Executive Summary andListing of Recommendations Show
PurposeThese 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 IssuesEach 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 DepartmentWhen 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 ManagementThe First 24 HoursOnce 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, β-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 β-adrenergic blocker therapy, followed by oral therapy, provided that there is no contraindication. β-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 β-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 β-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 HoursAfter the first day in the hospital, the patient with acute MI should continue to receive aspirin 160 to 325 mg/d indefinitely with a β-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, β-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 HospitalBefore 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 ManagementFor an indefinite period after acute MI, the patient should continue to receive aspirin, a β-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. RecommendationsThe 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 ClassesAs 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 IssuesClass 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 DepartmentClass 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 Measures1. 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. OxygenClass 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 NitroglycerinClass 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 None. 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). AspirinClass 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. AtropineClass 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. ThrombolysisClass 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 PTCAClass 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 PTCAClass I None. 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 SurgeryClass 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 CohortClass 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 ManagementEarly, General MeasuresClass 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 RiskManagement of Recurrent Chest DiscomfortClass I 1. Aspirin for pericarditis. 2. β-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 MonitoringBalloon Flotation Right-Heart Catheter MonitoringClass 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. Intra-arterial Pressure MonitoringClass 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 CounterpulsationClass 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 hemodynamic instability. 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 DisturbancesAtrial FibrillationClass 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 β-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 β-adrenoceptor blocking agents are contraindicated or ineffective. Ventricular Tachycardia/Ventricular FibrillationClass 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: a. 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). b. 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. c. 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. d. 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 β-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. Bradyarrhythmias and Heart BlockAtropineClass 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 None. 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. Temporary PacingPlacement 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. 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. Permanent Pacing After Acute Myocardial InfarctionClass 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.=s 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 InterventionsEmergency 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 PharmacotherapyAntithrombotics/AnticoagulantsHeparinClass 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 12 500 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. β-Adrenoceptor Blocking AgentsEarly Therapy Class I 1. Patients without a contraindication to β-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 β-adrenoceptor blocker therapy. Angiotensin Converting Enzyme InhibitorsClass 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 BlockersClass I None Class IIa 1. Verapamil or diltiazem may be given to patients in whom β-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. MagnesiumClass I None. 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 HospitalNoninvasive Evaluation of Low-Risk PatientsStress ECGClass I a. Before discharge for prognostic assessment or functional capacity (submaximal at 4 to 6 days or symptom limited at 10 to 14 days). b. Early after discharge for prognostic assessment and functional capacity (14 to 21 days). c. Late after discharge (3 to 6 weeks) for functional capacity and prognosis if early stress was submaximal. 2. 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 TestingClass I None. Class IIa None. 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 EvaluationCoronary Angiography and Possible PTCAClass 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 TherapyClass I None. Class IIa None. 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 PreventionManagement of LipidsClass 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 β-Adrenoceptor Blocker Therapy in Survivors of Myocardial InfarctionClass I 1. All but low-risk patients without a clear contraindication to β-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 β-adrenoceptor blocker therapy. Class III 1. Patients with a contraindication to β-adrenoceptor blocker therapy. AnticoagulantsLong-Term Anticoagulation After Acute Myocardial InfarctionClass 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 InfarctionClass 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. “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 [email protected] To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400. *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. =sAn 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.” Page 2
Reducing intake of saturated fat and dietary cholesterol and avoiding excess calories, which can lead to obesity, remain the cornerstore of the dietary approach to decreasing risk of atherosclerotic vascular disease. During the past 20 years, however, there has been renewed interest in other dietary components that might favorably improve lipid profiles and reduce risk of coronary heart disease (CHD). Fish and fish oil, rich sources of omega-3 fatty acids, have sparked intense interest in both epidemiological studies, which suggest a favorable effect on CHD, and metabolic ward studies, which show a striking improvement in lipid profiles in hyperlipidemic patients. Confusion has resulted from clinical trials of fish oil in patients with CHD, which did not corroborate early observational findings, and newer results, which suggest clinical benefit due to a mechanism independent of lipid effects. Fish and other marine life are rich sources of a special class of polyunsaturated fatty acids known as the omega-3 or n-3 fatty acids.12 They are so named because the first of the several double bonds occur three carbon atoms away from the terminal end of the carbon chain. The three n-3 polyunsaturated fatty acids (n-3 PUFAs) are alpha linolenic acid (LNA), eicosapentenoic acid (EPA), and docosahexenoic acid (DHA). LNA is an 18–carbon chain fatty acid with three double bonds; in the form of tofu, soybean, and canola oil and nuts, it is an important plant-based source of n-3 PUFA for vegetarians and non–seafood eaters. EPA and DHA are very long–chain fatty acids obtained from marine sources. These, along with n-6 polyunsaturated fatty acids (n-6 PUFAs) that cannot be synthesized from nonlipid precursors such as linoleic acid, are considered essential fatty acids that must be consumed in the diet. The n-6 PUFAs are obtained primarily from plant sources, especially seeds. Arachidonic acid is a long-chain n-6 PUFA that is found in meats, fish, and plants or is synthesized from linoleic acid. Arachadonic acid and marine lipids both serve as key intermediates for eicosanoids like thromboxanes and prostacyclins, which are important for platelet and vessel wall physiology. The addition of omega-3 fatty acids to the diet lowers triglyceride levels, an effect that is pronounced in those with marked hypertriglyceridemia.3 The triglyceride-lowering effect is not seen with plant sources of n-3 PUFA.4 In those patients with type V hyperlipidemia, the use of fish oil supplements is an important therapeutic option.5 Connor6 listed the following putative mechanisms of dietary n-3 PUFA on lipoprotein metabolism in humans: (1) inhibition of VLDL triglyceride synthesis, (2) decreased apoprotein B synthesis, (3) enhancement of VLDL turnover with an increased fractional catabolic rate of VLDL, (4) depression of LDL synthesis, and (5) reduction of postprandial lipemia. A critical review by Harris2 has clarified the discrepancy among fish oil studies reporting effects on LDL cholesterol (LDL-C). He noted that in the majority of studies reporting reductions in LDL-C levels, the saturated fat intake was lowered when subjects switched from the control diet to the fish oil diet. When fish oil is consumed and saturated fat intake is constant, LDL-C levels either do not change or may increase. Although fish oil is not recommended in the treatment of hypercholesterolemia, it does have a role in the treatment of lipoprotein disorders characterized by severe hypertriglyceridemia. It can be quite useful in those severely hypertriglyceridemic (triglyceride >1000 mg/dL) patients for whom attempts to correct secondary causes (through diet, exercise, and gemfibrozil) have proved inadequate.7 Although a negative aspect is the concomitant elevation in LDL-C that occurs when fish oils are given to these patients with lower plasma levels of triglyceride, this is usually not a problem for those with severe hypertriglyceridemia, because LDL-C values are usually quite low. It can be a problem for those with more modest elevations of triglycerides in whom the elevation of LDL-C will actually move the patient away from the desired LDL-C goal. Fish oil supplementation does not appear to impair glucose tolerance in nondiabetic coronary bypass patients.8 Among diabetics, initial studies showed deterioration of glucose tolerance with fish oil consumption.9 Nonetheless, Connor and coworkers10 designed a longer term study in which body weights were unchanged between fish oil and olive oil groups and no deterioration in glucose homeostasis was demonstrated in those individuals with diabetes. Westerveld and colleagues11 conducted a randomized, blinded, placebo-controlled trial that also documented reduced platelet aggregation as well as triglyceride lowering in the fish oil group. In both trials the fall in triglyceride level was accompanied by a rise in LDL-C similar to that seen in studies of patients with combined hyperlipidemia.12 This rise in LDL-C level was not seen when a low dose of omega-3 fatty acids was given to 20 ambulatory subjects with non–insulin-dependent diabetes mellitus in a randomized, double-blind, prospective, controlled clinical trial.13 Although sample size may have been inadequate to show an LDL-C effect, fish oil significantly inhibited platelet aggregation and thromboxane A2 production, while it reduced triglyceride levels by 44 mg/dL and decreased upright systolic blood pressure by 8 mm Hg compared with safflower oil. Finally, a recent study looking at vascular reactivity suggested that fish oil ingestion in diabetics could favorably alter arterial wall compliance without affecting fasting blood sugar, cholesterol, or blood pressure.14 Clearly, further research on the use of n-3 PUFA in diabetics is required. A meta-analysis of placebo-controlled studies showed that fish oil reduced blood pressure in a dose-response fashion in those with hypertension and hypercholesterolemia but not in those participants with normal blood pressures.15 The effects were small, and it is not clear whether this effect is sustained over the long term. A concise review of studies on the prevention of thrombosis in laboratory animals and in humans emphasized the important role of n-3 PUFA, which affects cellular responses in platelets, monocytes, and endothelial cells.16 The reduced platelet aggregation and prolonged bleeding times of the Greenland Eskimos suggested an important mechanism by which n-3 PUFAs could affect CHD.17 When bleeding times are measured, the effects of fish oil are additive to those of aspirin.18 Studies in swine fed high cholesterol diets with and without cod liver oil showed that there was less coronary atherosclerosis in the cod liver oil group but that there was no relationship to lipid changes. The pigs fed cod liver oil had significant decreases in serum thromboxane B2 levels and increases in platelet fatty acid deposition of EPA.19 Fish oil supplements increased levels of tissue plasminogen activator (TPA) and decreased concentrations of plasminogen activator inhibitor, both enhancers of fibrinolysis.20 One study comparing fish oil with rapeseed oil noted that fish oil decreased lipoprotein(a) by 14%.21 This effect was not seen in all male subjects who were hospitalized with CHD but did correlate with a large reduction in TPA. The Atherosclerosis Risk in Communities study compiled data from four US communities (15 000 participants, both black and white) on six hemostatic factors: fibrinogen, factor VII, factor VIII, von Willebrand factor, protein C, and antithrombin III.22 These were communities not known for their high intake of fish. Dietary intake of n-3 PUFA showed negative associations with levels of fibrinogen, factor VIII, and von Willebrand factor and a positive association with protein C (whites only). These findings may help explain, in part, the reduced incidence of vein graft occlusion seen in patients after coronary artery bypass grafting who receive n-3 PUFA.23 In a randomized controlled trial of dietary supplementation with n-3 fatty acids in bypass patients who received usual anticoagulation with aspirin or warfarin, an inverse relation between relative change in serum phospholipid n-3 fatty acids and vein graft occlusions was observed. Thus, the prevention of thrombosis remains a promising area for n-3 PUFA research. The potent anti-inflammatory effects of fish oils and their effects on the immune response are beyond the scope of this review. Worthy of mention are the detailed studies of Meydani et al24 on immune responses seen with dietary fish supplementation. They showed decreased cell-mediated immunity when the Step II National Cholesterol Education Program (or AHA) diet was supplemented with a high fish intake as compared with one low in fish intake (121 to 188 g of fish per day versus 33 g of fish per day). The clinical significance of this important finding needs further investigation. Early studies of Greenland Eskimos (Inuit) highlighted their lower coronary mortality compared with their Danish counterparts. The Eskimos' diet included a strikingly higher intake of n-3 PUFAs rich in marine sources such as seal and whale that resulted in lower blood cholesterol, lower triglycerides, lower LDL-C, lower VLDL cholesterol, increased HDL cholesterol, increased bleeding times, and lower rates of CHD. In addition, prospective epidemiological studies from the Netherlands, Chicago, and the Multiple Risk Factor Intervention Trial confirmed that men who ate at least some fish per week had a lower mortality from CHD than those men who ate none.25262728 On the other hand, two studies describing populations with high intakes of fish did not show such a beneficial effect.2930 There is no convincing role for fish oil supplements in the prevention of CHD. The strongest evidence indicating a beneficial effect of fish intake on CHD came from the Diet and Reinfarction Trial (DART), in which men who were instructed to eat fish after myocardial infarction (MI) had a 29% decline in all-cause mortality as compared with those in the placebo group.31 No significant lowering of cholesterol was seen, and very few men were taking aspirin. Yet the Health Professionals Follow-up Study,32 a large-scale prospective cohort study, reported no association between increasing fish intake and CHD. The authors concluded that increasing fish intake beyond one or two servings per week is not likely to improve the primary prevention of CHD. A nested case-control study was conducted among the 14 916 participants in the Physicians' Health Study.33 Each participant with MI was matched by smoking status and age with a randomly chosen control participant who had not developed CHD. Fish oil intake was estimated by measuring plasma levels in cholesterol esters and phospholipids. No association was found between fish oil levels and the incidence of MI even when results were adjusted for major cardiovascular risk factors. Although early trials suggested that fish oil held some promise if ingested early before angioplasty, a clinical trial large enough to find a significant effect did not, despite a dose of 8 g/d of n-3 PUFA.34 This trial did document the safety of fish oil supplementation without any evidence of excess bleeding in the patients who all took aspirin. Moreover, a clinical trial with angiographic end points showed that among normocholesterolemic men with CHD, fish oil treatment (6 g n-3 PUFA for 2 years) did not produce significant changes in the diameter of the coronary arteries.35 DART peaked interest in whether a diet rich in fish oil could reduce risk of sudden death because of the striking difference in sudden deaths seen early in the trial, suggesting a possible action on either thrombosis or arrhythmic death rather than on atherosclerosis.9 Support for the latter hypothesis came from the Lyon Trial,36 which compared a “Mediterranean-type” diet rich in LNA with the AHA Step I diet in patients with known MI. Although no improvement in lipids, lipoproteins, and body mass index was seen, there was a striking difference in mortality, with eight sudden deaths in the control group and none in the alpha LNA–rich diet group. The risk ratio of cardiac death was 0.19 (95% CI, 0.06 to 0.65), with P<.002. These findings were extended by the carefully done population-based case-control study from Seattle and King County, Washington.37 Among 334 patients with primary cardiac arrest, the intake of n-3 PUFA per month was significantly less than that seen in age- and sex-matched community controls. The data suggested that an intake of 5.5 g of n-3 PUFA per month (equivalent to one fatty fish meal per week) was associated with a 50% reduction in the risk of primary cardiac arrest after adjustment for potential confounding factors. Moreover, studies of red blood cell membrane n-3 PUFA in both patients and controls allowed calculation of risk based on this sensitive parameter of dietary n-3 PUFA intake. These findings were consistent with experimental evidence suggesting that the n-3 PUFAs have an important effect on vulnerability to ventricular fibrillation in the setting of myocardial ischemia.38 Of additional interest are recent data showing suppression of premature ventricular contractions (PVCs) in middle-aged patients with frequent PVCs randomly assigned to take either fish oil (as cod liver oil containing 2.4 g of n-3 PUFA) or sunflower seed oil.39 Clearly, further studies are needed to explore the potential of fish oil in the prevention of sudden cardiac death. When considering cardiovascular health, it seems premature to recommend general usage until compelling evidence for the beneficial action of fish oil supplements is at hand. Although doses of 3 to 8 g of n-3 PUFA per day in those with CHD were not associated with significant adverse effects in recent clinical trials,834 evidence for beneficial effects in CHD patients is either lacking or needs additional study. Currently, fish oil capsules can only be recommended for the infrequent patients with severe, treatment-resistant hypertriglyceridemia who are at increased risk for pancreatitis. Potential side effects should be kept in mind (Table140 ). On the other hand, inclusion of marine sources of the n-3 PUFA in the diet seems reasonable because they are good sources of protein without the accompanying high saturated fat seen in fatty meat products. Moreover, as Harris has noted, the potential for benefit remains high, since dietary fish oils affect “a myriad of potentially atherogenic processes.”41 This requires the continued support of cardiovascular research on the n-3 PUFA. Single reprints are free: Call 1-800-242-8721 (US only) or write American Heart Association, Public Information, 7272 Greenville, Dallas, TX 75231-4596. “Fish Consumption, Fish Oil, Lipids, and Coronary Heart Disease” was approved by the Science Advisory and Coordinating Committee of the American Heart Association in July 1996. Single reprints are free: Call 1-800-242-8721 (US only) or write American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Table 1. Potential Side Effects of Fish Oil Capsules1,37,38,40 References
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