ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction: Executive Summary


A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction)

Writing Group

Thomas J. Ryan, MD, FACC; Jeffrey L. Anderson, MD, FACC; Elliott M. Antman, MD, FACC; Blaine A. Braniff, MD, FACP; Neil H. Brooks, MD, FAAFP; Robert M. Califf, MD, FACC; L. David Hillis, MD, FACC; Loren F. Hiratzka, MD, FACC; Elliot Rapaport, MD, FACC; Barbara J. Riegel, DNSc, FAAN; Richard O. Russell, MD, FACC; Earl E. Smith; W. Douglas Weaver, MD, FACC

Footnotes

Executive Summary and Listing of Recommendations

Purpose

These guidelines are intended for physicians, nurses, and allied healthcare personnel who care for patients with suspected or established acute myocardial infarction (MI).

These guidelines have been officially endorsed by the American Society of Echocardiography, the American College of Emergency Physicians, and the American Association of Critical-Care Nurses.

This executive summary and listing of recommendations appears in the November 1, 1996, issue of Circulation. The guidelines in their entirety, including the ACC/AHA Class I, II, and III recommendations, are published in the November 1996 issue of the Journal of the American College of Cardiology. Beginning with these guidelines, the full text of ACC/AHA guidelines will be published in one journal and the executive summary and listing of recommendations in the other. Reprints of both the full text and the executive summary with its listing of recommendations are available from both organizations.

Prehospital Issues

Each year 900 000 people in the United States experience acute MI. Of these, roughly 225 000 die, including 125 000 who die "in the field" before obtaining medical care. Most of these deaths are arrhythmic in etiology. Because early reperfusion treatment of patients with acute MI improves left ventricular (LV) systolic function and survival, every effort must be made to minimize prehospital delay. Indeed, efforts are ongoing to promote rapid identification and treatment of patients with acute MI, including (1) patient education about the symptoms of acute MI and appropriate actions to take and (2) prompt initial care of the patient by the community emergency medical system. In treating the patient with chest pain, emergency medical system personnel must act with a sense of urgency.

Initial Recognition and Management in the Emergency Department

When the patient with suspected acute MI reaches the emergency department (ED), evaluation and initial management should take place promptly, because the benefit of reperfusion therapy is greatest if therapy is initiated early. The initial evaluation of the patient ideally should be accomplished within 10 minutes of his or her arrival in the ED; certainly no more than 20 minutes should elapse before an assessment is made. On arrival in the ED the patient with suspected acute MI should immediately receive (1) oxygen by nasal prongs; (2) sublingual nitroglycerin (unless systolic arterial pressure is less than 90 mm Hg or heart rate is less than 50 or greater than 100 beats per minute [bpm]); (3) adequate analgesia (with morphine sulfate or meperidine); and (4) aspirin, 160 to 325 mg orally. A 12-lead electrocardiogram (ECG) should also be performed. ST-segment elevation (equal to or greater than 1 mV) in contiguous leads provides strong evidence of thrombotic coronary arterial occlusion and makes the patient a candidate for immediate reperfusion therapy, either by fibrinolysis or primary percutaneous transluminal coronary angioplasty (PTCA). Symptoms consistent with acute MI and left bundle branch block (LBBB) should be managed like ST-segment elevation. In contrast, the patient without ST-segment elevation should not receive thrombolytic therapy. The benefit of primary PTCA in these patients remains uncertain.

In comparison with standard medical therapy, thrombolytic therapy exerts a highly significant 21% proportional reduction in 35-day mortality among patients with acute MI and ST elevation, corresponding to an overall reduction of 21 deaths per 1000 patients treated. A powerful time-dependent effect on mortality has been observed in the administration of thrombolytic agents. The greatest benefit occurs when thrombolysis is initiated within 6 hours of the onset of symptoms, although it exerts definite benefit when begun within 12 hours. An estimated 35 lives per 1000 patients treated are saved when thrombolysis is used within the first hour of symptom onset, compared with 16 lives saved per 1000 treated when given 7 to 12 hours after symptom onset. Thrombolysis benefits the patient irrespective of age and gender and the presence of comorbid conditions such as diabetes mellitus, although the degree of benefit varies among patient groups. Thrombolytic therapy is associated with a slightly increased risk of intracranial hemorrhage (ICH) that usually occurs within the first day of therapy. Variables that appear to predict an increased risk of ICH include age greater than 65 years, body weight less than 70 kg, systemic arterial hypertension, and administration of tissue plasminogen activator (TPA).

Primary PTCA may be performed as an alternative to thrombolytic therapy, provided that it can be accomplished in a timely fashion by persons skilled in the procedure and supported by experienced personnel. Prompt access to emergency coronary artery bypass graft (CABG) surgery must also be available if primary PTCA is to be undertaken.

Once reperfusion therapy is initiated, the patient with suspected acute MI should be hospitalized. Subsequent short- and long-term management is similar, irrespective of the appearance of the initial ECG. Thus, following the initial triage decision regarding reperfusion therapy, treatment of the patient whose ECG initially showed ST-segment elevation or presumably new LBBB and who received reperfusion therapy is similar to that for the patient whose initial ECG failed to show ST-segment elevation or LBBB and who did not receive reperfusion therapy.

Hospital Management

The First 24 Hours

Once hospitalized, the patient with acute MI should be continuously monitored by electrocardiography and the diagnosis of acute MI confirmed by serial ECGs and measurements of serum cardiac markers of myocyte necrosis, such as creatine kinase isoenzymes or cardiac specific troponin T or I. The patient should be monitored closely for adverse electrical or mechanical events because reinfarction and death occur most frequently within the first 24 hours. The patient's physical activities should be limited for at least 12 hours, and pain and/or anxiety should be minimized with appropriate analgesics. Although the use of prophylactic antiarrhythmic agents in the first 24 hours of hospitalization is not recommended, atropine, lidocaine, transcutaneous pacing patches or a transvenous pacemaker, a defibrillator, and epinephrine should be immediately available.

Patients who survive a large anterior MI or who have a LV mural thrombus seen on echocardiography are at high risk of having an embolic stroke. Some data suggest that this risk is reduced by early administration of intravenous heparin. For the patient without a large anterior MI or LV mural thrombus who did not receive reperfusion therapy, there are few data on the benefit of heparin beyond that of aspirin, -adrenoceptor blocking agents, nitrates, and angiotensin converting enzyme (ACE) inhibitors. For the patient given thrombolytic therapy, the recommendations for subsequent heparin administration are based more on current practice than on evidence and depend on the specific thrombolytic agent. There is only limited evidence that heparin (given intravenously or subcutaneously) is beneficial in the patient who receives a nonspecific fibrinolytic agent such as streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), or urokinase. When TPA (alteplase) is administered, intravenous heparin increases the likelihood of patency in the infarct-related artery (assessed angiographically), but this may not necessarily lead to improved clinical outcome. Considering the superior performance of accelerated TPA plus intravenous heparin in the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO) trial, it seems judicious to give heparin intravenously for at least 48 hours after alteplase is given. When primary PTCA is performed, high-dose intravenous heparin is recommended. Aspirin, 160 to 325 mg daily, initially given in the ED, should be continued indefinitely.

Despite the absence of definitive outcome data, it is reasonable to treat the patient with acute MI and without hypotension, bradycardia, or excessive tachycardia with intravenous nitroglycerin for 24 to 48 hours after hospitalization. Concern exists about oral nitrate preparations in the patient with acute MI because of inability to titrate the dose to effect in an acutely evolving hemodynamic situation, whereas intravenous infusion of nitroglycerin can be titrated successfully with frequent measurement of heart rate and cuff blood pressure. Nitroglycerin should not be used as a substitute for narcotic analgesics that are often required in the patient with acute MI.

The patient with evolving acute MI should receive early intravenous -adrenergic blocker therapy, followed by oral therapy, provided that there is no contraindication. -Adrenoceptor blocker therapy should be initiated regardless of whether reperfusion therapy was given, because several studies in the prethrombolytic as well as the thrombolytic era showed that -adrenoceptor blockers diminish morbidity and mortality. Calcium channel blockers have not been shown to reduce mortality in patients with acute MI, and in certain persons with cardiovascular disease they appear to be harmful. In the patient without ST-segment elevation or LBBB in whom pulmonary congestion is absent, diltiazem may reduce the incidence of recurrent ischemic events, but its benefit beyond that of -adrenoceptor blockers and aspirin is unclear. Immediate-release dihydropyridines (eg, nifedipine) are contraindicated in the patient with acute MI.

In the patient with evolving acute MI with ST-segment elevation or LBBB, an ACE inhibitor should be initiated within hours of hospitalization, provided that the patient does not have hypotension or a contraindication. Subsequently, the ACE inhibitor should be continued indefinitely in the patient with impaired LV systolic function (ejection fraction less than 40%) or clinical congestive heart failure (CHF). In patients without complications and no evidence of symptomatic or asymptomatic LV dysfunction by 6 weeks, ACE inhibitors can be stopped. On admission to the hospital, a lipid profile and serum electrolyte concentration (including magnesium) should be measured in all patients.

After the First 24 Hours

After the first day in the hospital, the patient with acute MI should continue to receive aspirin 160 to 325 mg/d indefinitely with a -adrenergic blocker; an ACE inhibitor should be administered for at least 6 weeks. Nitroglycerin should be infused intravenously for 24 to 48 hours, and magnesium sulfate should be given as needed to replete magnesium deficits for 24 hours. For the patient receiving alteplase, it is current practice to give intravenous heparin for an additional 48 hours.

Patients with myocardial ischemia that is spontaneous or provoked in the days to weeks after acute MI, irrespective of whether they received thrombolytic therapy, ordinarily should undergo elective angiographic evaluation, with subsequent consideration of percutaneous or surgical revascularization. There is considerable variability in the use of coronary angiography and catheter interventions among survivors of uncomplicated acute MI with preserved LV systolic function. Although some practitioners routinely perform angiography and PTCA during the days after acute MI in virtually all patients, the available data suggest that such a management strategy does not salvage myocardium nor reduce the incidence of reinfarction or death. Accordingly, coronary angiography and subsequent revascularization should be reserved for survivors of acute MI who have preserved LV systolic function and spontaneous or provoked ischemia.

During hospitalization the patient with acute MI should be closely observed for prompt recognition and management of complications. The patient with recurrent chest pain believed due to pericarditis should receive high-dose aspirin (650 mg every 4 to 6 hours). Recurrent chest discomfort thought to be caused by myocardial ischemia should be treated with intravenous nitroglycerin, analgesics, and antithrombotic medications (aspirin, heparin). Coronary angiography with subsequent revascularization therapy should be considered. The patient with heart failure should receive a diuretic (usually intravenous furosemide) and an afterload-reducing agent. For the patient in cardiogenic shock, consideration should be given to insertion of an intra-aortic balloon pump and emergency coronary angiography, followed by PTCA or CABG. The patient with right ventricular infarction and dysfunction should be treated vigorously with intravascular volume expansion (using normal saline) and inotropic agents if hypotension persists.

In the patient with acute MI, the appearance of atrial fibrillation is often a manifestation of extensive LV systolic dysfunction. If its occurrence causes hemodynamic compromise or ongoing ischemia, direct-current cardioversion should be performed. In the absence of these, -adrenoceptor blocking agents or digitalis should be given to slow the ventricular response. Episodes of ventricular fibrillation should be treated with immediate direct-current countershock; the same is true for episodes of monomorphic ventricular tachycardia associated with angina, pulmonary congestion, or hypotension. If monomorphic ventricular tachycardia is not accompanied by chest pain, pulmonary congestion, or hypotension, it should be treated with intravenous lidocaine, procainamide, or amiodarone.

The patient with acute MI and symptomatic sinus bradycardia or atrioventricular block should receive atropine. Temporary pacing should be performed in the patient with (1) sinus bradycardia unresponsive to drug therapy, (2) Mobitz type II second-degree atrioventricular block, (3) third-degree heart block, (4) bilateral bundle branch block (BBB), (5) newly acquired BBB, and (6) right or left BBB in conjunction with first-degree atrioventricular block.

Immediate surgical intervention is often required for the patient with (1) failed PTCA with persistent chest pain or hemodynamic instability; (2) persistent or recurrent ischemia refractory to medical therapy who is not a candidate for catheter intervention; (3) cardiogenic shock and coronary anatomy not amenable to PTCA; or (4) a mechanical abnormality leading to severe pulmonary congestion or hypotension, such as papillary muscle rupture (with resultant mitral regurgitation) or ventricular septal defect (VSD).

Preparation for Discharge From the Hospital

Before hospital discharge or shortly thereafter, the patient with recent acute MI should undergo standard exercise testing (submaximal at 4 to 7 days or symptom limited at 10 to 14 days). This is done to (1) assess the patient's functional capacity and ability to perform tasks at home and work, (2) evaluate the efficacy of the patient's current medical regimen, and (3) stratify risk for a subsequent cardiac event. The incremental value of radionuclide imaging or echocardiography during exercise is uncertain. Although markers of electrical instability such as abnormal baroreflex stimulation or the presence of late potentials on a signal-averaged ECG are associated with increased risk of death, their positive predictive value is low, and appropriate therapy when these findings are observed is yet to be determined.

Long-Term Management

For an indefinite period after acute MI, the patient should continue to receive aspirin, a -adrenoceptor blocker, and a selected dose of an ACE inhibitor. The patient should be instructed to achieve an ideal weight and educated about a diet low in saturated fat and cholesterol. The patient with a low-density lipoprotein (LDL) cholesterol measurement greater than 130 mg/dL despite diet should be given drug therapy with the goal of reducing LDL to less than 100 mg/dL. Smoking cessation is essential. Finally, the patient should be encouraged to participate in a formal rehabilitation program and ultimately to plan to engage in 20 minutes of exercise at the level of brisk walking at least three times a week.

Recommendations

The following is a listing of the recommendations made by the ACC/AHA Task Force on Practice Guidelines in the ACC/AHA Task Force Report "ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction." More detailed information regarding the evidence and the rationale for these recommendations can be found in the full text of the guidelines themselves, which appears in the November 1996 issue of the Journal of the American College of Cardiology.

Explanation of Classes

As in previous guidelines, the American College of Cardiology and the American Heart Association have used the following classification system in which indications for a diagnostic procedure, a particular therapy, or intervention are designated as:

    Class I: Conditions for which there is evidence for and/or general agreement that a given procedure or treatment is beneficial, useful, and effective.

    Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.

    Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.

    Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

    Class III: Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful/effective and in some cases may be harmful.

Prehospital Issues

Class I

  1. Availability of 911 access.
  2. Availability of an emergency medical services (EMS) system staffed by persons trained to treat cardiac arrest with defibrillation if indicated and to triage patients with ischemic-type chest discomfort.

Class IIa

  1. Availability of a first-responder defibrillation program in a tiered response system.
  2. Healthcare providers educate patients/families about signs and symptoms of acute MI, accessing EMS, and medications.

Class IIb

  1. Twelve-lead telemetry.
  2. Prehospital thrombolysis in special circumstances (eg, transport time greater than 90 minutes).

Initial Recognition and Management in the Emergency Department

Class I

  1. Emergency department acute MI protocol that yields a targeted clinical examination and a 12-lead ECG within 10 minutes and a door-to-needle time that is less than 30 minutes.

Routine Measures

  1. Supplemental oxygen, intravenous access, and continuous electrocardiographic monitoring should be established in all patients with acute ischemic-type chest discomfort.
  2. An ECG should be obtained and interpreted within 10 minutes of arrival in the ED in all patients with suspected acute ischemic-type chest discomfort.

Oxygen

Class I

  1. Overt pulmonary congestion.
  2. Arterial oxygen desaturation (SaO2 less than 90%).

Class IIa

  1. Routine administration to all patients with uncomplicated MI during the first 2 to 3 hours.

Class IIb

  1. Routine administration of supplemental oxygen to patients with uncomplicated MI beyond 3 to 6 hours.

Intravenous Nitroglycerin

Class I

  1. For the first 24 to 48 hours in patients with acute MI and CHF, large anterior infarction, persistent ischemia, or hypertension.
  2. Continued use (beyond 48 hours) in patients with recurrent angina or persistent pulmonary congestion.

Class IIa

Class IIb

  1. For the first 24 to 48 hours in all patients with acute MI who do not have hypotension, bradycardia, or tachycardia.
  2. Continued use (beyond 48 hours)* in patients with a large or complicated infarction.

Class III

  1. Patients with systolic blood pressure less than 90 mm Hg or severe bradycardia (less than 50 bpm).

Aspirin

Class I

  1. A dose of 160 to 325 mg should be given on day 1 of acute MI and continued indefinitely on a daily basis thereafter.

Class IIb

  1. Other antiplatelet agents such as dipyridamole or ticlopidine may be substituted if true aspirin allergy is present.

Atropine

Class I

  1. Sinus bradycardia with evidence of low cardiac output and peripheral hypoperfusion or frequent premature ventricular complexes at onset of symptoms of acute MI.
  2. Acute inferior infarction with type I second- or third-degree atrioventricular (AV) block associated with symptoms of hypotension, ischemic discomfort, or ventricular arrhythmias.
  3. Sustained bradycardia and hypotension after administration of nitroglycerin.
  4. For nausea and vomiting associated with administration of morphine.
  5. Ventricular asystole.

Class IIa

  1. Symptomatic patients with inferior infarction and type I second- or third-degree heart block at the level of the AV node (ie, with narrow QRS complex or with known existing BBB).

Class IIb

  1. Administration concomitant with (before or after) administration of morphine in the presence of sinus bradycardia.
  2. Asymptomatic patients with inferior infarction and type I second-degree heart block or third-degree heart block at the level of the AV node.
  3. Second- or third-degree AV block of uncertain mechanism when pacing is not available.

Class III

  1. Sinus bradycardia greater than 40 bpm without signs or symptoms of hypoperfusion or frequent premature ventricular contractions.
  2. Type II AV block and third-degree AV block and third-degree AV block with new wide QRS complex presumed due to acute MI.

Thrombolysis

Class I

  1. ST elevation (greater than 0.1 mV, two or more contiguous leads),* time to therapy 12 hours or less, age less than 75 years.
  2. Bundle branch block (obscuring ST-segment analysis) and history suggesting acute MI.

Class IIa

  1. ST elevation,* age 75 years or older.

Class IIb

  1. ST elevation,* time to therapy greater than 12 to 24 hours.
  2. Blood pressure on presentation greater than 180 mm Hg systolic and/or greater than 110 mm Hg diastolic associated with high-risk MI.

Class III

  1. ST elevation,* time to therapy greater than 24 hours, ischemic pain resolved.
  2. ST-segment depression only.

Primary PTCA

Class I

  1. As an alternative to thrombolytic therapy only if performed in a timely fashion by individuals skilled in the procedure and supported by experienced personnel in high-volume centers.§

Class IIa

  1. As a reperfusion strategy in patients who are candidates for reperfusion but who have a risk of bleeding contraindication to thrombolytic therapy.
  2. Patients in cardiogenic shock.

Class IIb

  1. As a reperfusion strategy in patients who fail to qualify for thrombolytic therapy for reasons other than a risk of bleeding contraindication.

Early Coronary Angiography in the ST-Segment Elevation or Bundle Branch Block Cohort Not Undergoing Primary PTCA

Class I

Class IIa

  1. Patients with cardiogenic shock or persistent hemodynamic instability.

Class IIb

  1. Patients with evolving large or anterior infarcts treated with thrombolytic agents in whom it is believed that the artery is not patent and adjuvant PTCA is planned.

Class III

  1. Routine use of angiography and subsequent PTCA within 24 hours of administration of thrombolytic agents.

Emergency or Urgent Coronary Artery Bypass Graft Surgery

Class I

  1. Failed angioplasty with persistent pain or hemodynamic instability in patients with coronary anatomy suitable for surgery.
  2. Acute MI with persistent or recurrent ischemia refractory to medical therapy in patients with coronary anatomy suitable for surgery who are not candidates for catheter intervention.
  3. At the time of surgical repair of postinfarction VSD or mitral valve insufficiency.

Class IIa

  1. Cardiogenic shock with coronary anatomy suitable for surgery.

Class IIb

  1. Failed PTCA and small area of myocardium at risk; hemodynamically stable.

Class III

  1. When the expected surgical mortality rate equals or exceeds the mortality rate associated with appropriate medical therapy.

Early Coronary Angiography and/or Interventional Therapy in Non-ST-Segment Elevation Cohort

Class I

  1. Patients with recurrent (stuttering) episodes of spontaneous or induced ischemia or evidence of shock, pulmonary congestion, or LV dysfunction.

Class IIa

  1. Patients with persistent ischemic-type discomfort despite medical therapy and an abnormal ECG or two or more risk factors for coronary artery disease.
  2. Patients with chest discomfort, hemodynamic instability, and an abnormal ECG.

Class IIb

  1. Patients with chest discomfort and an unchanged ECG.
  2. Patients with ischemic-type chest discomfort and a normal ECG and more than two risk factors for coronary artery disease.

Hospital Management

Early, General Measures

Class I

  1. Selection of electrocardiographic monitoring based on infarct location and rhythm.
  2. Bed rest with bedside commode privileges for initial 12 hours in hemodynamically stable patients free of ischemic-type chest discomfort.
  3. Avoidance of Valsalva.
  4. Careful attention to maximum pain relief.

Class IIb

  1. Routine use of anxiolytics.

Class III

  1. Prolonged bed rest (more than 12 to 24 hours) in stable patients without complications.

Identification and Treatment of the Patient at High Risk

Management of Recurrent Chest Discomfort

Class I

  1. Aspirin for pericarditis.
  2. -Adrenoceptor blockers intravenously, then orally for ischemic-type chest discomfort.
  3. (Re)administration of thrombolytic therapy (alteplase) for patients with recurrent ST elevation.
  4. Coronary arteriography for ischemic-type chest discomfort recurring after hours to days of initial therapy and associated with objective evidence of ischemia in patients who are candidates for revascularization.

Class IIa

  1. Nitroglycerin intravenously for 24 hours, then topically or orally for ischemic-type chest discomfort.

Class IIb

  1. Corticosteroids for pericarditis.
  2. Indomethacin for pericarditis.

Hemodynamic Monitoring

Class I

  1. Severe or progressive CHF or pulmonary edema.
  2. Cardiogenic shock or progressive hypotension.
  3. Suspected mechanical complications of acute infarction, ie, VSD, papillary muscle rupture, or pericardial tamponade.

Class IIa

  1. Hypotension that does not respond promptly to fluid administration in a patient without pulmonary congestion.

Class III

  1. Patients with acute infarction without evidence of cardiac or pulmonary complications.
  2. Intra-arterial Pressure Monitoring

Class I

  1. Patients with severe hypotension (systolic arterial pressure less than 80 mm Hg) and/or cardiogenic shock.
  2. Patients receiving vasopressor agents.

Class IIa

  1. Patients receiving intravenous sodium nitroprusside or other potent vasodilators.

Class IIb

  1. Hemodynamically stable patients receiving intravenous nitroglycerin for myocardial ischemia.
  2. Patients receiving intravenous inotropic agents.

Class III

  1. Patients with acute infarction who are hemodynamically stable.

Intra-aortic Balloon Counterpulsation

Class I

  1. Cardiogenic shock not quickly reversed with pharmacological therapy as a stabilizing measure for angiography and prompt revascularization.
  2. Acute mitral regurgitation or VSD complicating MI as a stabilizing therapy for angiography and repair/revascularization.
  3. Recurrent intractable ventricular arrhythmias with h.Áž
  4. Refractory post-MI angina as a bridge to angiography and revascularization.

Class IIa

  1. Signs of hemodynamic instability, poor LV function, or persistent ischemia in patients with large areas of myocardium at risk.

Class IIb

  1. In patients with successful PTCA after failed thrombolysis or those with three-vessel coronary disease to prevent reocclusion.
  2. In patients known to have large areas of myocardium at risk with or without active ischemia.

Rhythm Disturbances

Class I

  1. Electrical cardioversion for patients with severe hemodynamic compromise or intractable ischemia.
  2. Rapid digitalization to slow a rapid ventricular response and improve LV function.
  3. Intravenous -adrenoceptor blockers to slow a rapid ventricular response in patients without clinical LV dysfunction, bronchospastic disease, or AV block.
  4. Heparin should be given.

Class IIa

  1. Either diltiazem or verapamil intravenously to slow a rapid ventricular response if -adrenoceptor blocking agents are contraindicated or ineffective.
  2. Ventricular Tachycardia/Ventricular Fibrillation

Class I

  1. Ventricular fibrillation (VF) should be treated with an unsynchronized electric shock with an initial energy of 200 J; if unsuccessful, a second shock of 200 to 300 J should be given, and, if necessary, a third shock of 360 J.
  2. Sustained (more than 30 seconds or causing hemodynamic collapse) polymorphic ventricular tachycardia (VT) should be treated with an unsynchronized electric shock using an initial energy of 200 J; if unsuccessful, a second shock of 200 to 300 J should be given, and, if necessary, a third shock of 360 J.
  3. Episodes of sustained monomorphic VT associated with angina, pulmonary edema, or hypotension (blood pressure less than 90 mm Hg) should be treated with a synchronized electric shock of 100 J initial energy. Increasing energies may be used if not initially successful.
  4. Sustained monomorphic VT not associated with angina, pulmonary edema, or hypotension (blood pressure less than 90 mm Hg) should be treated with one of the following regimens:
    1. Lidocaine: bolus 1.0 to 1.5 mg/kg. Supplemental boluses of 0.5 to 0.75 mg/kg every 5 to 10 minutes to a maximum of 3 mg/kg total loading dose may be given as needed. Loading is followed by infusion of 2 to 4 mg/min (30 to 50 µg/kg per minute).
    2. Procainamide: 20 to 30 mg/min loading infusion, up to 12 to 17 mg/kg. This may be followed by an infusion of 1 to 4 mg/min.
    3. Amiodarone: 150 mg infused over 10 minutes followed by a constant infusion of 1.0 mg/min for 6 hours and then a maintenance infusion of 0.5 mg/min.
    4. Synchronized electrical cardioversion starting at 50 J (brief anesthesia is necessary).

Class IIa

  1. Infusions of antiarrhythmic drugs may be used after an episode of VT/VF but should be discontinued after 6 to 24 hours and the need for further arrhythmia management assessed.
  2. Electrolyte and acid-base disturbances should be corrected to prevent recurrent episodes of VF when an initial episode of VF has been treated.

Class IIb

  1. Drug-refractory polymorphic VT should be managed by aggressive attempts to reduce myocardial ischemia, including therapies such as -adrenoceptor blockade, intra-aortic balloon pumping, and emergency PTCA/CABG surgery. Amiodarone, 150 mg infused over 10 minutes followed by a constant infusion of 1.0 mg/min for up to 6 hours and then a maintenance infusion of 0.5 mg/min may also be helpful.

Class III

  1. Treatment of isolated ventricular premature beats, couplets, runs of accelerated idioventricular rhythm, and nonsustained VT.
  2. Prophylactic administration of antiarrhythmic therapy when using thrombolytic agents.
  3. Bradyarrhythmias and Heart Block

    Atropine

Class I

  1. Symptomatic sinus bradycardia (generally, heart rate less than 50 bpm associated with hypotension, ischemia, or escape ventricular arrhythmia).
  2. Ventricular asystole.
  3. Symptomatic AV block occurring at the AV nodal level (second-degree type I or third degree with a narrow-complex escape rhythm).

Class IIa

Class III

  1. Atrioventricular block occurring at an infranodal level (usually associated with anterior MI with a wide-complex escape rhythm).
  2. Asymptomatic sinus bradycardia.
  3. Temporary Pacing

Placement of Transcutaneous Patches* and Active (Demand) Transcutaneous Pacing

Class I

  1. Sinus bradycardia (rate less than 50 bpm) with symptoms of hypotension (systolic blood pressure less than 80 mm Hg) unresponsive to drug therapy.
  2. Mobitz type II second-degree AV block.
  3. Third-degree heart block.
  4. Bilateral BBB (alternating BBB, or RBBB and alternating left anterior fascicular block [LAFB], left posterior fascicular block [LPFB]) (irrespective of time of onset).*
  5. Newly acquired or age indeterminate LBBB, LBBB and LAFBa, RBBB, and LPFBa.*
  6. RBBB or LBBB and first-degree AV block.*

Class IIa

  1. Stable bradycardia (systolic blood pressure greater than 90 mm Hg, no hemodynamic compromise, or compromise responsive to initial drug therapy).*
  2. Newly acquired or age-indeterminate RBBB.*

Class IIb

  1. Newly acquired or age-indeterminate first-degree AV block.*

Class III

  1. Uncomplicated acute MI without evidence of conduction system disease.
  2. Temporary Transvenous Pacing

Class I

  1. Asystole.
  2. Symptomatic bradycardia (includes sinus bradycardia with hypotension and type I second-degree AV block with hypotension not responsive to atropine).
  3. Bilateral BBB (alternating BBB or RBBB with alternating LAFB/LPFB) (any age).
  4. New or indeterminate age bifascicular block (RBBB with LAFB or LPFB, or LBBB) with first-degree AV block.
  5. Mobitz type II second-degree AV block.

Class IIa

  1. RBBB and LAFB or LPFB (new or indeterminate).
  2. RBBB with first-degree AV block.
  3. LBBB, new or indeterminate.
  4. Incessant VT, for atrial or ventricular overdrive pacing.
  5. Recurrent sinus pauses (greater than 3 seconds) not responsive to atropine.

Class IIb

  1. Bifascicular block of indeterminate age.
  2. New or age-indeterminate isolated RBBB.

Class III

  1. First-degree heart block.
  2. Type I second-degree AV block with normal hemodynamics.
  3. Accelerated idioventricular rhythm.
  4. Bundle branch block or fascicular block known to exist before acute MI.
  5. Permanent Pacing After Acute Myocardial Infarction

Class I

  1. Persistent second-degree AV block in the His-Purkinje system with bilateral BBB or complete heart block after acute MI.
  2. Transient advanced (second- or third-degree) AV block and associated BBB.§
  3. Symptomatic AV block at any level.

Class IIb

  1. Persistent advanced (second- or third-degree) block at the AV node level.

Class III

  1. Transient AV conduction disturbances in the absence of intraventricular conduction defects.
  2. Transient AV block in the presence of isolated LAFB.
  3. Acquired LAFB in the absence of AV block.
  4. Persistent first-degree AV block in the presence of BBB that is old or age indeterminate.

Other Surgical Interventions

Emergency or Urgent Cardiac Repair of Mechanical Defects

Class I

  1. Papillary muscle rupture with severe acute mitral insufficiency.
  2. Postinfarction VSD or free wall rupture and pulmonary edema or cardiogenic shock (emergency or urgent).
  3. Postinfarction ventricular aneurysm associated with intractable ventricular tachyarrhythmias and/or pump failure (urgent).

Class III

  1. Acute infarctectomy in hemodynamically stable patients.

Rationale and Approach to Pharmacotherapy

Antithrombotics/Anticoagulants

Heparin

Class I

  1. Patients undergoing percutaneous or surgical revascularization.

Class IIa

  1. Intravenously in patients undergoing reperfusion therapy with alteplase.
  2. Subcutaneously (7500 U twice daily) (intravenous heparin is an acceptable alternative) in all patients not treated with thrombolytic therapy who do not have a contraindication to heparin. In patients who are at high risk for systemic emboli (large or anterior MI, atrial fibrillation [AF], previous embolus, or known LV thrombus), intravenous heparin is preferred.
  3. Intravenously in patients treated with nonselective thrombolytic agents (streptokinase, anistreplase, urokinase) who are at high risk for systemic emboli (large or anterior MI, AF, previous embolus, or known LV thrombus).

Class IIb

  1. Patients treated with nonselective thrombolytic agents, not at high risk, subcutaneous heparin, 7500 U to 12500 U twice a day until completely ambulatory.

Class III

  1. Routine intravenous heparin within 6 hours to patients receiving a nonselective fibrinolytic agent (streptokinase, anistreplase, urokinase) who are not at high risk for systemic embolism.

-Adrenoceptor Blocking Agents

Early Therapy

Class I

  1. Patients without a contraindication to -adrenoceptor blocker therapy who can be treated within 12 hours of onset of infarction, irrespective of administration of concomitant thrombolytic therapy.
  2. Patients with continuing or recurrent ischemic pain.
  3. Patients with tachyarrhythmias, such as AF with a rapid ventricular response.

Class IIb

  1. Non-Q-wave MI.

Class III

  1. Patients with moderate or severe LV failure or other contraindications to -adrenoceptor blocker therapy.

Angiotensin Converting Enzyme Inhibitors

Class I

  1. Patients within the first 24 hours of a suspected acute MI with ST-segment elevation in two or more anterior precordial leads or with clinical heart failure in the absence of significant hypotension or known contraindications to use of ACE inhibitors.
  2. Patients with MI and LV ejection fraction less than 40% or patients with clinical heart failure on the basis of systolic pump dysfunction during and after convalescence from acute MI.

Class IIa

  1. All other patients within the first 24 hours of a suspected or established acute MI, provided significant hypotension or other clear-cut contraindications are absent.
  2. Asymptomatic patients with mildly impaired LV function (ejection fraction 40% to 50%) and a history of old MI.

Class IIb

  1. Patients who have recently recovered from MI but have normal or mildly abnormal global LV function.

Calcium Channel Blockers

Class I

Class IIa

  1. Verapamil or diltiazem may be given to patients in whom -adrenoceptor blockers are ineffective or contraindicated (ie, bronchospastic disease) for relief of ongoing ischemia or control of a rapid ventricular response with AF after acute MI in the absence of CHF, LV dysfunction, or AV block.

Class IIb

  1. In non-ST-elevation infarction, diltiazem may be given to patients without LV dysfunction, pulmonary congestion, or CHF. It may be added to standard therapy after the first 24 hours and continued for 1 year.

Class III

  1. Nifedipine (short acting) is generally contraindicated in routine treatment of acute MI because of its negative inotropic effects and the reflex sympathetic activation, tachycardia, and hypotension associated with its use.
  2. Diltiazem and verapamil are contraindicated in patients with acute MI and associated LV dysfunction or CHF.

Magnesium

Class I

Class IIa

  1. Correction of documented magnesium (and/or potassium) deficits, especially in patients receiving diuretics before onset of infarction.
  2. Episodes of torsades de pointes-type VT associated with a prolonged QT interval should be treated with 1 to 2 g magnesium administered as a bolus over 5 minutes.

Class IIb

  1. Magnesium bolus and infusion in high-risk patients such as the elderly and/or those for whom reperfusion therapy is not suitable.

Preparation for Discharge From the Hospital

Noninvasive Evaluation of Low-Risk Patients

Stress ECG

Class I

  1. Before discharge for prognostic assessment or functional capacity (submaximal at 4 to 6 days or symptom limited at 10 to 14 days).
  2. Early after discharge for prognostic assessment and functional capacity (14 to 21 days).
  3. Late after discharge (3 to 6 weeks) for functional capacity and prognosis if early stress was submaximal.
  1. Exercise, vasodilator stress nuclear scintigraphy, or exercise stress echocardiography when baseline abnormalities of the ECG compromise interpretation.*

Class IIa

  1. Dipyridamole or adenosine stress perfusion nuclear scintigraphy or dobutamine echocardiography before discharge for prognostic assessment in patients judged to be unable to exercise.
  2. Exercise two-dimensional echocardiography or nuclear scintigraphy (before or early after discharge for prognostic assessment).

Class III

  1. Stress testing within 2 to 3 days of acute MI.
  2. Either exercise or pharmacological stress testing at any time to evaluate patients with unstable postinfarction angina pectoris.
  3. At any time to evaluate patients with acute MI who have uncompensated CHF, cardiac arrhythmia, or noncardiac conditions that severely limit their ability to exercise.
  4. Before discharge to evaluate patients who have already been selected for cardiac catheterization. In this situation an exercise test may be useful after catheterization to evaluate function or identify ischemia in distribution of a coronary lesion of borderline severity.

Assessment of Ventricular Arrhythmia--Routine Testing

Class I

Class IIa

Class IIb

  1. Ambulatory (Holter) monitoring, signal-averaged ECG, heart rate variability, baroreflex sensitivity monitoring, alone or in combination with these or other tests, including functional tests (ejection fraction, treadmill testing) for risk assessment after MI, especially in patients at higher perceived risk, when findings might influence management issues, or for clinical research purposes.

Invasive Evaluation

Coronary Angiography and Possible PTCA

Class I

  1. Patients with spontaneous episodes of myocardial ischemia or episodes of myocardial ischemia provoked by minimal exertion during recovery from infarction.
  2. Before definitive therapy of a mechanical complication of infarction such as acute mitral regurgitation, VSD, pseudoaneurysm, or LV aneurysm.
  3. Patients with persistent hemodynamic instability.

Class IIa

  1. When MI is suspected to have occurred by a mechanism other than thrombotic occlusion at an atherosclerotic plaque. This would include coronary embolism, certain metabolic or hematological diseases, or coronary artery spasm.
  2. Survivors of acute MI with depressed LV systolic function (LV ejection fraction less than or equal to 40%), CHF, prior revascularization, or malignant ventricular arrhythmias.
  3. Survivors of acute MI who had clinical heart failure during the acute episode but subsequently demonstrated well-preserved LV function.

Class IIb

  1. Coronary angiography performed in all patients after infarction to find persistently occluded infarct-related arteries in an attempt to revascularize the artery or to identify patients with three-vessel disease.
  2. All patients after a non-Q wave MI.
  3. Recurrent VT or VF or both, despite antiarrhythmic therapy in patients without evidence of ongoing myocardial ischemia.

Class III

  1. Routine use of coronary angiography and subsequent PTCA of the infarct-related artery within days after receiving thrombolytic therapy.
  2. Survivors of MI who are thought not to be candidates for coronary revascularization.

Routine Coronary Angiography and PTCA After Successful Thrombolytic Therapy

Class I

Class IIa

Class III

  1. Routine PTCA of the stenotic infarct-related artery immediately after thrombolytic therapy.
  2. Percutaneous transluminal coronary angioplasty of the stenotic infarct-related artery within 48 hours of receiving a thrombolytic agent in asymptomatic patients without evidence of ischemia.

Secondary Prevention

Management of Lipids

Class I

  1. The AHA Step II diet, which is low in saturated fat and cholesterol (less than 7% of total caloriesas saturated fat and less than 200 mg/d cholesterol), should be instituted in all patients after recovery from acute MI.
  2. Patients with LDL cholesterol levels greater than 125 mg/dL despite the AHA Step II diet should be placed on drug therapy with the goal of reducing LDL to less than 100 mg/dL.
  3. Patients with normal plasma cholesterol levels who have a high-density lipoprotein (HDL) cholesterol level less than 35 mg/dL should receive nonpharmacological therapy (eg, exercise) designed to raise it.

Class IIa

  1. Drug therapy may be added to diet in patients with LDL cholesterol levels less than 130 mg/dL but greater than 100 mg/dL after an appropriate trial of the AHA Step II diet alone.*
  2. Patients with normal total cholesterol levels but HDL cholesterol less than 35 mg/dL despite diet and other nonpharmacological therapy may be started on drugs such as niacin to raise HDL levels.

Class IIb

  1. Drug therapy using either niacin or gemfibrozil may be added to diet regardless of LDL and HDL levels when triglyceride levels are greater than 400 mg/dL.

Long-Term -Adrenoceptor Blocker Therapy in Survivors of Myocardial Infarction

Class I

  1. All but low-risk patients without a clear contraindication to -adrenoceptor blocker therapy. Treatment should begin within a few days of the event (if not initiated acutely) and continue indefinitely.

Class IIa

  1. Low-risk patients without a clear contraindication to -adrenoceptor blocker therapy.

Class III

  1. Patients with a contraindication to -adrenoceptor blocker therapy.

Anticoagulants

Class I

  1. For secondary prevention of MI in post-MI patients unable to take daily aspirin.
  2. Post-MI patients in persistent AF.
  3. Patients with LV thrombus.

Class IIa

  1. Post-MI patients with extensive wall motion abnormalities.
  2. Patients with paroxysmal AF.

Class IIb

  1. Post-MI patients with severe LV systolic dysfunction with or without CHF.

Estrogen Replacement Therapy (ERT) and Myocardial Infarction

Class IIa

  1. All postmenopausal patients who have an MI should be carefully counseled about the potential beneficial effects of ERT and offered the option of ERT if they desire it.

 




 

 

*Oral or topical preparations may be substituted.

 

 

*Repeat ECGs recommended during medical observation in clinical settings when initial ECG is nondiagnostic of ST elevation.

 

 

†Time of symptom onset is defined as beginning of continuous persistent discomfort that brought the patient to the hospital.

 

 

†Individuals who perform more than 75 PTCA procedures per year.

 

 

§Centers that perform more than 200 PTCA procedures per year.

 

 

*Transcutaneous patches applied; system may be attached and activated within a brief time if needed. Transcutaneous pacing may be very helpful as an urgent expedient. Because it is associated with significant pain, high-risk patients likely to require pacing should receive a temporary pacemaker.

 

 

†Apply patches and attach system; system is in either active or standby mode to allow immediate use on demand as required. In facilities in which transvenous pacing or expertise are not available to place an intravenous system, consideration should be given to transporting the patient to one equipped and competent in placing transvenous systems.

 

 

‡It should be noted that in choosing an intravenous pacemaker system, patients with substantially depressed ventricular performance, including right ventricular infarction, may respond better to atrial/AV sequential pacing than ventricular pacing.

 

 

§An electrophysiology study should be considered to assess the site and extent of heart block in uncertain cases.

 

 

*Marked abnormalities in the resting ECG such as LBBB, LV hypertrophy with strain, ventricular pre-excitation, or a ventricular paced rhythm render a displacement of ST segments virtually uninterpretable. For patients taking digoxin or who have less than 1 mm ST depression on their resting tracing who undergo standard stress electrocardiographic testing, it must be realized that further ST depression with exercise may have minimal diagnostic significance.

 

 

*HmG CoA reductase drugs provide the greatest lowering of LDL cholesterol. Niacin is less effective in lowering LDL, although it is more effective in raising HDL levels. Resins are rarely sufficiently effective to be used alone, but they may be used to supplement lowering LDL with either niacin or HmG CoA reductase drugs.

 

 

†See "Initial Recognition and Management in the Emergency Department," "Aspirin."

 

 


"ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction" was approved by the American College of Cardiology Board of Trustees on July 10, 1996, and by the American Heart Association Science Advisory and Coordinating Committee on June 20, 1996.

When citing this document, the American College of Cardiology and the American Heart Association request that the following format be used: Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM, Hillis LD, Hiratzka LF, Rapaport E, Riegel BJ, Russell RO, Smith EE III, Weaver WD. ACC/AHA guidelines for the management of patients with acute myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol. 1996;28:1328-1428.

A single reprint of this document (Executive Summary and Listing of Recommendations) is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0092. To obtain a reprint of the complete Guidelines published in the November issue of the Journal of the American College of Cardiology, ask for reprint No. 71-0094. To purchase additional reprints, specify version reprint number: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or E-mail pubauth@amhrt.org. To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400.

(Circulation. 1996;942341-2350.)

© 1996 American College of Cardiology and American Heart Association, Inc.

 

© 1998 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.

The information contained in this American Heart Association (AHA) Web site is not a substitute for medical advice or treatment, and the AHA recommends consultation with your doctor or health care professional.