The surgical mortality rate remains high, especially among patients with shock, ranging Mortality risk is higher for patients with inferior-basal defects than for those with anterior-apical defects. Percutaneous closure is a less invasive option that might allow for initial hemodynamic stabilization, but experience with this approach is limited, and residual shunts are common. Further technical developments and prospective trials are required to identify patients best suited for transcatheter closure. 9.4.4. LV Free-Wall Rupture Free-wall rupture is characterized by recurrent chest pain and ST-T-wave changes, with rapid progression to hemodynamic collapse, electromechanical dissociation, and death.484 It is observed most frequently in patients with first MI, anterior infarction, the elderly, and women. Other risk factors include hypertension during the acute phase of STEMI, lack of ante- cedent angina or prior MI, absence of collateral blood flow, Q waves on ECG, use of corticosteroids or nonsteroidal anti-inflammatory drugs, and administration of fibrinolytic therapy >14 hours after symptom onset.485,486 Pseudoaneu- rysm formation with contained rupture and tamponade can be recognized with transthoracic echocardiography, and emergency surgery should be considered. Most case series of patients reaching the operating room for management of this complication are of small size, with mortality rates 9.4.5. LV Aneurysm Ventricular aneurysm formation after STEMI occurs in <5% of patients and is more frequent in those with anterior infarc- tion. Incidence rates have declined with timely reperfusion. Surgery for LV aneurysm after STEMI is rarely needed but may be considered for treatment of HF, ventricular arrhyth- mias not amenable to drugs or radiofrequency ablation, or recurrent thromboembolism despite appropriate anticoagulant therapy. 9.5. Electrical Complications During the Hospital Phase of STEMI 9.5.1. Ventricular Arrhythmias Ventricular arrhythmias are common early after onset of STEMI, and not all require intervention. Out-of-hospital cardiac arrest with STEMI is most often due to lethal ven- tricular arrhythmias, including sustained VT and VF (Sec- tion 3.6.1). The mechanisms for these arrhythmias are multifactorial and include ongoing ischemia, hemodynamic and electrolyte abnormalities, reentry, and enhanced auto- maticity. As many as 10% of hospitalized patients receiv- ing fibrinolytic therapy in the GUSTO-I trial had sustained VT/VF complicating their course.488 An analysis of patients referred for primary PCI in the APEX-AMI (Assessment of Pexelizumab in Acute Myocardial Infarction) trial reported a lower incidence of sustained VT/VF (5.7%); 90% of cases occurred within 48 hours of presentation.489 Compared with patients without VT/VF, 90-day mortality risk was 2-fold higher for patients with early VT/VF (ie, before the comple- tion of primary PCI) and 5-fold higher for patients with late VT/VF (ie, after primary PCI). Several factors were asso- ciated with the occurrence of both early and late VT/VF, including HF, hypotension, tachycardia, shock, and TIMI flow grade. Treatment consists of immediate defibrillation or cardioversion for VF or pulseless sustained VT, respectively, and antiarrhythmic drug therapy in accordance with the 2010 Advanced Cardiac Life Support guidelines for sustained VT with a pulse.490 Prevention of VT/VF is directed to correction of electrolyte and acid/base abnormalities, optimization of myocardial perfusion, eradication of ongoing ischemia, and treatment of associated complications such as HF or shock. Early (within 24 hours of presentation) administration of beta blockers has been associated with a reduction in the incidence and is recommended for all patients without con- traindications (Section 8.1). The prophylactic use of lidocaine is not recommended. Premature ventricular complexes, non- sustained VT not associated with hemodynamic compromise, and accelerated idioventricular rhythms that emerge after reperfusion are not indicative of increased SCD risk and do not require specific therapy in the acute phase of STEMI. 9.5.2. Implantable Cardioverter-Defibrillator Therapy Before Discharge Class I 1. Implantable cardioverter-defibrillator (ICD) therapy is indicated before discharge in patients who develop sustained VT/VF more than 48 hours after STEMI, provided the arrhythmia is not due to transient or reversible ischemia, reinfarction, or metabolic ab- (Level of Evidence: B) Life-threatening ventricular arrhythmias that occur >48 hours after STEMI usually are associated with signifi- cant LV systolic dysfunction and signify poor prognosis. Although previous RCTs492,494,495 have not specifically addressed this population of patients with STEMI, they have shown clear and consistent benefit of ICD therapy for survivors of sustained VT or VF arrest.493 In the absence of a reversible cause, late (>48 hours) in-hospital sustained VT/VF is an indication for ICD therapy for secondary prevention of SCD. For other at-risk patients, particularly those with significantly reduced left ventricular ejection fraction (LVEF), candidacy for ICD therapy for primary prevention of SCD should be reassessed at 40 days after discharge (Section 10.3). See the 2008 ACCF/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm 9.5.3. AF and Other Supraventricular Tachyarrhythmias AF, atrial flutter, and other supraventricular tachyarrhythmias occur frequently in patients with STEMI and are triggered by excessive sympathetic stimulation, atrial stretch due to LV or RV volume/pressure overload, atrial infarction, pericarditis, electrolyte abnormalities, hypoxia, or underlying lung dis- ease. By far the most common supraventricular arrhythmia is AF, which occurs in 8% to 22% of patients with STEMI, with higher rates in elderly patients and those with HF and hyper- tension. In a contemporary study, the incidence of new-onset AF during hospitalization was 6.3%.497 New-onset AF was significantly associated with shock, HF, stroke, and 90-day These observations mirrored those seen in earlier The cumulative incidence of AF among MI survivors with EF 0.40 over approximately 2 years of follow-up approaches 30%.500 Management of AF during hospitalization for STEMI is based on the usual considerations of rhythm versus rate con- trol and the indications for anticoagulation according to cur- For hemodynamically unstable patients or those with ongoing ischemic symptoms, treatment should be implemented according to the 2010 Advanced Cardiac Life Support guideline for management of unstable supra- If medical treatment is unsuccessful, synchronized, direct current cardioversion may be indicated. Provision of anticoagulation in the context of DAPT creates additional challenges related to the risk of bleeding (Section 9.7). 9.5.4. Bradycardia, AV Block, and Intraventricular Conduction Defects 9.5.4.1. Pacing in STEMI: Recommendation Class I 1. Temporary pacing is indicated for symptomatic bradyarrhythmias unresponsive to medical treat- ment. (Level of Evidence: C) Sinus bradycardia is common early after STEMI, particularly with inferior location. It is mediated through increased vagal tone, is usually self-limited, and gener- ally requires no treatment. It may be necessary to withhold beta blockers until the bradycardia resolves. Symptom- atic or hemodynamically important sinus bradycardia should be treated with atropine or temporary pacing if not The development of AV block and intraventricular conduc- tion delays is associated with the extent of infarction. The incidence of abnormal conduction has decreased substantially in the reperfusion era. In a survey of nearly 3 million hospi- tal discharges after MI from 1996 to 2003, the incidence of complete heart block was 3.7% in inferior/posterior MI and AV block of varying degree and persistent bundle-branch block develop in approximately 7% and 5% of patients with STEMI, respectively.506,507 High- grade (ie, second- or third-degree) AV block and persistent bundle-branch block are independently associated with worse short- and long-term prognosis in both inferior/posterior and anterior/lateral MI but are more ominous in anterior/lat- eral MI because of a relatively greater extent of myocardial First-degree AV block does not require treatment. High- grade AV block with inferior/posterior STEMI usually is transient and associated with a narrow complex/junc- tional escape rhythm that can be managed conservatively. Application of transcutaneous pacing pads for potential use is reasonable. Prophylactic placement of a temporary pac- ing system is recommended for high-grade AV block and/ or new bundle-branch (especially LBBB) or bifascicular block in patients with anterior/lateral MI. Choice of pacing system (transcutaneous versus transvenous) varies across institutions. Indications for permanent pacing for persis- tent AV block or bundle-branch block after STEMI are reviewed in the 2008 ACC/AHA/HRS device-based therapy 9.6.1. Management of Pericarditis After STEMI: Recommendations Class I 1. Aspirin is recommended for treatment of pericarditis (Level of Evidence: B) Class IIb 1. Administration of acetaminophen, colchicine, or narcotic analgesics may be reasonable if aspirin, even in higher doses, is not effective. (Level of Evidence: C) Class III: Harm 1. Glucocorticoids and nonsteroidal anti-inflammatory drugs are potentially harmful for treatment of peri- carditis after STEMI.510,511 (Level of Evidence: B) The incidence of acute pericarditis after STEMI has decreased with the aggressive use of reperfusion ther- Pericarditis should be considered in the differential diagnosis of recurrent chest pain after STEMI, particularly when the discomfort is pleuritic or posi- tional, radiates to the trapezius ridge, and is associated with a pericardial friction rub. Recurrent or worsening ST elevation without early T-wave inversion may be present. Distinction from reinfarction or acute stent thrombosis is crucial. In rare circumstances, if pain is persistent (>1 week) and accompa- nied by systemic features of malaise, fever, and increased inflammatory biomarkers, Dressler syndrome should be con- sidered. In most cases, the pain is self-limited and responds to conservative measures. The use of colchicine has been extrap- olated from its efficacy in other settings. Although pericarditis is not an absolute contraindication to anticoagulation,514 cau- tion should be exercised because of the potential for hemor- Asymptomatic pericardial effusions are common after It is important to exclude free-wall rupture when a pericardial effusion is present,518,519 especially if the O Gara et al 2013 ACCF/AHA STEMI Guideline e395 Whentamponadeispresent,free- wall rupture, hemorrhagic conversion, or aortic dissection should be considered.Anticoagulation should be discontinued in the pres- ence of a significant ( 1 cm) or enlarging pericardial effusion. 9.7. Thromboembolic and Bleeding Complications 9.7.1. Thromboembolic Complications 9.7.1.1. Anticoagulation: Recommendations Class I 1. Anticoagulant therapy with a vitamin K antagonist should be provided to patients with STEMI and AF with CHADS2 score# greater than or equal to 2, me- chanical heart valves, venous thromboembolism, or hypercoagulable disorder. (Level of Evidence: C) 2. The duration of triple antithrombotic therapy with a vitamin K antagonist, aspirin, and a P2Y12 receptor inhibitor should be minimized to the extent possible to limit the risk of bleeding.** (Level of Evidence: C) Class IIa 1. Anticoagulant therapy with a vitamin K antagonist is reasonable for patients with STEMI and asymptom- atic LV mural thrombi. (Level of Evidence: C) Class IIb 1. Anticoagulant therapy may be considered for pa- tients with STEMI and anterior apical akinesis or dyskinesis. (Level of Evidence: C) 2. Targeting vitamin K antagonist therapy to a lower international normalized ratio (eg, 2.0 to 2.5) might be considered in patients with STEMI who are re- ceiving DAPT. (Level of Evidence: C) Previous recommendations for the use of vitamin K antagonists, either alone or in combination with low-dose aspirin, for second- ary prevention or for reducing the risk of systemic thromboem- bolism after STEMI, must be reconsidered in the era of DAPT.4,48 The availability of several P2Y12 receptor inhibitors has virtually eliminated the former reliance on vitamin K antagonists as an alternative to aspirin for aspirin-allergic patients. A meta-analy- sis of RCTs comparing warfarin plus aspirin to aspirin alone in patients with ACS showed that in studies with an international normalized ratio goal of 2.0 to 3.0, combination therapy was associated with a significant reduction in major adverse events at the expense of an increased risk of major bleeding.521 None of the trials included patients treated with primary PCI or DAPT. Triple therapy with a vitamin K antagonist, aspirin, and a receptor inhibitor should be restricted to specific clini- cal situations after STEMI in which the risk of systemic or venous thromboembolism or stent thrombosis is considered to exceed that of bleeding. Patient preferences and values should be taken into consideration, because individuals may weigh these outcomes differently. The novel oral anticoagulants such as dabigatran have not been evaluated in this context, and thus no recommendation for their use can be made. The duration of vitamin K antagonist therapy can be limited to 3 months in patients with or at risk for LV thrombus (eg, those with antero- apical akinesis or dyskinesis), whereas the duration of DAPT could be predicated on stent type or whether STEMI treatment included a stent.219,522,523 For patients undergoing primary PCI who require anticoagulation, avoidance of a DES is strongly preferred. When triple therapy is used, an international nor- malized ratio targeted to a range of 2.0 to 2.5 might be rea- sonable, though prospective data are lacking. Use of DAPT alone with aspirin and clopidogrel also might be considered for patients with STEMI who have AF and low to intermediate CHADS2 scores (0 to 1), with reconsideration of the indica- tions for anticoagulation over time.296,522 The incidence of venous thromboembolic events after STEMI has declined significantly,526 though patients with HF or on prolonged bed rest remain at risk.527 The approach to the prevention and treatment of venous thromboembolic disease during hospitalization, with both pharmacological and mechan- ical measures, is similar to that for other critically ill patients.528 9.7.1.2. Heparin-Induced Thrombocytopenia HIT, with or without associated thrombosis, can infrequently particularlypatients who previously have been exposed to heparin or who receive hep- arin over several hospital days. From 1% to 5% of all patients receiving heparin will develop HIT, and of these, 25% to 50% will develop thrombotic complications. In the CATCH (Complica- tions After Thrombocytopenia Caused by Heparin) registry,530,531 thrombocytopenia was common among those who received hepa- rin for >96 hours (36.4%) and was associated with a significantly increased risk of death, MI, or HF. Recognition of HIT frequently was delayed, and treatment often did not include a direct thrombin inhibitor. Data on the use of direct thrombin inhibitors in patients with STEMI who develop HIT are limited.532,533 For patients with STEMI and HIT who require stenting, bivalirudin would be the preferred anticoagulant. Management of patients with HIT who require urgent CABG can be more difficult.534 9.7.2. Bleeding Complications Despite variable definitions for major and minor bleeding used in clinical trials, bleeding that complicates the course of an ACS, including STEMI, is independently associated with recurrent MI, stroke, death, longer hospital stay, and increased cost. The risk of death increases as a function of the severity of bleeding, independent of the success or failure of reperfusion therapy. In a pooled analysis from 4 ACS tri- als, the adjusted hazard ratio for death within 30 days ranged from 1.6 with mild bleeding to 10.6 with severe bleeding.535 Most bleeding is procedure related, although gastrointestinal and intracerebral bleeding may be more life threatening. Fac- tors likely to contribute to adverse outcomes with ACS-related These recommendations apply to patients who receive intracoronary stents during PCI for STEMI. Among individuals with STEMI who do not receive an intracoronary stent, the duration of DAPT beyond 14 days has not been studied adequately for patients who undergo balloon angioplasty alone, are treated with fibrinolysis alone, or do not receive reperfusion therapy. In this subset of patients with STEMI who do not receive an intracoronary stent, the threshold for initiation of oral anticoagulation for secondary prevention, either alone or in combination with aspirin, may be lower, especially if a shorter duration (ie, 14 days) of DAPT is planned.521 #CHADS2 (Congestive heart failure, Hypertension, Age 75 years, Diabetes mellitus, previous Stroke/transient ischemic attack [doubled risk weight]) score. **Individual circumstances will vary and depend on the indications for triple therapy and the type of stent placed during PCI. After this initial treatment period, consider therapy with a vitamin K antagonist plus a single antiplatelet agent. For patients treated with fibrinolysis, consider triple therapy for 14 days, followed by a vitamin K antagonist plus a single antiplatelet agent.522 525 bleeding include patient comorbidities,536,537 discontinuation of antiplatelet or anticoagulant therapy in response to bleeding,536,538 and blood transfusion.539,540 Additional considerations include types of antiplatelet or anticoagulant agent at time of PCI,248,541,542 number of antithrombotic agents used,533 duration of therapy, crossover from low-molecular-weight heparin to UFH, HF or shock, diabetes mellitus, peripheral artery disease, and prior warfarin use. If triple antithrombotic therapy is required after discharge, the risk of bleeding increases (Figure 4).533 Risk factors for bleeding in patients with ACS have been identified from several clinical trials535,544 546 (Table 13). Predictive models for major bleeding in patients with ACS and in patients undergoing PCI have been reported from the NCDR ACTION Registry GWTG.547,548 An analy- sis from the ACTION Registry GWTG suggests that the CRUSADE bleeding risk score, developed in patients with non ST-elevation MI, may be extended to the STEMI popula- Major bleeding occurred in 2.8% of >40000 patients with acute MI in the GRACE Registry.536 Patients who expe- rienced a major bleeding episode were more likely to die in hospital than were those who did not bleed (20.9% versus 5.6%; P<0.001), even after adjustment for several relevant demographic and clinical variables. One in 5 patients with a major bleed did not survive to hospital discharge; these patients accounted for 10% of all hospital deaths and were older, more severely ill, and more likely to undergo invasive proce- dures. In ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment Thrombolysis In Myocardial Infarction 25), high 30-day mor- tality rates after major bleeding in patients with STEMI treated with fibrinolysis and either unfractionated or low-molecular- weight heparin were driven largely by the very poor progno- sis associated with ICH (65% mortality rate).537 The overall incidence of ICH in this study was 0.6%.332 The relationship between non-ICH bleeding and death in both ExTRACT-TIMI 25 and TRITON-TIMI 38 may have been confounded by patient attributes, severity of illness, and treatment protocols.537,550 To minimize the risk of bleeding complications, an assessment of patient, procedural, and pharmacological risk factors should be performed at time of presentation with STEMI and continu- ously thereafter. As an example, a longer time to PCI may be justifiable if the risk of hemorrhage with fibrinolysis is consid- ered prohibitive. Evidence suggests that although anemia is a risk factor for bleeding, the threshold for transfusion should be high.551 Absent ongoing ischemia, transfusion should be avoided unless the hemoglobin level is <8 mg/dL. The optimal hemo- globin level in the transfused patient is not known, but the number of units provided should be minimized.539,552 9.7.2.1. Treatment of ICH Older age, female sex, low body weight (<70 kg [female] and <80 kg [male]), prior stroke, and hypertension on presenta- tion (with a graded increase beginning at >160 to 170 mmHg systolic) are the major risk factors for ICH. Once ICH is rec- ognized, all antiplatelet and anticoagulant therapy should be stopped. Brain imaging with emergency neurological and neurosurgical consultation is required. Consideration can be given to the use of protamine, fresh frozen plasma, prothrom- bin complex concentrates, activated factor VII,555 and platelets as indicated. Resumption and timing of anticoagulant and/or antiplatelet therapy after ICH should be individualized and guided by neurosurgical consultation.556 9.7.2.2. Vascular Access Site Bleeding Vascular access site bleeding is the most common type of bleeding after STEMI, particularly after PCI. PCI trials have identified female sex, advanced age, renal insufficiency, ane- mia, IABP, use of GP IIb/IIIa antagonists, and low-molecu- lar-weight heparin within 48 hours of PCI as risk factors for femoral access site bleeding.557 Larger sheath size, postpro- cedural heparin use, higher activated clotting times, and late postprocedural sheath removal increases the risk of access site bleeding and should be avoided. Radial artery access may decrease bleeding complications and should be con- sidered whenever feasible,558 but procedural success with this technique is dependent on operator experience.559,560 Among patients with STEMI in the RIVAL (Radial Versus Femoral Access for Coronary Angiography and Interven- tion in Patients with Acute Coronary Syndromes) trial, radial artery access appeared to reduce the rate of the primary composite outcome (death, MI, stroke, non CABG-related Figure 4. Adjusted risk of nonfatal and fatal bleeding in patients treated with aspirin, clopidogrel, and/or vitamin K antagonists after first MI. Compared with aspirin alone, triple therapy is associated with a 3- to 4-fold increased risk of fatal and nonfa- tal bleeding. CI indicates confidence interval; HR, hazard ratio; and MI, myocardial infarction. Adapted with permission from S rensen et al.533 Table 13. Selected Risk Factors for Bleeding in Patients With ACS Advanced age (>75 y) Female sex HF or shock Diabetes mellitus Body size History of GI bleeding Presentation with STEMI or NSTEMI (vs UA) Severe renal dysfunction (CrCl <30 mL/min) Elevated white blood cell count Anemia Use of fibrinolytic therapy Invasive strategy Inappropriate dosing of antithrombotic medications Chronic oral anticoagulant therapy ACS indicates acute coronary syndrome; CrCl, creatinine clearance; GI, gastro intestinal; HF, heart failure; NSTEMI, non ST-elevation myocardial infarction; STEMI, ST-elevation myocardial infarction; and UA, unstable O Gara et al 2013 ACCF/AHA STEMI Guideline e397 major bleeding) and the individual secondary outcomes of death, MI, stroke, and overall mortality. However, rates of major bleeding were not lower with radial versus femoral access in patients with STEMI, though rates of major vascular complications were significantly reduced.561 Although arterial closure devices have been associated with decreased femoral access site bleeding, more rapid hemostasis, and shorter dura- tion of bed rest,251,562,563 their routine use cannot be advocated specifically to reduce vascular complications after PCI, given the lack of robust, directionally consistent data on their effi- cacy and safety compared with manual compression.564 566 Retroperitoneal bleeding should be suspected when the fol- lowing are seen: unheralded intraprocedural or postprocedural hypotension and bradycardia (or tachycardia), high vascular puncture site, and an otherwise unexplained decrease in hemo- globin. Prompt computed tomographic imaging of the abdo- men and pelvis may be helpful. Conservative management usually suffices, but early vascular interventional or surgical consultation should be obtained.219 9.8. Acute Kidney Injury The risk of renal failure with STEMI relates to a host of factors, including patient age, prehospital renal function, medications, contrast volume, and hemodynamic status. Contrast-induced nephropathy after angiography and intervention for STEMI is always a risk, and attention to minimization of contrast vol- ume and optimal hydration is required.219 There is a U-shaped relationship between glucose levels and death in STEMI andACS.567 The mortality rate associated with hypoglycemia appears to be as high as the mortality rate asso- ciated with hyperglycemia.568,569 Concern about overly aggres- sive glycemic control in critically ill patients was raised by the NICE-SUGAR (Normoglycemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation) trial.570 In this study of medical and surgical intensive care unit patients, tight glucose control (81 to 108 mg/dL) compared to modest control (<180 mg/dL) was associated with increased mortality rate (primarily from cardiovascular causes) and more episodes of hypoglycemia. Blood glucose levels should be maintained below 180 mg/dL if possible while avoiding hypoglycemia. There is no established role for glucose-insulin-potassium infusions in patients with STEMI.571 573 10. Risk Assessment After STEMI Initial risk stratification should be performed early (Section 3) with the use of information available at the time of pre- sentation. However, risk assessment is a continuous process that requires recalibration on the basis of data obtained dur- ing the hospital stay. Such data include the success of reper- fusion therapy, events that occur during the hospital course (such as hemorrhagic complications), and the findings from noninvasive and invasive testing, particularly as they relate to the assessment of LV systolic function. For example, in patients treated with fibrinolytic therapy, clinical and ECG indicators of failed reperfusion identify individuals who should undergo urgent coronary angiography with intent to In addition, the emergence of HF or signifi- cant LV systolic dysfunction is among the strongest predictors of higher-mortality risk after STEMI. Stable patients with a low risk of complications may be candidates for early discharge. Among patients with STEMI managed with fibrinolysis, it has been suggested that an uncomplicated course after 72 hours of hospitalization identi- fies a group with sufficiently low risk to enable discharge.574,575 Newby and colleagues calculated that extending the hospital stay of these patients by another day would cost $105629 per year of life saved. However, the duration of hospitalization in patients treated with reperfusion therapy may be determined by other needs, such as patient education or titration of medi- cations to optimum doses.576 Physicians and patients must individualize strategies for risk reduction, using lifestyle interventions, disease-modifying pharmacological therapies, and additional coronary revascular- ization when indicated.All patients with STEMI are considered to be at sufficiently high risk to merit interventions for second- ary prevention, including the use of cardiac rehabilitation, aspi- rin, lipid-lowering therapy, beta blockers, and ACE inhibitors Additional risk assessment should be used to guide decisions about performance of coronary angiography in patients who did not undergo an invasive evaluation as part of their initial treatment strategy and to guide consideration of interventions to reduce the risk of SCD due to arrhythmia. 10.1. Use of Noninvasive Testing for Ischemia Before Discharge: Recommendations Class I 1. Noninvasive testing for ischemia should be performed before discharge to assess the presence and extent of inducible ischemia in patients with STEMI who have not had coronary angiography and do not have high- risk clinical features for which coronary angiogra- phy would be warranted.577 579 (Level of Evidence: B) Class IIb 1. Noninvasive testing for ischemia might be considered before discharge to evaluate the functional signifi- cance of a noninfarct artery stenosis previously iden- tified at angiography. (Level of Evidence: C) 2. Noninvasive testing for ischemia might be considered before discharge to guide the postdischarge exercise prescription. (Level of Evidence: C) Noninvasive testing for ischemia provides valuable informa- tion about the presence of residual ischemia in patients who have not undergone cardiac catheterization during initial management of STEMI and may be useful in assessing the functional significance of a noninfarct artery stenosis identi- fied at angiography. In the latter instance, stress imaging to localize ischemia would be appropriate.580,581 Exercise test- ing early after STEMI may also be performed to 1) assess functional capacity and the ability to perform tasks at home and at work, 2) evaluate the efficacy of medical therapy, and 3) assess the risk of a subsequent cardiac event. Symptom- limited exercise testing is a key feature of the intake evalua- tion for enrollment in a program of cardiac rehabilitation 2 weeks after discharge.582 Low-level exercise testing after MI appears to be safe if patients have undergone in-hospital cardiac rehabilitation, including low-level exercise; have had no symptoms of angina or HF; and have a stable baseline ECG 48 to 72 hours before Two different protocols have been used for early post-MI exercise testing: the traditional submaximal exercise test (done at 3 to 5 days in patients without complications) or a symptom-limited exercise test (done at 5 days or later) with- out stopping at a prespecified target heart rate or metabolic equivalent level. RCTs of early exercise testing after PCI have excluded patients with recent MI.584 Limited data exist on the safety of early symptom-limited exercise testing after MI; therefore, clinical judgment must be used.585 Pharmacological stress myocardial perfusion imaging has been shown to have predictive value for postinfarction cardiac events and is useful and safe in patients who are unable to exercise.586 The opti- mum timing for provocative testing for ischemia after STEMI remains unresolved. It is argued that a predischarge exercise test may provide psychological benefit to the patient and will permit detection of profound ischemia or other indicators of high risk that could be associated with postdischarge cardiac events that might occur before a symptom-limited stress test scheduled weeks later.585 A predischarge study also provides parameters for exercise prescription in the first few days after return home, before enrollment in cardiac rehabilitation. On the other hand, deferring exercise testing until approximately 3 weeks after STEMI in clinically low-risk patients appears safe and reasonable and enables more optimal assessment of functional capacity. It is the consensus of the writing com- mittee that patients without complications who have not undergone coronary angiography and who might be potential candidates for revascularization should undergo provocative testing before hospital discharge. In patients with noninfarct artery disease who have undergone successful PCI of the infarct artery and have an uncomplicated course, it is reason- able to proceed with discharge and plans for close clinical follow-up with stress imaging within 3 to 6 weeks. 10.2. Assessment of LV Function: Recommendation Class I 1. LVEF should be measured in all patients with STEMI. (Level of Evidence: C) LV function is one of the strongest predictors of survival in patients with STEMI. LV function most commonly is evalu- ated with contrast ventriculography at the time of cardiac catheterization or with transthoracic echocardiography on day 2 or 3. Echocardiography is the most frequently used imag- ing modality to evaluate regional and global LV function after STEMI and can help characterize any associated mechanical complications when they are clinically suspected. Because of the dynamic nature of LV functional recovery after STEMI, clinicians should consider the timing of the imaging study relative to the index event. In patients with significant LV sys- tolic dysfunction revealed during the initial hospitalization, LV function should be reevaluated 40 days later, especially to address the potential need for ICD therapy after allowance for recovery from myocardial stunning.496,587,588 10.3. Assessment of Risk for SCD: Recommendation Class I 1. Patients with an initially reduced LVEF who are possible candidates for ICD therapy should under- go reevaluation of LVEF 40 or more days after dis- (Level of Evidence: B) The timing and character of ventricular arrhythmias and resid- ual LV systolic function are the strongest predictors of SCD risk after STEMI. Management considerations for patients with ventricular arrhythmias during the hospital phase are reviewed in Section 9.5. Hospital survivors with an initially reduced LVEF ( 0.40) who do not merit ICD therapy before discharge should undergo reassessment of LV function 40 days later to determine their eligibility for ICD therapy. The recommended delay to ICD therapy in this setting stems from the results of DINAMIT (Defibrillator in Acute Myocardial Infarction Trial), in which defibrillator implantation 6 to 40 days after MI in patients with EF 0.35 and impaired cardiac autonomic function was not shown to reduce overall cardiac death risk. The observed reduction in arrhythmic deaths was offset by a relative increase in the numbers of nonarrhythmic The IRIS (Immediate Risk Stratification Improves also showed that early ICD therapy in patients with LVEF 0.40 and a high heart rate, nonsustained VT regardless of LVEF, or both did not result in improved survival. The utility of a wearable cardioverter-defibrillator in high-risk patients during the first 4 to 6 weeks after STEMI is under investigation http://clinicaltrials.gov/ct2/show/ NCT00628966). The indications for ICD therapy 40 days after STEMI are based on LVEF and New York Heart Association class, as derived from the results of the landmark MADIT 2 (Multicenter Automatic Defibrillator Implantation Trial 2) and SCDHeFT (Sudden Cardiac Death in Heart Failure) tri- If LVEF remains 0.35 and the patient has New York Heart Association class II or III HF symptoms, or if the LVEF is 0.30 independent of symptoms, then ICD implanta- tion is recommended.496 Indications for cardiac resynchroniza- tion therapy in the late, convalescent phase of STEMI include residual LV function, NewYork Heart Association class, QRS duration, and LBBB morphology.592 In addition to determination of LVEF, several other non- invasive strategies have been proposed to identify patients at high risk for arrhythmic events after STEMI, such as sig- nal-averaged or high-resolution ECG, heart rate variability, baroreflex sensitivity, and T-wave alternans.591 These strate- gies have not been adopted widely because of their limited O Gara et al 2013 ACCF/AHA STEMI Guideline e399 performance characteristics and are not recommended for routine use. 11. Posthospitalization Plan of Care 11.1. Posthospitalization Plan of Care: Recommendations Class I 1. Posthospital systems of care designed to prevent hos- pital readmissions should be used to facilitate the transition to effective, coordinated outpatient care for all patients with STEMI.593 597 (Level of Evidence: B) 2. Exercise-based cardiac rehabilitation/secondary prevention programs are recommended for patients (Level of Evidence: B) 3. A clear, detailed, and evidence-based plan of care that promotes medication adherence, timely follow- up with the healthcare team, appropriate dietary and physical activities, and compliance with interven- tions for secondary prevention should be provided to patients with STEMI. (Level of Evidence: C) 4. Encouragement and advice to stop smoking and to avoid secondhand smoke should be provided to pa- tients with STEMI.602 605 (Level of Evidence: A) 11.1.1. The Plan of Care for Patients With STEMI Education of patients with STEMI and their families is criti- cal and often challenging, especially when transitions of care occur. Failure to understand and comply with a plan of care may account for the high rate of STEMI rehospitalization rates seen in the United States.19,606 One key intervention to ensure effective coordination is to provide to patients and caregiv- ers, during the hospital stay, a comprehensive plan of care and educational materials that promote compliance with recom- mended evidence-based therapies.607 609 The posthospitaliza- tion plan of care for patients with STEMI should address in detail several complex issues, including medication adherence and titration, timely follow-up, dietary interventions, physical and sexual activities, cardiac rehabilitation, compliance with interventions for secondary prevention (Table 14), and reas- sessment of arrhythmic and HF risks. In addition, providers should pay close attention to psychosocial and socioeconomic issues, including access to care, risk of depression, social iso- lation, and healthcare disparities.610 612 11.1.2. Smoking Cessation The value of smoking cessation for the secondary prevention of cardiovascular disease has been demonstrated in several prospective observational studies. A meta-analysis of cohort studies in patients after acute MI showed that smoking cessa- tion reduced the subsequent cardiovascular mortality rate by ranking it among the most powerful secondary The SAVE (Sleep Apnea Cardiovas- cular Endpoints) study investigators reported that in selected patients with LV systolic dysfunction after MI, smoking ces- sation, compared with continued smoking, is associated with a 40% lower hazard of all-cause mortality and a 30% lower hazard of death, recurrent MI, or HF hospitalization.605 Reasonable evidence from RCTs indicates that counseling hospitalized smokers after acute MI increases smoking cessa- tion rates, provided that the initial contact during the hospital stay is followed by repeated contacts, usually by telephone, for 3 months after discharge.603,604 Similarly, the odds of smoking cessation are greater among patients who receive discharge recommendations for cardiac rehabilitation.604 Patients with depressive symptoms during the MI hospitaliza- tion and early convalescence are less likely to quit smoking and may require more intensive treatment to achieve cessa- Counseling should be provided to the patient and family, along with pharmacological therapy as deemed safe, and access to formal smoking-cessation programs should be facilitated. 11.1.3. Cardiac Rehabilitation The objectives of contemporary exercise-based cardiac reha- bilitation are to increase functional capacity, decrease or alle- viate anginal symptoms, reduce disability, improve quality of life, modify coronary risk factors, and reduce morbidity and mortality rates.598,613,614 Core components include patient assessment; ongoing medical surveillance; nutritional coun- seling; BP, lipid, and diabetes mellitus management; smoking cessation; psychosocial counseling; physical activity coun- seling; exercise training; and pharmacological treatment, as Among 601099 US Medicare beneficiaries who were hospitalized for coronary conditions or revascularization procedures, mortality rates were 21% to 34% lower among participants in cardiac rehabilitation programs than among It has been suggested that contemporary reperfusion and cardioprotective drug therapies may dimin- ish the impact of adjunctive exercise-based cardiac reha- bilitation programs on post-MI survival rate. Taylor et al600 conducted a systematic review and meta-analysis of RCTs of cardiac rehabilitation with 6 months of follow-up. The study population included 8940 patients, a greater number were women (20% of the cohort), patients 65 years of age, and individuals who had undergone revascularization pro- cedures. Compared with usual care, cardiac rehabilitation was associated with a reduction in total and cardiac mor- tality rates of 20% and 26%, respectively. Subgroup analy- ses showed that the decreased mortality rates did not differ across several patient subsets, between programs limited to exercise and those providing more comprehensive secondary interventions, or between pre- and post-1995 studies, which suggests that the mortality benefits of cardiac rehabilitation persist in the modern era. However, despite these impres- sive outcomes, cardiac rehabilitation services remain vastly 11.1.4. Systems of Care to Promote Care Coordination Meaningful evidence has facilitated a much better under- standing of the systems changes necessary to achieve safer This includes the adoption by all US hospitals of a standardized set of Safe Practices endorsed by the National which overlap in many ways with the National Patient Safety Goals espoused by The Joint Com- Examples of patient safety standards that should be ensured for all patients discharged after STEMI include Table 14. Plan of Care for Patients With STEMI Plan of Care Resources/References Medications Antithrombotic therapies Beta blockers ACE inhibitors/ARBs/aldosterone antagonists Statins ESC STEMI Guideline48 Physical activity/cardiac rehabilitation Physical activity Cardiorespiratory fitness (MET capacity) AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 AACVPR/ACCF/AHA 2010 Update: Performance Measures on Cardiac Rehabilitation616 Risk factor modification/lifestyle interventions Smoking cessation AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 ACCP Tobacco Cessation Toolkit615 Diet/nutrition AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 Management of comorbidities Overweight/obesity Lipids Hypertension Diabetes HF Arrhythmia/arrhythmia risk AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 NHLBI National Hypertension Education Program (JNC VII)617 AHA/ADA CVD Prevention in DM Patients618 ACC/AHA/HFSA HF Guideline619 ACC/AHA/HRS DBT & AF Guidelines496,501 Psychosocial factors Sexual activity Gender-specific issues Depression, stress, and anxiety Alcohol use Culturally sensitive issues AHA Scientific Statement on Sexual Activity and Cardiovascular Disease627a Cardiovascular Disease Prevention in Women Guidelines620 AHA Scientific Statement on Depression621 AHA/ACC 2011 Update: Secondary Prevention and Risk Reduction Therapy249 Provider follow-up Cardiologist Primary care provider Advanced practice nurse/physician assistant Other relevant medical specialists Electronic personal health records Influenza vaccination Centers for Disease Control Adult Vaccinations622 Patient/family education Plan of care for acute MI Recognizing symptoms of MI Activating EMS, signs and symptoms for urgent vs emergency evaluations CPR training for family members Risk assessment & prognosis Advanced directives Social networks/social isolation AHA CPR Guideline201 Socioeconomic factors Access to health insurance coverage Access to healthcare providers Disability Social services Community services http://www.qualityforum.org/Topics/Care_Coordination.Aspx AACVPR indicates American Association of Cardiovascular and Pulmonary Rehabilitation; ACC, American College of Cardiology; ACCF, American College of Cardiology Foundation; ACCP, American College of Chest Physicians; ACE, angiotensin-converting enzyme; ADA, American Diabetes Association; AF, atrial fibrillation; AHA, American Heart Association; ARB, angiotensin receptor blocker; CPR, cardiopulmonary resuscitation; CVD, cardiovascular disease; DBT, device-based therapy; DM, diabetes mellitus; EMS, emergency medical services; ESC, European Society of Cardiology; H2H, hospital-to-home; HF, heart failure; HFSA, Heart Failure Society of America; HRS, Heart Rhythm Society; JNC, Joint National Committee; MET, metabolic equivalent; MI, myocardial infarction; NHLBI, National Heart, Lung, and Blood Institute; SIHD, stable ischemic heart disease; and STEMI, ST-elevation myocardial infarction. O Gara et al 2013 ACCF/AHA STEMI Guideline e401 improved communication among physicians, nurses, and pharmacists; medication reconciliation; careful transitions between care settings; and consistent documentation. The National Quality Forum also has endorsed a set of patient- centered Preferred Practices for Care Coordination, 619 which detail comprehensive specifications that are necessary to achieve the goals of successful care coordination for patients and their families. Systems of care designed to support patients with STEMI and other cardiac diseases can result in signifi- cant improvement in patient outcomes. To provide the inter- ventions and services listed in Table 14, appropriate resources must be applied to ensure that all patients with STEMI have full access to evidence-based therapies and follow-up care. There is a growing emphasis on penalizing hospitals for avoid- able hospital readmissions. Hence, it is imperative for health systems to work in partnership with physicians, nurses, phar- macists, communities, payers, and public agencies to support the interventions that achieve such comprehensive care. Patient characteristics may be important predictors of read- mission after MI; however, only a few variables have been From a policy perspective, a vali- dated risk-standardized model that uses readmission rates to profile hospitals is not currently available. 12. Unresolved Issues and Future Research Directions The writing committee has identified several areas pertain- ing to the management of patients with STEMI that deserve further research. Although the observations from the Swedish STEMI registry showing an association between the increased use of evidence-based treatments and declining mortality rates after STEMI are encouraging,18 additional efforts to improve patient outcomes are needed. There is widespread acknowl- edgment that progress in closing existing knowledge and per- formance gaps will require contributions from a wide range of investigators, dedicated clinicians, hospital and health plan administrators, regional emergency response systems, and both government and private payers.631 12.1. Patient Awareness Delay times from onset of symptoms to activation of STEMI care pathways remain unacceptably long.51,631 Multicultural efforts to educate, reassure, and motivate at-risk patients and their families are needed. Comparable efforts to improve adher- ence and attention to healthy lifestyle behaviors as the corner- stones of secondary prevention are required at time of discharge and as an integral feature of cardiac rehabilitation programs. 12.2. Regional Systems of Care The adoption of regional systems of care for patients with STEMI across diverse geographical areas has proved challeng- ing, and inappropriate delays to initiation of reperfusion ther- apy are common.632 As previously emphasized, attention should be focused on reducing the total ischemic time, from onset of symptoms to successful reperfusion. Several factors in addi- tion to patient activation of EMS contribute to delays, not all of which can be reconciled. Areas for continued research include prehospital EMS protocols, the approach to out-of-hospital car- diac arrest, triage and transfer algorithms, rapid availability of expert PCI services, and further refinement of the clinical and time-related factors that should prompt earlier use of fibrino- lytic therapy coupled with immediate transfer for PCI.129,633 635 The lack of correlation between shorter D2B times and reduced mortality should drive further efforts to improve all aspects of STEMI care.636 Regional systems should track, analyze, and report all STEMI and out-of-hospital cardiac arrest events as part of an ongoing process-improvement program. 12.3. Transfer and Management of Non High-Risk Patients After Administration of Fibrinolytic Therapy The indications for and timing of transfer for angiography with a view toward revascularization of non high-risk patients after successful fibrinolysis are still debated. Although there has been increasing activation of this pathway, the evidence base for its justification is still limited.358,360,365 12.4. Antithrombotic Therapy The optimum choice of P2Y12 receptor inhibitor and antico- agulant agents for patients with STEMI can be challenging. Individual genetic variability in drug absorption, metabolism, and effectiveness has been highlighted by the experience with clopidogrel in patients with ACS.285,637 The risks of bleeding also may vary across racial and ethnic groups.12 The roles of platelet function testing and genetic screening for clopidogrel metabolism in the acute phase of STEMI care are uncertain,289 especially with the availability of alternative P2Y12 receptor inhibitors. More information specific to patients with STEMI is needed with regard to the use of prasugrel, ticagrelor, novel factor Xa and IIa antagonists, and platelet protease activated The efficacy and safety of com- bination ( triple ) antithrombotic therapy must be addressed while less hazardous approaches are tested. Bleeding rates with radial versus femoral artery access for PCI warrant further prospective study.561 12.5. Reperfusion Injury Aside from manual aspiration thrombectomy, efforts to counter- act the no-reflow phenomenon and to limit myocardial reper- fusion injury have had limited success. The value of aspiration thrombectomy in patients with anterior STEMI has been ques- Remote ischemic preconditioning has engendered little enthusiasm. Trials evaluating the use of antithrombotic and vasodilator agents have been disappointing. New bio- logical, pharmacological, and mechanical strategies should be investigated to facilitate prompt recovery of tissue-level perfu- In addition, high-dose statin pretreatment before primary or delayed PCI for STEMI requires further study.645 12.6. Approach to Noninfarct Artery Disease There is great variability in the evaluation and management of nonculprit coronary artery disease in stable patients without HF or shock, both at the time of primary PCI and later during the hospital course. Physiological assessment of lesion sig- nificance is often not performed, and the decision to proceed with PCI is made on anatomic grounds. More work is needed to clarify the indications for and timing of noninfarct artery 12.7. Prevention of SCD Prediction of electrical vulnerability and SCD risk after STEMI is fraught with imprecision. Treatment decisions rely almost exclusively on parameters of LV systolic function. Optimal therapy for at-risk individuals in the time window between discharge and 40 days, the time point after which ICD therapy is currently recommended, has not been estab- lished. Improved prediction rules and validated treatment rec- ommendations are urgently needed.646 12.8. Prevention of HF Much progress has been made to limit LV remodeling, though there remains substantial room for improvement, beginning with the timeliness of reperfusion and initiation of ACE inhib- The superimposition of ischemic mitral regurgitation adds further to the risks of HF and death. Contin- ued exploration of the roles of cell- and gene-based therapies after STEMI is encouraged.647 656 Presidents and Staff American College of Cardiology Foundation William A. Zoghbi, MD, FACC, President Thomas E. Arend, Jr, Esq, CAE, Interim Chief Staff Officer William J. Oetgen, MD, MBA, FACC, Senior Vice President, Science and Quality Charlene L. May, Senior Director, Science and Clinical Policy American College of Cardiology Foundation/ American Heart Association Lisa Bradfield, CAE, Director, Science and Clinical Policy Debjani Mukherjee, MPH, Associate Director, Evidence- Based Medicine Sarah Jackson, MPH, Specialist, Science and Clinical Policy American Heart Association Donna K. Arnett, PhD, MSPH, BSN, FAHA, President Nancy Brown, Chief Executive Officer Rose Marie Robertson, MD, FAHA, Chief Science Officer Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science Operations Judy Bezanson, DSN, RN, CNSMS, FAHA, Science and Medicine Advisor, Office of Science Operations Jody Hundley, Production Manager, Scientific Publications, Office of Science Operations References 1. ACCF/AHA Task Force on Practice Guidelines. Manual for ACCF/AHA Guideline Writing Committees: Methodologies and Policies from theACCF/ AHA Task Force on Practice Guidelines. 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