ACC/AHA 2007 STEMI Guidelines Focused Update Slide Set

ACC/AHA 2007 STEMI Guidelines Focused Update Slide Set
Based on the 2007 Focused Update of the ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (STEMI): A Report of the ACC/AHA Task Force on Practice Guidelines

This slide set was adapted from the 2007 Focused Update of the ACC/AHA Guidelines for Management of Patients With ST-Elevation Myocardial Infarction (Journal of the American College of Cardiology published ahead of print on December 10, 2007, available at The full-text guidelines are also available on the Web sites: ACC ( and, AHA (

Special Thanks to Slide Set Editor Elliott M. Antman, MD, FACC, FAHA
and The 2007 STEMI Guidelines Focused Update Writing Committee Members Elliott M. Antman, MD, FACC, FAHA, Co-Chair* Mary Hand, MSPH, RN, FAHA, Co-Chair Paul W. Armstrong, MD, FACC, FAHA† Eric R. Bates, MD, FACC, FAHA Lee A. Green, MD, MPH Lakshmi K. Halasyamani, MD Judith S. Hochman, MD, FACC, FAHA Harlan M. Krumholz, MD, FACC, FAHA Gervasio A. Lamas, MD, FACC Charles J. Mullany, MB, MS, FACC David L. Pearle, MD, FACC, FAHA Michael A. Sloan, MD, FACC Sidney C. Smith, Jr., MD, FACC, FAHA *2004 Writing Committee Chair †Representing the Canadian Cardiovascular Society

Applying Classification of Recommendations and Level of Evidence
Class I Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Class IIa Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Class IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Class III Risk ≥ Benefit No additional studies needed Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL should is recommended is indicated is useful/effective/ beneficial is reasonable can be useful/effective/ beneficial is probably recommended or indicated may/might be considered may/might be reasonable usefulness/effectiveness is unknown /unclear/uncertain or not well established is not recommended is not indicated should not is not useful/effective/beneficial may be harmful

Applying Classification of Recommendations and Level of Evidence
Class I Benefit >>> Risk Procedure/ Treatment SHOULD be performed/ administered Class IIa Benefit >> Risk Additional studies with focused objectives needed IT IS REASONABLE to perform procedure/administer treatment Class IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Procedure/Treatment MAY BE CONSIDERED Class III Risk ≥ Benefit No additional studies needed Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluated Level C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated

1994 AHCPR/NHLBI UA E. Braunwald
Evolution of Guidelines for ACS 1990 1992 1994 1996 1998 2000 2002 2004 2007 1990 ACC/AHA AMI R. Gunnar 1994 AHCPR/NHLBI UA E. Braunwald Rev Upd ACC/AHA AMI T. Ryan Rev Upd Rev ACC/AHA UA/NSTEMI E. Braunwald J. Anderson Evolution of Guidelines for Management of Patients with AMI The first guideline published by the ACC/AHA described the management of patients with acute myocardial infarction (AMI). The subsequent three documents were the Agency for Healthcare and Quality/National Heart, Lung and Blood Institute sponsored guideline on management of unstable angina (UA), the revised/updated ACC/AHA guideline on AMI, and the revised/updated ACC/AHA guideline on unstable angina/non-ST segment myocardial infarction (UA/NSTEMI). The present guideline is a revision and deals strictly with the management of patients presenting with ST segment elevation myocardial infarction (STEMI). The names of the chairs of the writing committees for each of the guidelines are shown at the bottom of each box Rev, Revised; Upd, Update Rev Upd ACC/AHA STEMI E. Antman

Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)
1.57 Million Hospital Admissions - ACS UA/NSTEMI† STEMI 1.24 million Admissions per year .33 million Admissions per year Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115: *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.

Analgesia

Analgesia Morphine remains Class I for STEMI although may increase adverse events in UA/NSTEMI NSAID medications increase mortality, reinfarction, and heart failure in proportion to degree of COX-2 selectivity Discontinue on admission for STEMI Do not initiate during acute phase of management

Analgesia Patients routinely taking nonsteroidal anti-inflammatory drugs (NSAIDs) (except for aspirin), both non-selective as well as COX-2 selective agents, prior to STEMI should have those agents discontinued at the time of presentation with STEMI because of the increased risks of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.

Analgesia I IIa IIb III NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, should not be administered during hospitalization for STEMI because of the increased risks of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.

Beta-Blockers

COMMIT: Study design TREATMENT: Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placebo INCLUSION: Suspected acute MI (ST change or LBBB) within 24 h of symptom onset EXCLUSION: Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV block 1 OUTCOMES: Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge) Mean treatment and follow-up: 16 days

Increased early risk of shock
Effects of Metoprolol COMMIT (N = 45,852) Totality of Evidence (N = 52,411) Death 13% P=0.0006 ReMI 22% P=0.0002 Increased early risk of shock VF 15% P=0.002 Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms Lancet. 2005;366:1622.

Beta-Blockers Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). I IIa IIb III B I IIa IIb III B *Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age > 70 years, systolic blood pressure < 120 mmHg, sinus tachycardia > 110 or heart rate < 60, increased time since onset of symptoms of STEMI.

Beta-Blockers IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). I IIa IIb III A *Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age > 70 years, systolic blood pressure < 120 mmHg, sinus tachycardia > 110 or heart rate < 60, increased time since onset of symptoms of STEMI.

Primary PCI

Primary PCI I IIa IIb III A STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal. STEMI patients presenting to a hospital without PCI capability, and who cannot be transferred to a PCI center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated. I IIa IIb III B Note “medical contact” is defined as the “time of EMS arrival on scene” after the patient calls EMS/9-1-1 or the “time of arrival at the emergency department door” (whether PCI-capable or non–PCI-capable hospital) when the patient self-transports.

Options for Transport of Patients With STEMI and Initial Reperfusion Treatment
Hospital fibrinolysis: Door-to-Needle within 30 min. Not PCI capable Call 9-1-1 Call fast EMS on-scene Encourage 12-lead ECGs. Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min. Onset of symptoms of STEMI 9-1-1 EMS Dispatch EMS Triage Plan Inter-Hospital Transfer PCI capable GOALS 5 min. 8 min. EMS Transport Options for Transportation of STEMI Patients and Initial Reperfusion Treatment: Goals Reperfusion in patients with STEMI can be accomplished by the pharmacologic (fibrinolysis) or catheter-based (primary PCI) approaches. The overarching goal is to keep total ischemic time within 120 minutes (ideally within 60 minutes) from symptom onset to initiation of reperfusion treatment. The medical system goal is to facilitate rapid recognition and treatment of patients with STEMI such that door-to-needle (or medical-contact-to-needle) for initiation of fibrinolytic therapy can be achieved within 30 minutes or door-to-balloon (or medical-contact-to-balloon) for PCI can be achieved within 90 minutes. These goals should not be understood as “ideal” times, but rather the longest times that should be considered acceptable for a given system. Systems that are able to achieve even more rapid times for treatment of patients with STEMI should be encouraged. Note “medical contact” is defined as the “time of EMS arrival on scene” after the patient calls EMS/9-1-1 or the “time of arrival at the emergency department door” (whether PCI-capable or non-PCI-capable hospital) when the patient self-transports. Patient EMS Prehospital fibrinolysis EMS-to-needle within 30 min. EMS transport EMS-to-balloon within 90 min. Patient self-transport Hospital door-to-balloon within 90 min. Dispatch 1 min. Golden Hour = first 60 min. Total ischemic time: within 120 min. Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at Figure 1.

Facilitated PCI

Meta-analysis: Facilitated PCI vs Primary PCI
Mortality Reinfarction Major Bleeding Lytic alone N=2953 IIb/IIIa alone N=1148 Lytic +IIb/IIIa N=399 All (N=4500) 1.43 ( ) ( ) 1.03 ( ) ( ) 3.07 ( ) 1.03 ( ) 1.38 ( ) 1.71 ( ) 1.51 ( ) 0.1 1 10 0.1 1 10 0.1 1 10 Fac. PCI Better PPCI Better Fac. PCI Better PPCI Better Fac. PCI Better PPCI Better Keeley E, et al. Lancet 2006;367:579.

Facilitated PCI I IIa IIb III B A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI is not recommended and may be harmful. Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of the following are present: a. Patients are at high risk, b. PCI is not immediately available within 90 minutes, and c. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight). I IIa IIb III C

Facilitated PCI Further Studies Ongoing
Prehospital fibrinolytic therapy Better anticoagulant and antiplatelet therapy Use in circumstances of longer delays to PCI However, based on available data, facilitated PCI offered no clinical benefit, and was associated with harm when full dose fibrinolytics were used.

Rescue and Late PCI

Meta-analysis: Rescue PCI vs Conservative Tx
Outcome Rescue PCI Conservative Treatment RR (95% CI) P Mortality, % (n) 7.3 (454) 10.4 (457) 0.69 (0.46–1.05) .09 HF, % (n) 12.7 (424) 17.8 (427) 0.73 (0.54–1.00) .05 Reinfarction, % (n) 6.1 (346) 10.7 (354) 0.58 (0.35–0.97) .04 Stroke, % (n) 3.4 (297) 0.7 (295) 4.98 (1.10–22.48) Minor bleeding, % (n) 16.6 (313) 3.6 (307) 4.58 (2.46–8.55) <.001 Wijeysundera and colleagues performed a meta-analysis of 8 randomized trials enrolling 1177 patients to estimate the benefits and risks associated with rescue PCI and repeat fibrinolytic therapy compared with conservative management in patients with failed fibrinolytic therapy for STEMI. As shown on the slide, rescue PCI was associated with no significant reduction in all-cause mortality (relative risk [RR] 0.69; 95% CI, ), but was associated with significant risk reductions in heart failure (RR 0.73; 95% CI, ) and reinfarction (RR 0.58; 95% CI, ) compared with conservative treatment. Rescue PCI also was associated with an increased risk of stroke (RR 4.98; 95% CI, ) and minor bleeding (RR 4.58; 95% CI, ). In 3 trials enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and heart failure, rescue PCI was associated with a significant relative risk reduction of 28% (RR 0.72, 95% CI, ; P=.001). Further, there was an 11% absolute risk reduction (95% CI, 5%-18%; P<.001) in this composite end point with an incidence of 29.2% in the PCI arm and 41.0% in the conservative arm, leading to a number needed to treat of 9. Repeat fibrinolytic therapy was not associated with significant improvements in all-cause mortality (RR 0.68; 95% CI, ) or reinfarction (RR 1.79; 95% CI, ), but was associated with an increased risk for minor bleeding (RR 1.84; 95% CI, ). Thus, the investigators concluded that rescue PCI is associated with improved clinical outcomes for STEMI patients after failed fibrinolytic therapy, but these benefits must be interpreted in the context of potential risks. On the other hand, repeat fibrinolytic therapy is not associated with significant clinical improvement and may be associated with increased harm. In 3 trials, enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and HF, rescue PCI was associated with a significant RR reduction of 28% (RR 0.72; 95% CI, ; P=.001) Wijeysundera HC, et al. J Am Coll Cardiol. 2007;49: Wijeysundera HC, Vijayaraghavan R, Nallamothu BK, et al. Rescue angioplasty or repeat fibrinolysis after failed fibrinolytic therapy for ST-segment myocardial infarction: a meta-analysis of randomized trials. J Am Coll Cardiol. 2007;49:

Rescue PCI B B c A strategy of coronary angiography with intent to
perform PCI (or emergency CABG) is recommended in patients who have received fibrinolytic therapy and have: Cardiogenic shock in patients < 75 years who are suitable candidates for revascularization b. Severe congestive heart failure and/or pulmonary edema (Killip class III) c. Hemodynamically compromising ventricular arrhythmias. I IIa IIb III B I IIa IIb III B I IIa IIb III c

Rescue PCI A strategy of coronary angiography with intent to
perform PCI (or emergency CABG) is reasonable in patients ≥ 75 years who have received fibrinolytic therapy, and are in cardiogenic shock, provided they are suitable candidates for revascularization.

Rescue PCI A strategy of coronary angiography with intent to perform rescue PCI is reasonable for patients in whom fibrinolytic therapy has failed (ST-segment elevation < 50% resolved after 90 min following initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and a moderate or large area of myocardium at risk [anterior MI, inferior MI with right ventricular involvement or precordial ST-segment depression]. I IIa IIb III B

Rescue PCI A strategy of coronary angiography with intent to perform PCI in the absence of any of the above Class I or IIa indications might be reasonable in moderate- or high-risk patients, but its benefits and risks are not well established. The benefits of rescue PCI are greater the earlier it is initiated after the onset of ischemic discomfort. I IIa IIb III C

Rescue PCI A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is not recommended in patients who have received fibrinolytic therapy if further invasive management is contraindicated or the patient or designee do not wish further invasive care. I IIa IIb III c

Occluded Artery Trial (OAT)
Eligibility: Confirmed Index MI Total IRA occlusion 3-28 days (>24 hours) Exclusion criteria: Significant left main or 3 vessel CAD Hemodynamic or electrical instability Rest or low-threshold angina NYHA Class III-IV HF or shock RESULTS 2166 randomized 1082 PCI + optimal medical therapy 1084 Optimal medical therapy (MED) Death, MI, CHF Class IV 4 year event rate: 17.2% PCI vs 15.6% MED Hazard Ratio: PCI vs MED=1.16; 95% Cl (0.92, 1.45); p=0.20 Fatal and Non fatal MI 7.0% PCI vs 5.3% MED Hazard Ratio: PCI vs MED=1.36; 95% Cl (0.92, 2.00); p=0.13 Hochman JS, et al. Am Heart J 2005;150:627-42; Hochman JS, et al. N Engl J Med 2006;355:

Late PCI after Fibrinolysis or for Patients Not Undergoing Primary Reperfusion
IIa IIb III B PCI of a hemodynamically significant stenosis in a patent infarct artery > 24 hours after STEMI may be considered as part of a invasive strategy. PCI of a totally occluded infarct artery > 24 hours after STEMI is not recommended in asymptomatic patients with 1- or 2-vessel disease if they are hemodynamically and electrically stable and do not have evidence of severe ischemia. I IIa IIb III B

Anticoagulants

Anticoagulants Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). (Level of Evidence: A) Anticoagulant regimens with established efficacy include: ♥ UFH (LOE: C) ♥ Enoxaparin (LOE:A) ♥ Fondaparinux (LOE:B) I IIa IIb III C I IIa IIb III A Dosing regimens for UFH, enoxaparin and fondaparinux in patients undergoing reperfusion with fibrinolytics or PCI can be found in the 2007 STEMI Focused Update (Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at

Anticoagulants C For patients undergoing PCI after having
received an anticoagulant regimen, the following dosing recommendations should be followed: a. For prior treatment with UFH: administer additional boluses of UFH as needed to support the procedure taking into account whether GP IIb/IIIa receptor antagonists have been administered. (Level of Evidence: C) Bivalirudin may also be used in patients treated previously with UFH. (Level of Evidence: C) I IIa IIb III C Recommendation continues on the next slide.

Anticoagulants b. For prior treatment with enoxaparin: if the last SC dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg/kg of enoxaparin should be given. c. For prior treatment with fondaparinux: administer additional intravenous treatment with an anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa receptor antagonists have been administered. I IIa IIb III B I IIa IIb III C

Anticoagulants C Because of the risk of catheter thrombosis,
IIa IIb III C Because of the risk of catheter thrombosis, fondaparinux should not be used as the sole anticoagulant to support PCI. An additional anticoagulant with anti-IIa activity should be administered.

Unfractionated Heparin
Advantages Disadvantages Immediate anticoagulation Multiple sites of action in coagulation cascade Long history of successful clinical use Readily monitored by aPTT and ACT Indirect thrombin inhibitor so does not inhibit clot-bound thrombin Nonspecific binding to: Serine proteases Endothelial cells (can lead to variability in level of anticoagulation) Reduced effect in ACS Inhibited by PF-4 Causes platelet aggregation Nonlinear pharmacokinetics Risk of HIT Some of the advantages of unfractionated heparin include immediate anticoagulation with a bolus, multiple sites of action in the clotting cascade, and a long history of successful clinical use. UFH can be readily monitored by either activated partial thromboplastin time (aPTT) or by activated coagulation time (ACT). Some of the disadvantages of UFH include that it is an indirect thrombin inhibitor and thus, does not have the ability to inhibit clot-bound thrombin. It is characterized by areas of nonspecific binding, which can lead to variability in the level of anticoagulation. The inhibition of platelet factor 4 (PF-4) also contributes to variability in anticoagulation. Paradoxically, the long chains on UFH can actually cause platelet aggregation. Other disadvantages include nonlinear pharmacokinetics, which make the anticoagulant response to UFH nonlinear at therapeutic doses, with both the intensity and duration of effect rising disproportionately with increasing dose. Moreover, the possibility of heparin-induced thrombocytopenia (HIT) exists with UFH administration. HIT is an antibody-mediated adverse reaction to heparin that can result in venous or arterial thrombosis. Hirsh J, et al. Circulation. 2001;103: aPTT = activated partial thromboplastin time; ACT = activated coagulation time; PF-4 = platelet factor 4; HIT = heparin-induced thrombocytopenia. Hirsh J, Anand SS, Halperin JL, Fuster V. Guide to anticoagulant therapy: Heparin: A statement for healthcare professionals from the American Heart Association. Circulation. 2001;103:

ExTRACT-TIMI 25: Primary End Point (ITT) Death or Nonfatal MI
UFH 12.0% 17% RRR 9.9% Enoxaparin Primary End Point (%) Relative Risk 0.83 (95% CI, 0.77 to 0.90) P<.001 This slide shows the primary endpoint with a highly significant (P<.001) 17% reduction in the relative risk of death or nonfatal MI in an intention-to-treat analysis. As shown, the curves begin to separate early and then separate more widely beginning after the first 48 hours. There is, however, a reduction of events in the enoxaparin group even during the first 48 hours. Lost to follow-up = 3 Days after Randomization Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354: Antman EM, Morrow DA, McCabe CH, Murphy SA, Ruda M, Sadowski Z, Budaj A, Lopez-Sendon JL, Guneri S, Jiang F, White HD, Fox KA, Braunwald E, for the ExTRACT-TIMI 25 Investigators. Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction. N Engl J Med. 2006;354:

Low-Molecular-Weight Heparin
Advantages Disadvantages Increased anti-Xa to anti-IIa activity  inhibits thrombin generation more effectively Induces ↑ release of TFPI vs UFH Not neutralized by platelet factor 4 Less binding to plasma proteins (eg, acute-phase reactant proteins)  more consistent anticoagulation Lower rate of HIT vs UFH Lower fibrinogen levels Easy to administer (SC administration) Long history of clinical studies and experience, FDA-approved indications Monitoring typically unnecessary Indirect thrombin inhibitor Less reversible Difficult to monitor (no aPTT or ACT) Renally cleared Long half-life Risk of HIT This slide shows some of the advantages and disadvantages of low-molecular weight heparin. Compared with UFH, the increased anti-Xa to anti-2A activity will inhibit thrombin generation to a greater degree. LMWH also induces tissue factor pathway inhibitor release as compared with UFH and other anticoagulants, thereby enhancing anti-clotting effects. It's not neutralized by platelet factor 4, and has less binding to all the proteins resulting in more consistent anticoagulation. With fewer long chains, there is a lower rate of heparin-induced thrombocytopenia, and there are lower fibrinogen levels. LMWH is also easier to administer because of its subcutaneous administration, and has a long history of use in clinical trials and is FDA-approved for multiple different indications. Some of the disadvantages include that it has an indirect action and therefore does not bind to clot-bound thrombin. It is less reversible because of its subcutaneous administration, which makes reversal with protamine more difficult, albeit it possible. LMWH is difficult to monitor, but monitoring is typically unnecessary. It is renally cleared which necessitates does adjustments for renal dysfunction. Hirsh J, et al. Circulation. 2001;103: TFPI = tissue factor pathway inhibitor; UFH = unfractionated heparin; SC = subcutaneous; aPTT = activated partial thromboplastin time; ACT = activated coagulation time. Hirsh J, Anand SS, Halperin JL, Fuster V. Guide to anticoagulant therapy: Heparin: A statement for healthcare professionals from the American Heart Association. Circulation. 2001;103:

OASIS-6 Trial: Results Reduction in Death/MI at 30 days: Stratum 1 (No UFH indicated) P<.05 14% 14% Primary End Point: Death/Reinfarction (%) 12% 11.2% 10% 14.8% 15% 8% 13.4% 6% 12% 11.2% 9.7% 4% 8.9% 9% 2% 7.4% Frequency 0% 6% Fondaparinux Placebo Reduction in Death/MI: Stratum 2 (UFH Indicated) P=NS 3% 14% The overall results are shown on the left of this slide. The primary endpoint was reduced from 11.2% for control (either placebo or unfractionated heparin) to 9.7% with fondaparinux, a highly significant P value of This was also seen at the earlier time point of 9 days and at the later follow-up of three to six months. There were some differences at the 30 day time period in the results by strata. A significant difference in stratum one (fondaparinux vs placebo) was seen with an absolute 3% reduction in death or MI, whereas in patients who had unfractionated heparin in the control group, there was a nonsignificant difference that went from 8.7% for unfractionated heparin down to 8.3% for fondaparinux. P=.008 P=.003 P=.008 12% 0% 10% 8.3% 8.7% 30 days 9 days 3-6 months 8% p=0.97 Fondaparinux (n=6036) Control (n=6056) 6% 4% 2% 0% Yusuf S, et al. JAMA. 2006;295: Adapted with permission from Fondaparinux UFH Yusuf S, Mehta SR, Chrolavicius S, et al. for the OASIS-6 Trial Group. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA. 2006;295:

Fondaparinux Advantages Disadvantages SC administration
Potential exists for outpatient management Once-daily administration Predictable anticoagulant response Fixed dose No antigenicity Potentially no need for serologic parameters Does not cross the placenta HIT antibodies do not cross-react Decreased bleeding complications vs UFH or LMWH Difficult to monitor (no aPTT or ACT) Long half-life Catheter thrombosis during PCI The advantages of fondaparinux include that it is administered subcutaneously, which facilitates possible outpatient management with once-daily administration. It has a predictable anticoagulant response and is administered using a fixed dose (uses a milligram dose as opposed to a milligram per kilogram dose). It has no antigenicity, and thus, no need for serologic parameters. It does not cross the placenta and does not cross react with HIT antibodies. It has been shown to have decreased bleeding complications as compared with either unfractionated heparin or low molecular weight heparin. Some of the disadvantages are that it is difficult to monitor. It has a long half life (15 hours), and thrombosis on catheters has been noted when using only fondaparinux in the cath lab. Simoons ML, et al. J Am Coll Cardiol. 2004;43: Yusuf S, et al. N Engl J Med. 2066;354: Simoons ML, Bobbink IWG, Boland J, et al. A dose-finding study of fondaparinux in patients with non-ST-segment elevation acute coronary syndromes. The Pentasaccharide in Unstable Angina (PENTUA) Study. J Am Coll Cardiol. 2004;43: Yusuf S, Mehta SR, Chrolavicius S, et al. for the Fifth Organization to Assess Strategies in Acute Ischemic Syndromes Investigators. N Engl J Med. 2006;354:

Summary of Observations from Trials of Anticoagulants for STEMI
Efficacy (through 30 d) Safety Use During PCI Reviparin Fibrinolysis: probably superior to placebo.* No reperfusion: probably superior to placebo.* ↑ risk of serious bleeds† No data on reviparin alone during PCI. Additional anticoagulant with anti-IIa activity, such as UFH or bivalirudin, recommended. Fondaparinux Fibrinolysis: appears superior to control rx (placebo/UFH). Relative benefit vs placebo and UFH separately cannot be reliably determined from available data.* Primary PCI: when used alone, no advantage over UFH and trend toward worse outcome. No reperfusion: appears superior to control therapy (placebo/UFH). Relative benefit versus placebo and UFH separately cannot be reliably determined from available data.* Trend toward ↓ risk of serious bleeds† ↑ risk of catheter thrombosis when fondaparinux used alone. Additional anticoagulant with anti-IIa activity, such as UFH or bivalirudin, recommended. Enoxaparin Fibrinolysis: appears superior to UFH Enoxaparin can be used to support PCI after fibrinolysis. No additional anticoagulant needed. * See 2007 STEMI Focused Update for further discussion and subgroup analysis (Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at † Definitions of significant bleeds varied among the trials. The original references should be consulted for details. Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at Table 10.

Thienopyridines

CLARITY-TIMI 28 Primary Endpoint: Occluded Artery (or D/MI thru Angio/HD)
Odds Ratio 0.64 (95% CI ) 36% Odds Reduction 21.7 25 20 P= 15.0 Occluded Artery or Death/MI (%) 15 10 5 0.4 0.6 0.8 1.0 1.2 1.6 n=1752 n=1739 Clopidogrel better Placebo better Clopidogrel LD 300 mg MD 75 mg Placebo Sabatine N Eng J Med 2005;352:1179. STEMI, Age 18-75

COMMIT: Effect of CLOPIDOGREL on Death In Hospital
Placebo + ASA: 1,846 deaths (8.1%) Clopidogrel + ASA: 1,728 deaths (7.5%) 0.6% ARD 7% RRR P = 0.03 Dead (%) N = 45,852 No Age limit ; 26% > 70 y Lytic Rx 50% No LD given Chen ZM, et al. Lancet. 2005;366:1607. Days Since Randomization (up to 28 days)

Thienopyridines Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. Treatment with clopidogrel should continue for at least 14 days. I IIa IIb III A I IIa IIb III B

Thienopyridines In patients < 75 years who receive fibrinolytic therapy or who do not receive reperfusion therapy, it is reasonable to administer an oral clopidogrel loading dose of 300 mg. (No data are available to guide decision making regarding an oral loading dose in patients ≥ 75 years of age.) Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) can be useful in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. I IIa IIb III C I IIa IIb III C

Hospital Care

Anticoagulants It is reasonable for patients with STEMI who do not undergo reperfusion therapy to be treated with anticoagulant therapy (non-UFH regimen) for the duration of the index hospitalization, up to 8 days. Convenient strategies that can be used include those with LMWH (Level of Evidence: C) or fondaparinux (Level of Evidence: B) using the same dosing regimens as for patients who receive fibrinolytic therapy. I IIa IIb III B I IIa IIb III C I IIa IIb III B

Invasive Evaluation B C
IIa IIb III B Coronary arteriography may be considered as part of an invasive strategy for risk assessment after fibrinolytic therapy (Level of Evidence: B) or for patients not undergoing primary reperfusion. (Level of Evidence: C) I IIa IIb III C

Secondary Prevention and Long-Term Management

Secondary Prevention Ask, advise, assess, and assist patients to stop smoking – I (B) Clopidogrel 75 mg daily: PCI – I (B) no PCI – IIa (C) Statin goal: LDL-C < 100 mg/dL – I (A) consider LDL-C < 70 mg/dL – IIa (A) Daily physical activity 30 min 7 d/wk, minimum 5 d/wk – I (B) Annual influenza immunization – I (B)

Secondary Prevention and Long Term Management
Goals Class I Recommendations Smoking 2007 Goal: Complete cessation. No exposure to environmental tobacco smoke. Status of tobacco use should be asked at every visit. Every tobacco user and family member who smoke should be advised to quit at every visit. The tobacco user’s willingness to quit should be assessed. The tobacco user should be assisted by counseling and developing a plan for quitting. Follow-up, referral to special programs, or pharmacotherapy (including nicotine replacement and pharmacological rx) should be arranged. Exposure to environmental tobacco smoke at home and work should be avoided. NEW NEW

Goals Class I Recommendations Blood pressure control: 2007 Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes If blood pressure is ≥ 140/90 mm Hg or ≥ 130/80 mm Hg for patients with chronic kidney disease or diabetes: • It is recommended to initiate or maintain lifestyle modification (weight control, ↑ physical activity, alcohol moderation, sodium ↓, and emphasis on ↑ consumption of fresh fruits, vegetables, and low-fat dairy products). • It is useful as tolerated, to add blood pressure medication, treating initially with beta-blockers and/or ACE inhibitors, with the addition of other drugs such as thiazides as needed to achieve goal BP. CHANGED TEXT

Goals Class I Recommendations Lipid management: 2007 goal: LDL-C << than 100 mg/dL (if TG ≥ 200 mg/dL, non–HDL-C < 130 mg/dL Starting dietary therapy in all patients is recommended. ↓ intake of sat. fats (< 7% of total calories), trans fatty acids and cholesterol (< 200 mg/d). Adding plant stanol/sterols (2 g/d) and/or viscous fiber (> 10 g/d) is reasonable to further lower LDL-C. (Class IIa; LOE:A) Promotion of daily physical activity and weight management is recommended. It may be reasonable to encourage ↑ consumption of omega-3 fatty acids in the form of fish or in capsule form (1 g/d) for risk reduction. For treatment of elevated TG, higher doses are usually necessary for risk reduction. (Class IIb; LOE: B) NEW

Goals Class I Recommendations A fasting lipid profile should be assessed in all patients and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiation of lipid-lowering medication is indicated as recommended below before discharge according to the following schedule: LDL-C should be < 100 mg/dL. Further reduction to < 70 mg /dL is reasonable. (Class IIa; LOE: A) If baseline LDL-C is ≥ 100 mg/dL, LDL-lowering drug rx should be initiated. If on-treatment LDL-C is ≥ 100 mg/dL intensify LDL-lowering drug rx (may require LDL-lowering combination is recommended. If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-C < 70 mg/dL. (Class IIa; LOE: B) Lipid management: 2007 goal: LDL-C << than 100 mg/dL (if TG ≥ 200 mg/dL, non–HDL-C < 130 mg/dL NEW NEW

Goals Class I Recommendations Lipid management: (TG 200 mg/dL or greater) Primary goal: Non–HDL-C < 130 mg/dL If TG are ≥ 150 mg per dL or HDL-C < 40 mg per dL, weight management, physical activity, and smoking cessation should be emphasized. If TGs are 200 to 499 mg per dL, non–HDL-C target should be less than 130 mg per dL. If TGs are 200 to 499 mg/dL, non–HDL-C target is < 130 mg/dL. (Class I; LOE: B); further reduction of non–HDL-C to < 100 mg dL is reasonable. (Class IIa; LOE: B) Therapeutic options to reduce non–HDL-C include: More intense LDL-C-lowering rx is indicated Niacin (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B) Fibrate therapy (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B) If TG are ≥ 500 mg/dL, therapeutic options indicated and useful to prevent pancreatitis are fibrate or niacin before LDL-lowering rx; and treat LDL-C to goal after TG- lowering rx. Achieving non–HDL-C < 130 mg/dL is recommended. NEW

Goals Class I Recommendations Physical activity: 2007 Goal: 30 min 7 d per wk; minimum 5 d per wk For all patients, it is recommended that risk be assessed with a physical activity history and/or an exercise test to guide prescription. For all patients, encouraging 30 to 60 min of moderate-intensity aerobic activity, such as brisk walking, on most, preferably all, days of the week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work). Advising medical supervised programs (cardiac rehabilitation) for high-risk patients (e.g., recent acute coronary syndrome or revascularization, HF) is recommended. Encouraging resistance training 2 d per week may be reasonable (Class IIb; LOE: C) NEW

Goals Class I Recommendations Weight management: Goal: BMI 18.5 to 24.9 kg/m2 Waist circumference: Women: < 35 in. (102 cm) Men: < 40 in. (89 cm) It is useful to assess body mass index and/or waist circumference on each visit and consistently encourage weight maintenance/reduction through an appropriate balance of physical activity, caloric intake, and formal behavioral programs when indicated to maintain/achieve a body mass index between 18.5 and 24.9 kg/m2. The initial goal of weight loss therapy should be to reduce body weight by approximately 10% from baseline. With success, further weight loss can be attempted if indicated through further assessment. If waist circumference (measured horizontally at the iliac crest) is ≥ 35 inches (102 cm) in women and ≥ 40 inches (89 cm) in men, it is useful to initiate lifestyle changes and consider treatment strategies for metabolic syndrome as indicated.

Goals Class I Recommendations Diabetes management: Goal: HbA1c < 7% It is recommended to initiate lifestyle and pharmacotherapy to achieve near-normal HbA1c. Beginning vigorous modification of other risk factors (e.g., physical activity, weight management, BP control, and cholesterol management as recommended above) is beneficial. Coordination of diabetic care with patient’s primary care physician or endocrinologist is beneficial. NEW

Goals Class I Recommendations Antiplatelet agents/ anticoagulants: Aspirin For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162 to 325 mg daily should be given for at least 1 month after bare-metal stent implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75 to 162 mg daily. CHANGED TEXT

Goals Recommendations Antiplatelet agents/ anticoagulants: Aspirin In patients where the physician is concerned about the risk of bleeding lower-dose 75 to 162 mg of aspirin is reasonable during the initial period after stent implantation. (Class IIa; LOE: C) NEW REC

Goals Class I Recommendations Antiplatelet agents/ anticoagulants: Clopidogrel For all post-PCI patients who receive a drug-eluting stent (DES), clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a bare metal stent (BMS), clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks). CHANGED TEXT

Goals Recommendations Antiplatelet agents/ anticoagulants: Clopidogrel For all STEMI patients not undergoing stenting (medical therapy alone or PTCA without stenting), treatment with clopidogrel should continue for at least 14 d. (Class I; LOE: B) Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Class IIa; LOE: C) NEW RECS

Goals Class I Recommendations Managing warfarin to INR = 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter is recommended, and in post-STEMI patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus). Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely. In patients requiring warfarin, clopidogrel, and aspirin therapy, an INR of 2 to 2.5 is recommended with low dose aspirin (75 to 81 mg) and a 75 mg dose of clopidogrel. Antiplatelet agents/ anticoagulants: Warfarin CHANGED TEXT NEW REC NEW REC

Antiplatelet agents: NSAIDs At the time of preparation for hospital discharge, the patient’s need for treatment of chronic musculoskeletal discomfort should be assessed and a stepped care approach to pain management should be used for selection of treatments. Pain relief should begin with acetaminophen or aspirin, small doses of narcotics, or non-acetylated salicylates. It is reasonable to use non-selective NSAIDs such as naproxen if initial therapy with acetaminophen, small doses of narcotics, or non-acetylated salicylates is insufficient. I IIa IIb III C NEW REC I IIa IIb III C NEW REC

Antiplatelet agents: NSAIDs NSAIDs with increasing degrees of relative COX-2 selectivity may be considered for pain relief only for situations where intolerable discomfort persists despite attempts at stepped care therapy with acetaminophen, small doses of narcotics, nonacetylated salicylates, or non-selective NSAIDs. In all cases, the lowest effective doses should be used for the shortest possible time. NSAIDs with increasing degrees of relative COX-2 selectivity should not be administered to STEMI patients with chronic musculoskeletal discomfort when therapy with acetaminophen, small doses of narcotics, non-acetylated salicylates, or non-selective NSAIDs provides acceptable levels of pain relief. I IIa IIb III C NEW REC I IIa IIb III C CHANGED TEXT

Acetaminophen, ASA, tramadol, narcotic analgesics (short term)
Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal Symptoms with Known Cardiovascular Disease or Risk Factors for Ischemic Heart Disease Acetaminophen, ASA, tramadol, narcotic analgesics (short term) Nonacetylated salicylates Non COX-2 selective NSAIDs Select patients at low risk of thrombotic events NSAIDs with some COX-2 activity Prescribe lowest dose required to control symptoms Regular monitoring for sustained hypertension or worsening of prior blood pressure control), edema, worsening renal function, or gastrointestinal bleeding. If these events occur, consider reduction of the dose or discontinuation of the offending drug, a different drug, or alternative therapeutic modalities, as dictated by clinical circumstances. Add ASA 81 mg and PPI to patients at increased risk of thrombotic events * COX-2 Selective NSAIDs * Addition of ASA may not be sufficient protection against thrombotic events Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at

Goals Class I Recommendations Renin-Angiotensin-Aldosterone System Blockers: ACE Inhibitors ACE inhibitors should be started and continued indefinitely in all patients recovering from STEMI with LVEF ≤ 40% and for those with hypertension, diabetes, or chronic kidney disease, unless contraindicated. ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI who are not lower risk (lower risk defined as those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated. Among lower risk patients recovering from STEMI (i.e., those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed) use of ACE inhibitors is reasonable. (Class IIa; LOE: B) CHANGED TEXT NEW REC NEW REC

Goals Class I Recommendations Renin-Angiotensin-Aldosterone System Blockers: ARBs Use of ARBs is recommended in patients who are intolerant of ACE inhibitors and have HF or have had a STEMI with LVEF ≤ 40%. It is beneficial to use ARB therapy in other patients who are ACE-inhibitor intolerant and have hypertension. Considering use in combination with ACE inhibitors in systolic dysfunction HF may be reasonable. CHANGED TEXT NEW REC NEW REC

Goals Class I Recommendations Renin-Angiotensin-Aldosterone System Blockers: Aldosterone Blockade Use of aldosterone blockade in post-STEMI patients without significant renal dysfunction or hyperkalemia is recommended in patients who are already receiving therapeutic doses of an ACE inhibitor and beta blocker, have an LVEF of ≤ 40% and have either diabetes or HF. CHANGED TEXT Significant renal dysfunction: creatinine should be < 2.5 mg/dL in men and < 2.0 mg/dL in women. Hyperkalemia: potassium should be < 5.0 mEq/L.

Goals Class I Recommendations Beta- Blockers It is beneficial to start and continue beta- blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without HF symptoms, unless contraindicated. CHANGED TEXT

Goals Class I Recommendations Influenza Vaccination Patients with cardiovascular disease should have an annual influenza vaccination. NEW REC

ACC/AHA 2007 STEMI Guidelines Focused Update Slide Set

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ACC/AHA 2007 STEMI Guidelines Focused Update Slide Set

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