-2 data-base. Gruppo Italiano per lo Studio della Sopravvivenza Nell'Infarto. Lancet. 1995;346:523 9. 142. Keller T, Zeller T, Ojeda F, et al. Serial changes in highly sensitive troponin I assay and early diagnosis of myocardial infarction. JAMA. 2011;306:2684 93. 143. Eggers KM, Jaffe AS, Venge P, et al. Clinical implications of the change of cardiac troponin I levels in patients with acute chest pain - an evalu- ation with respect to the Universal Definition of Myocardial Infarction. Clin Chim Acta. 2011;412:91 7. 144. Apple FS, Smith SW, Pearce LA, et al. Delta changes for optimizing clinical specificity and 60-day risk of adverse events in patients present- ing with symptoms suggestive of acute coronary syndrome utilizing the ADVIA Centaur TnI-Ultra assay. Clin Biochem. 2012;45:711 13. 145. Giannitsis E, Becker M, Kurz K, et al. High-sensitivity cardiac troponin T for early prediction of evolving non-ST-segment elevation myocardial infarction in patients with suspected acute coronary syndrome and nega- tive troponin results on admission. Clin Chem. 2010;56:642 50. 146. Lindahl B, Venge P, James S. The new high-sensitivity cardiac troponin T assay improves risk assessment in acute coronary syndromes. Am Heart J. 2010;160:224 9. 147. Reichlin T, Irfan A, Twerenbold R, et al. Utility of absolute and relative changes in cardiac troponin concentrations in the early diagnosis of acute myocardial infarction. Circulation. 2011;124:136 45. 148. Apple FS, Pearce LA, Smith SW, et al. Role of monitoring changes in sensitive cardiac troponin I assay results for early diagnosis of myo- cardial infarction and prediction of risk of adverse events. Clin Chem. 2009;55:930 7. 149. Hammarsten O, Fu ML, Sigurjonsdottir R, et al. Troponin T percentiles from a random population sample, emergency room patients and patients with myocardial infarction. Clin Chem. 2012;58:628 37. 150. Santalo M, Martin A, Velilla J, et al. Using high- sensitivity tro- ponin T: the importance of the proper gold standard. Am J Med. 2013;126:709 17. 151. Aguirre FV, Varghese JJ, Kelley MP, et al. Rural interhospital trans- fer of ST-elevation myocardial infarction patients for percutane- ous coronary revascularization: the Stat Heart Program. Circulation. 2008;117:1145 52. 14 152. Henry TD, Sharkey SW, Burke MN, et al. A regional system to provide timely access to percutaneous coronary intervention for ST-elevation myocardial infarction. Circulation. 2007;116:721 8. 153. Jollis JG, Roettig ML, Aluko AO, et al. Implementation of a statewide system for coronary reperfusion for ST-segment elevation myocardial infarction. JAMA. 2007;298:2371 80. 154. American Heart Association. Get With The Guidelines. Available at: http://www.heart.org/HEARTORG/HealthcareResearch/GetWith TheGuidelinesHFStroke/Get-With-The-Guidelines HFStroke_ UCM_001099_SubHomePage.jsp. Accessed: June 2, 2017. 155. ASSENT-4 PCI Investigators. Primary versus tenecteplase-facilitated percutaneous coronary intervention in patients with ST-segment el- evation acute myocardial infarction (ASSENT-4 PCI): randomised trial. Lancet. 2006;367:569 78. 156. Bonow RO, Masoudi FA, Rumsfeld JS, et al. ACC/AHA classification of care metrics: performance measures and quality metrics: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. Circulation. 2008;118:2662 6. 157. Le May MR, So DY, Dionne R, et al. A citywide protocol for prima- ry PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2008;358:231 40. 158. National Cardiovascular Data Registry. Action Registry GWTG. Available at: http://www.ncdr.com/webncdr/ACTION/Default.aspx. Accessed: June 2, 2017. 159. QualityNet.com. Measure Comparison (Inpatient Hospital Quality Measures). Available at: http://www.qualitynet.org/dcs/ContentServer? 1138900297065. Accessed: June 10, 2009. 160. The Joint Commission. Acute Myocardial Infarction Core Measure Set. Available at: http://www.jointcommission.org/core_measure_sets.aspx. Accessed: August 28, 2014. 161. Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital mor- tality in the Global Registry of Acute Coronary Events. Arch Intern Med. 2003;163:2345 53. 162. Morrow DA, Antman EM, Giugliano RP, et al. A simple risk index for rapid initial triage of patients with ST-elevation myocardial infarction: an InTIME II substudy. Lancet. 2001;358:1571 5. 163. Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for un- stable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000;284:835 42. 164. Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation. 2000;101:2557 67. 165. Abu-Assi E, Ferreira-Gonzalez I, Ribera A, et al. Do GRACE (Global Registry of Acute Coronary events) risk scores still maintain their perfor- mance for predicting mortality in the era of contemporary management of acute coronary syndromes? . Am Heart J. 2010;160:826 34. 166. Eagle KA, Lim MJ, Dabbous OH, et al. A validated prediction mod- el for all forms of acute coronary syndrome: estimating the risk of 6-month postdischarge death in an international registry. JAMA. 2004;291:2727 33. 167. Go J, Narmi A, Sype J, et al. Impact of renal dysfunction on the prognos- tic value of the TIMI risk score in patients with non-ST elevation acute coronary syndrome. Coron Artery Dis. 2011;22:411 15. 168. Huynh T, Nasmith J, Luong TM, et al. Complementary prognostic val- ues of ST segment deviation and Thrombolysis In Myocardial Infarction (TIMI) risk score in non-ST elevation acute coronary syndromes: Insights from the Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) study. Can J Cardiol. 2009;25:e417 21. 169. Meune C, Drexler B, Haaf P, et al. The GRACE score's performance in predicting in-hospital and 1-year outcome in the era of high-sensi- tivity cardiac troponin assays and B-type natriuretic peptide. Heart. 2011;97:1479 83. 170. Pollack CV Jr, Sites FD, Shofer FS, et al. Application of the TIMI risk score for unstable angina and non-ST elevation acute coronary syndrome to an unselected emergency department chest pain population. Acad Emerg Med. 2006;13:13 18. 171. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med. 2001;344:1879 87. 172. Dolor RJ, Melloni C, Chatterjee R, et al. Treatment strategies for women with coronary artery disease. Comparative effectiveness review No. 66. Rockville, MD: Agency for Healthcare Research and Quality. Available CER66_Treatment-Coronary-Artery-Disease_FinalReport_20120816. pdf. Accessed: July 30, 2014. 173. Glaser R, Herrmann HC, Murphy SA, et al. Benefit of an early invasive management strategy in women with acute coronary syndromes. JAMA. 2002;288:3124 9. 174 Effects of tissue plasminogen activator and a comparison of early in- vasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia. Circulation. 1994;89:1545 56. 175. Lagerqvist B, Safstrom K, Stahle E, et al. Is early invasive treatment of unstable coronary artery disease equally effective for both women and men? FRISC II Study Group Investigators. J Am Coll Cardiol. 2001;38:41 8. 176. O'Donoghue ML, Vaidya A, Afsal R, et al. An invasive or conservative strategy in patients with diabetes mellitus and non-ST-segment elevation acute coronary syndromes: a collaborative meta-analysis of randomized trials. J Am Coll Cardiol. 2012;60:106 11. 177. Fox KA, Clayton TC, Damman P, et al. Long-term outcome of a routine versus selective invasive strategy in patients with non-ST-segment eleva- tion acute coronary syndrome a meta-analysis of individual patient data. J Am Coll Cardiol. 2010;55:2435 45. 178. O'Donoghue M, Boden WE, Braunwald E, et al. Early invasive vs con- servative treatment strategies in women and men with unstable angina and non-ST-segment elevation myocardial infarction: a meta-analysis. JAMA. 2008;300:71 80. 179. Damman P, Hirsch A, Windhausen F, et al. 5-year clinical outcomes in the ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes) trial a randomized comparison of an early in- vasive versus selective invasive management in patients with non- ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2010;55:858 64. 180. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med. 2001;344:1879 87. 181. de Winter RJ, Windhausen F, Cornel JH, et al. Early invasive versus se- lectively invasive management for acute coronary syndromes. N Engl J Med. 2005;353:1095 104. 182. Fox KA, Poole-Wilson PA, Henderson RA, et al. Interventional versus conservative treatment for patients with unstable angina or non-ST- elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet. 2002;360:743 51. 183. Invasive compared with non-invasive treatment in unstable coronary- artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary ar- tery disease Investigators. Lancet. 1999;354:708 15. 184. Damman P, Clayton T, Wallentin L, et al. Effects of age on long-term outcomes after a routine invasive or selective invasive strategy in patients presenting with non-ST segment elevation acute coronary syndromes: a collaborative analysis of individual data from the FRISC II - IC. Heart. 2012;98:207 13. 185. Devlin G, Gore JM, Elliott J, et al. Management and 6-month outcomes in elderly and very elderly patients with high-risk non-ST-elevation acute coronary syndromes: The Global Registry of Acute Coronary Events. Eur Heart J. 2008;29:1275 82. 186. Gale CP, Cattle BA, Woolston A, et al. Resolving inequalities in care? Reduced mortality in the elderly after acute coronary syndromes. The Myocardial Ischaemia National Audit Project 2003-2010. Eur Heart J. 2012;33:630 9. 187. Alexander KP, Newby LK, Cannon CP, et al. Acute coronary care in the elderly, part I: non-ST-segment-elevation acute coronary syndromes: a scientific statement for healthcare professionals from the American Heart Association Council on Clinical Cardiology. Circulation. 2007;115: 2549 69. 188. Bach RG, Cannon CP, Weintraub WS, et al. The effect of routine, early invasive management on outcome for elderly patients with non- ST-segment elevation acute coronary syndromes. Ann Intern Med. 2004;141:186 95. 189. Fox KA, Poole-Wilson P, Clayton TC, et al. 5-year outcome of an in- terventional strategy in non-ST-elevation acute coronary syndrome: the British Heart Foundation RITA 3 randomised trial. Lancet. 2005;366:914 20. 15 190. Mehta SR, Cannon CP, Fox KA, et al. Routine vs selective inva- sive strategies in patients with acute coronary syndromes: a col- laborative meta-analysis of randomized trials. JAMA. 2005;293: 2908 17. 191. Bhatt DL, Roe MT, Peterson ED, et al. Utilization of early invasive management strategies for high-risk patients with non-ST-segment el- evation acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. JAMA. 2004;292:2096 104. 192. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survi- vors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557 63. 193. HACA Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346: 549 56. 194. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation12218 suppl 32010S768 86. 195. Gislason GH, Jacobsen S, Rasmussen JN, et al. Risk of death or reinfarc- tion associated with the use of selective cyclooxygenase-2 inhibitors and nonselective nonsteroidal antiinflammatory drugs after acute myocardial infarction. Circulation. 2006;113:2906 13. 196. Kearney PM, Baigent C, Godwin J, et al. Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ. 2006;332:1302 8. 197. Silverman HS, Pfeifer MP. Relation between use of anti-inflammatory agents and left ventricular free wall rupture during acute myocardial in- farction. Am J Cardiol. 1987;59:363 4. 198. Bulkley BH, Roberts WC. Steroid therapy during acute myocardial in- farction. A cause of delayed healing and of ventricular aneurysm. Am J Med. 1974;56:244 50. KEY WORDS: AHA Scientific Statements acute myocardial infarction non ST-elevation myocardial infarction performance measures quality indicators quality measures ST-elevation myocardial infarction 16 Appendix A. STEMI and NSTEMI Performance Measures Performance Measures for Use in Patients With Inpatient STEMI and NSTEMI Inpatient Measures Short Title: PM-1: Aspirin at Arrival PM-1: AMI: Aspirin Received at Arrival Measure Description: Percentage of patients, age 18 y, hospitalized with AMI who received aspirin within 24 h before or after hospital arrival. Numerator Patients with AMI who have received aspirin within 24 h before or after hospital arrival Denominator All patients with AMI Denominator Exclusions Patients age <18 y Patients who leave against medical advice on day of or day after arrival Patients who die during hospitalization on day of or day after arrival Patients who are on comfort measures/hospice only documented on day of or day after arrival Patients who are transferred to another hospital for inpatient care on day of or day after arrival Patients received in transfer from the inpatient, outpatient, or ED of another facility Patients discharged on day of or day after arrival Denominator Exceptions Documentation of a medical reason for not prescribing aspirin at arrival (eg, aspirin allergy or intolerance, oral anticoagulant therapy as prearrival medication, active bleeding) Patient currently enrolled in a clinical trial precluding the use of aspirin in its protocol (eg, trials of triple versus dual therapy in atrial fibrillation patients) Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale Coronary heart disease with atherosclerotic plaque disruption (eg, rupture, erosion, ulceration) and superimposed platelet-rich thrombus formation are the main pathophysiological mechanisms causing MI (type 1 or spontaneous MI). Acute occlusion of the coronary artery by the plaque + superimposed thrombus complex results in acute imbalance in myocardial oxygen demand and supply which, when prolonged and unabated, leads to myocardial cell necrosis and infarction. Acute and complete occlusion of the coronary artery usually results in STEMI, which usually presents with persistent ST-elevation on the ECG or as an STEMI equivalent (hyperacute T-wave changes, true posterior MI, multilead ST depression with coexistent ST-elevation in lead aVR, characteristic diagnostic criteria in the setting of LBBB). On the other hand, severely obstructive but incompletely occlusive coronary lesions usually result in NSTEMI, characterized by the absence of persistent ST elevation on ECG, but rather the presence of ST depression, T-wave inversion or other nonspecific changes. Aspirin inhibits the formation of thromboxane A2, a potent stimulator of platelet aggregation, and is the first-line therapy for AMI.30 A loading dose of 162 to 325 mg of non enteric-coated aspirin formulation should be administered as soon as possible (to be crushed or chewed to achieve rapid absorption), followed preferably by an 81-mg daily dose to minimize bleeding risk.30 34 In the ISIS-2 (Second International Study of Infarct Survival) trial,30 aspirin therapy administered within the first 24 h after acute STEMI resulted in a 23% relative risk reduction in 5-week vascular mortality (or 2.4% absolute risk reduction) in patients with STEMI. Significant reductions in the incidence of non-fatal reinfarction and stroke were also observed with aspirin.30 Clinical Recommendation(s) 2013 ACCF/AHA Guideline for the Management of Patients With ST-Elevation Myocardial Infarction12 1. Aspirin 162 to 325 mg should be given before primary PCI.33,35,36 (Class I, Level of Evidence: B) 2. Aspirin (162- to 325-mg loading dose) and clopidogrel (300-mg loading dose for patients <75 years of age, 75-mg dose for patients >75 years of age) should be administered to patients with STEMI who receive fibrinolytic therapy.30,37,38 (Class I, Level of Evidence: A) 2014 AHA/ACC Guideline for the Management of Patients With Non ST-Elevation Acute Coronary Syndromes11 1. Non enteric-coated, chewable aspirin (162 mg to 325 mg) should be given to all patients with NSTE-ACS without contraindications as soon as possible after presentation, and a maintenance dose of aspirin (81 mg/d to 162 mg/d) should be continued indefinitely.7,39 42 (Class I, Level of Evidence: A) 2. Patients not on aspirin therapy should be given non enteric-coated aspirin (325 mg) as soon as possible before PCI.35,36,43,44 (Class I, Level of Evidence: B) 3. In patients with NSTE-ACS who are unable to take aspirin because of hypersensitivity or major gastrointestinal intolerance, a loading dose of clopidogrel followed by a daily maintenance dose should be administered.45 (Class I, Level of Evidence: B) ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart Association, AMI, acute myocardial infarction; ED, emergency department; ISIS-2, Second International Study of Infarct Survival; LBBB, left bundle branch block; MI, myocardial infarction; NSTE-ACS, non ST-elevation acute coronary syndrome; NSTEMI, non ST-elevation myocardial infarction; PCI, percutaneous coronary intervention; and STEMI, ST-elevation myocardial infarction. 17 Short Title: PM-2: Aspirin at Discharge PM-2: AMI: Aspirin Prescribed at Discharge Measure Description: Percentage of patients, age 18 y, hospitalized with AMI who are prescribed aspirin at hospital discharge. Numerator Patients with AMI who are prescribed aspirin at hospital discharge Denominator All patients with AMI Denominator Exclusions Patients age <18 y Patients who leave against medical advice Patients who die during hospitalization Patients who are on comfort care measures only or hospice Patients who are transferred to another hospital for inpatient acute care Denominator Exceptions Documentation of a medical reason for not prescribing aspirin at discharge (eg, aspirin allergy or intolerance, oral anticoagulant therapy at discharge, active bleeding) Patient currently enrolled in a clinical trial precluding the use of aspirin in its protocol (eg, trials of triple versus dual therapy in atrial fibrillation patients) Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale Coronary heart disease with atherosclerotic plaque disruption (eg, rupture, erosion, ulceration) and superimposed platelet-rich thrombus formation are the main pathophysiological mechanisms causing MI (type 1 or spontaneous MI). Acute occlusion of the coronary artery by the plaque + superimposed thrombus complex results in acute imbalance in myocardial oxygen demand and supply which, when prolonged and unabated, leads to myocardial cell necrosis and infarction. Aspirin inhibits the formation of thromboxane A2, a potent stimulator of platelet aggregation, and is the first-line therapy for AMI.30 Following an initial loading dose of 162 to 325 mg of non enteric-coated aspirin, an 81-mg daily dose is preferred to higher doses to minimize bleeding risk.31 34 Aspirin should be continued indefinitely after a MI.46 The Antithrombotic Trialists Collaboration s meta-analyses firmly confirmed the benefits of long-term aspirin therapy in patients at high-risk of occlusive vascular events, including patients with prior or acute MI.32 A subsequent meta-analysis inclusive of 16 secondary prevention trials (n=17000 patients) compared long-term aspirin versus control and demonstrated that aspirin allocation was associated with a 1.5% significantly lower risk of serious vascular events per year, as well as significant reductions in coronary events and total stroke events.39 Clinical Recommendation(s) 2013 ACCF/AHA Guideline for the Management of Patients With ST-Elevation Myocardial Infarction12 1. After PCI, aspirin should be continued indefinitely.13,32,47 (Class I, Level of Evidence: A) 2. Aspirin should be continued indefinitely30,37,38 (Class I, Level of Evidence: A), and clopidogrel (75 mg daily) should be continued for at least 14 days37,38 (Class I, Level of Evidence: A) and up to 1 year (Class I, Level of Evidence: C) in patients with STEMI who receive fibrinolytic therapy. 2014 AHA/ACC Guideline for the Management of Patients With Non ST-Elevation Acute Coronary Syndromes11 1. After PCI, aspirin should be continued indefinitely at a dose of 81 mg to 325 mg daily.13,39,47 (Class I, Level of Evidence: B) 2. Aspirin should be continued indefinitely. The maintenance dose should be 81 mg daily in patients treated with ticagrelor and 81 mg to 325 mg daily in all (Class I, Level of Evidence: A) ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart Association; AMI, acute myocardial infarction; MI, myocardial infarction; PCI, percutaneous coronary intervention; and STEMI, ST-elevation myocardial infarction. Appendix A. Continued 18 Short Title: PM-3: Beta Blocker at Discharge PM-3: AMI: Beta Blocker Prescribed at Discharge Measure Description: Percentage of patients, age 18 y, hospitalized with AMI, who are prescribed a beta blocker at hospital discharge. Numerator Patients with AMI who are prescribed a beta blocker* at hospital discharge *Appropriate beta blockers to be used in patients with AMI and LVSD are: bisoprolol, carvedilol, extended-release metoprolol. Denominator All patients with AMI Denominator Exclusions Patients age <18 y Patients who leave against medical advice Patients who die during hospitalization Patients who are on comfort care measures only or hospice Patients who are transferred to another hospital for inpatient acute care Denominator Exceptions Documentation of a medical reason for not prescribing a beta blocker at hospital discharge (eg, beta-blocker allergy or intolerance, advanced heart block and no pacemaker, significant bradycardia or hypotension prior to discharge, active asthma or reactive airways disease, increased risk of heart failure/cardiogenic shock, recent history of cocaine or methamphetamine use with signs of acute intoxication) Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale Beta blockers are excellent anti-ischemic and antianginal medications that decrease myocardial oxygen demand by reducing the heart rate, blood pressure, and contractility. They also reduce cardiac automaticity and the risk of VF after MI. In addition, they improve coronary perfusion by prolonging diastole. Oral beta blockers should therefore be administered to all patients with MI without contraindications for their use. Common contraindications for beta blockers use include heart failure or risk for cardiogenic shock, bradycardia, hypotension, heart block, or active bronchospasm, or acute cocaine ingestion. Patients with initial contraindications to beta blockers in the first 24 h after an AMI should be reevaluated to determine their subsequent eligibility. A systematic review of randomized controlled trials inclusive of 54234 patients with acute or prior MI demonstrated that beta blockers are effective in secondary prevention after MI and impart a 23% reduction in the odds of death in long-term trials.48 Notably, the evidence is established predominantly in the pre-reperfusion era among patients with STEMI. The effects of beta blockers appear also to be greatest among patients with MI complicated by heart failure, systolic cardiomyopathy, or ventricular arrhythmias.48 Although not prospectively studied, the AHA/ACCF secondary prevention guidelines recommend a 3-year treatment course with beta blockers for patients with Many of these patients, however, have either hypertension or heart failure/systolic cardiomyopathy, and are usually continued on an oral beta blocker indefinitely. It is advisable to use beta blockers without intrinsic sympathomimetic activity, and in patients with MI complicated with systolic cardiomyopathy with or without heart failure, 1 of the 3 proven beta blockers should be used: carvedilol, sustained-release metoprolol succinate, or bisoprolol. Clinical Recommendation(s) 2013 ACCF/AHA Guideline for the Management of Patients With ST-Elevation Myocardial Infarction12 1. Beta blockers should be continued during and after hospitalization for all patients with STEMI and with no contraindications to their use.48,49 (Class I, Level of Evidence: B) 2014 AHA/ACC Guideline for the Management of Patients With Non ST-Elevation Acute Coronary Syndromes11 1. In patients with concomitant NSTE-ACS, stabilized HF, and reduced systolic function, it is recommended to continue beta-blocker therapy with 1 of the 3 drugs proven to reduce mortality in patients with HF: sustained-release metoprolol succinate, carvedilol, or bisoprolol. (Class I, Level of Evidence: C) 2. Beta blockers should not be administered to patients with ACS with a recent history of cocaine or methamphetamine use who demonstrate signs of acute intoxication due to the risk of potentiating coronary spasm. (Class III, Level of Evidence: C) ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; ACS, acute coronary syndrome; AHA, American Heart Association; AMI, acute myocardial infarction; HF, heart failure; LVSD, left ventricular systolic dysfunction; MI, myocardial infarction; NSTE-ACS, non ST-elevation acute coronary syndrome; STEMI, ST-elevation myocardial infarction; and VF, ventricular fibrillation. Appendix A. Continued 19 Short Title: PM-4: High-Intensity Statin at Discharge PM-4: AMI: High-Intensity Statin Prescribed at Discharge Measure Description: Percentage of patients age 18 y, hospitalized with AMI, who were prescribed a high-intensity statin at hospital discharge. Numerator Patients with AMI who are prescribed a high-intensity statin* at hospital discharge *High-intensity statin dose is defined in Table 5 of the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults14 Denominator All patients with AMI Denominator Exclusions Patients age <18 y Patients who leave against medical advice Patients who die during hospitalization Patients who are discharged to hospice or who are on comfort care measures only Patients who are transferred to another acute care hospital Denominator Exceptions Documentation of a medical reason for not prescribing a high-intensity statin (eg, allergy, intolerance or contraindications to high-intensity statin(s), risk of interaction between drugs, or other medical reasons) Documentation of prescription of a moderate-intensity statin for patients >75 y of age Documentation of a patient reason for not prescribing a statin (eg, patient refusal) Patient currently enrolled in a clinical trial related to lipid-lowering therapy Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale Patients with an MI are at high risk for recurrent cardiovascular events. Statins inhibit the HMG-CoA reductase enzyme, the rate-limiting step in cholesterol biosynthesis, and are powerful drugs for lowering LDL-C, with reductions 50% observed with the high-intensity statin regimens. Statins have been shown in multiple secondary prevention trials to reduce cardiovascular events, including coronary heart disease death, recurrent MI, cerebrovascular events, coronary revascularization, and all-cause mortality.50 52 They have also been shown to delay coronary atherosclerosis progression and possibly induce plaque regression, on serial angiographic and intravascular ultrasonographic studies. Given that the clinical evidence does not support the notion of titrating statin therapy to achieve a proposed LDL-C target and that statins are beneficial in all patients at high cardiovascular risk irrespective of their LDL-C levels, the paradigm of treating patients to LDL-C targets is largely abandoned.14,18 On the other hand, high-intensity statin therapy appears to confer incremental clinical benefit compared with less intensive therapy.53 The Cholesterol Treatment Trialists conducted meta-analyses of individual participant data from randomized trials of more versus less intensive statin regimens (5 trials; 39612 patients).53 They demonstrated that more intensive regimens produced a highly significant 15% further reduction in major vascular events, driven by reductions in coronary death or non-fatal MI, coronary revascularization, and ischemic stroke.53 The 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults recommends treatment of patients 75 y of age who have clinical atherosclerotic cardiovascular disease (including those with MI) with high-intensity statin.14 Moderate-intensity statins are recommended in their counterparts >75 y of age and in those who have contraindications/intolerance to high-intensity regimens. The guideline emphasizes that statin therapy should be individualized in persons >75 y of age according to the potential for ASCVD risk-reduction benefits, adverse effects, drug-drug interactions, and patient preferences.14 Improved compliance with therapy is an impetus for timing the initiation of statin therapy before discharge in patients hospitalized with acute MI. Clinical Recommendation(s) The 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults14 : 1. High-intensity statin therapy should be initiated or continued as first-line therapy in women and men 75 years of age who have clinical ASCVD, unless contraindicated. (Class I, Level of Evidence: A) 2. In individuals with clinical ASCVD* in whom high-intensity statin therapy would otherwise be used, when high-intensity statin therapy is contraindicated or when characteristics predisposing to statin-associated adverse effects are present, moderate-intensity statin therapy should be used as the second option if tolerated. (Class I, Level of Evidence: A) 3. In individuals with clinical ASCVD* >75 years of age, it is reasonable to evaluate the potential for ASCVD risk-reduction benefits and for adverse effects, drug-drug interactions and to consider patient preferences, when initiating a moderate- or high-intensity statin. It is reasonable to continue statin therapy in those who are tolerating it. (Class IIA; Level of Evidence: B) *Clinical ASCVD includes acute coronary syndromes, history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin. Contraindications, warnings, and precautions are defined for each statin according to the manufacturer s prescribing information.14 ACC indicates American College of Cardiology; ASCVD, atherosclerotic cardiovascular disease; AHA, American Heart Association; AMI, acute myocardial infarction; HMG-CoA, 3-hydroxy-3-methylglutaryl-coenzyme A; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; and TIA, transient ischemic attack. Appendix A. Continued 20 Short Title: PM-5: Evaluation of LVEF PM-5: AMI: Evaluation of LVEF Measure Description: Percentage of patients, age 18 y, hospitalized with AMI, with documentation in the hospital record that LVEF is evaluated during hospitalization or is planned for after discharge. Numerator Patients with AMI with documentation in the hospital record that LVEF assessment, which can be either qualitative or quantitative, is done during the hospitalization or is planned for after discharge Denominator All patients with AMI Denominator Exclusions Patients age <18 y Patients who leave against medical advice Patients who die during hospitalization Patients who are on comfort care measures only or hospice Patients who are transferred to another hospital for inpatient acute care Denominator Exceptions None Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale LVEF is important from a therapeutic and prognostic standpoint for patients with acute AMI for many reasons: Patients with reduced LVEF may benefit from specific medical therapies, such as inhibitors of the renin-angiotensin-aldosterone system. The presence of LVSD may help inform and guide the invasive strategy and revascularization modality (eg, further risk stratification in patients with NSTEMI, use of percutaneous circulatory assist devices during percutaneous coronary interventions, choice of surgical revascularization). LVEF is one of the strongest predictors of long-term survival following AMI. LVEF measurement during hospitalization provides a baseline and dictates outpatient reassessment a few weeks later in patients with initially depressed post-MI LVEF. This will help guide the need for device therapy. LV function can be assessed by a variety of modalities (eg, contrast ventriculography, echocardiography, CT angiography). However, a transthoracic echocardiogram is most useful. It is noninvasive, relatively inexpensive, and helps provide a comprehensive assessment of the LV function (regional and global) and size, and rule out post-MI mechanical and other complications. Clinical Recommendation(s) 2013 ACCF/AHA Guideline for the Management of Patients With ST-Elevation Myocardial Infarction12 1. LVEF should be measured in all patients with STEMI. (Class I, Level of Evidence: C) 2014 AHA/ACC Guideline for the Management of Patients With Non ST-Elevation Acute Coronary Syndromes11 1. A noninvasive imaging test is recommended to evaluate LV function in patients with definite ACS.54 58 (Class I, Level of Evidence: C) ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; ACS, acute coronary syndrome; AHA, American Heart Association; AMI, acute myocardial infarction; CT, computed tomography; LV, left ventricular; LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction; LVSF, left ventricular systolic function, MI, myocardial infarction; NSTEMI, non ST-elevation myocardial infarction; and STEMI, ST-elevation myocardial infarction. Appendix A. Continued 21 Short Title: PM-6: ACEI or ARB for LVSD PM-6: AMI: ACEI or ARB Prescribed for LVSD at Discharge Measure Description: Percentage of patients, age 18 y, hospitalized with AMI and LVSD who are prescribed an ACEI or ARB at hospital discharge. Numerator Patients with AMI with LVSD (defined as chart documentation of a LVEF <40% or a narrative description of LVSF consistent with moderate or severe systolic dysfunction) who are prescribed an ACEI or ARB* at hospital discharge *Fixed dose combination medications that contain ACEI or ARB therapy fulfill the numerator criteria if prescribed (eg, the ARNI, sacubitril/valsartan, contains the ARB valsartan and would fulfill the measure criteria if prescribed). Denominator All AMI patients with LVSD Denominator Exclusions Patients age <18 y Patients who leave against medical advice Patients who die during hospitalization Patients who are on comfort care measures only or hospice Patients who are transferred to another hospital for inpatient care Denominator Exceptions Documentation of medical reasons for not prescribing an ACEI and not prescribing an ARB at discharge (eg, allergy or intolerance to ACEI and ARB including: angioedema, hyperkalemia, hypotension, renal artery stenosis, worsening renal function) Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale ACEIs improve survival in patients with AMI, particularly in those with reduced LVEF. They attenuate LV remodeling and infarct expansion and have a variety of additional beneficial effects (effects on ischemic preconditioning, fibrinolysis, recurrent MI, sudden death). The SAVE (Survival and Ventricular Enlargement) trial demonstrated the benefits of captopril in reducing mortality, recurrent MI and HF hospitalization in AMI patients with an LVEF <40%, but without overt HF on entry.59 Other studies showed comparable findings.60,61 ARBs are reasonable alternatives to ACEIs in patients with AMI and LVSD and can be used for patients who are intolerant to ACEIs. In the VALIANT (Valsartan in Acute Myocardial Infarction) trial, losartan was noninferior to captopril in patients with MI complicated by LVSD, HF, or both.62 Common contraindications to the use of these agents include hypotension, shock, bilateral renal artery stenosis, worsening of renal function with ACEI/ARB exposure, and drug allergy. The ARNI, valsartan/sacubitril, is the first approved ARNI for the treatment of patients with HF and reduced ejection fraction. Compared with the ACEI, enalapril, it reduced the composite endpoint of cardiovascular death or HF hospitalization in the pivotal PARADIGM-HF (Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure) trial.17 The ARNI is even recommended as a replacement therapy for symptomatic HF reduced ejection fraction with New York Heart Association class II or III who tolerate an ACEI or ARB.17 An ACEI should not be added to AMI patients already treated with an ARNI given the increased risk of angioedema and other complications (eg, hypotension, renal insufficiency). Additionally, an ARB is already a component of the ARNI regimen and as such, adding ARB is not clinically advocated. Clinical Recommendation(s) 2013 ACCF/AHA Guideline for the Management of Patients With ST-Elevation Myocardial Infarction12 1. An angiotensin-converting enzyme inhibitor (ACE) should be administered within the first 24 hours to all patients with STEMI with anterior location, HF, or ejection fraction (EF) less than or equal to 0.40, unless contraindicated.59,63 65 (Class I, Level of Evidence: A) 2. An angiotensin receptor blocker (ARB) should be given to patients with STEMI who have indications for but are intolerant of ACE inhibitors.62,66 (Class I, Level of Evidence: B) 2014 AHA/ACC Guideline for the Management of Patients With Non ST-Elevation Acute Coronary Syndromes11 1. ACE inhibitors should be started and continued indefinitely in all patients with LVEF <0.40 and in those with hypertension, diabetes mellitus, or stable chronic kidney disease (CKD), unless contraindicated.67,68 (Class I, Level of Evidence: A) 2. ARBs are recommended in patients with HF or MI with LVEF less than 0.40 who are ACE inhibitor intolerant.62,69 (Class I, Level of Evidence: A) ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; ACEI, angiotensin-converting enzyme inhibitor; AHA, American Heart Association; AMI, acute myocardial infarction; ARB, angiotensin receptor blocker; ARNI, angiotensin receptor-neprilysin inhibitor; HF, heart failure; LV, left ventricular; LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction; LVSF, left ventricular systolic function; MI; myocardial infarction; and STEMI, ST-elevation myocardial infarction. Appendix A. Continued 22 Short Title: PM-7: Door-to-Needle Time PM-7: Acute STEMI: Time to Fibrinolytic Therapy Measure Description: Percentage of patients, age 18 y, with acute STEMI, or its equivalent, who receive fibrinolytic therapy (as the primary reperfusion modality) with a time from hospital arrival to fibrinolysis 30 min. Numerator Patients with acute STEMI (or its equivalent*) defined by characteristic symptoms of myocardial ischemia with diagnostic ST elevation on ECG, whose time from hospital arrival to fibrinolytic therapy (DTN time) is 30 min *Patients with STEMI equivalent on ECG may have: hyperacute T-wave changes, true posterior MI, multilead ST depression with coexistent ST elevation in lead aVR, characteristic diagnostic criteria in the setting of LBBB. Denominator All patients with acute STEMI and its equivalent Denominator Exclusions Patients age <18 y Patients received in transfer from the inpatient, outpatient, or ED of another facility Denominator Exceptions Documentation of a medical reason for delayed fibrinolytic therapy (eg, cardiopulmonary arrest, initial suspicion of bleeding/stroke or other contraindications to use fibrinolytic therapy, respiratory failure requiring intubation, intra-aortic balloon pump insertion, late presentation >12 h after symptom onset) Documentation of a patient reason (eg, initial patient concern with bleeding hazards) Measurement Period Encounter Sources of Data Medical record or other database (eg, administrative, clinical, registry) Attribution Measure reportable at the facility or provider level Care Setting Inpatient Rationale In the ISIS-2 (Second International Study of Infarct Survival) trial,30 the fibrinolytic streptokinase significantly reduced 5-week vascular mortality by 2.8% compared to placebo, which remained significant at a median follow-up of 15 mo. 