The Journal of Emergency
Medicine,
Printed in the USA . Copyright 0 1992 Pergamon Press Ltd.
Vol 10, pp 455-461, 1992
THE DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION IN THE EMERGENCY DEPARTMENT; PART 1 Charles H. Herr, MD, FACEP Department of Medicine, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Reprint Address: Charles Herr, MD, Emergency Department, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756
0 Abstract-Despite major advances in treatment, the accurate diagnosis of acute myocardial infarction (AMI) in the emergency department (ED) remains a difficult clinical problem and is still mainly based on the history and interpretation of the electrocardiogram. Although the physician’s clinical impression is a highly sensitive indicator for AMI, at least 4% of patients presenting to the ED with AMI may be mistakenly sent home. Althoagh chest pain is the most common chief complaint, the clinical presentation can be extremely variable, particularly in the elderly. Complaints of sharp chest pain or chest wall tenderness should not be relied upon to exclude AMI. Radiation of chest pain is an important symptom. With careful analysis, the electrocardiogram may yield a higher diagnostic sensitivity than is commonly accepted.
remained an elusive goal. However, the accurate diagnosis of AM1 in the emergency department is important for reasons of morbidity and mortality prevention, cost-effectiveness, and liability. The rationale for admission to the coronary care unit (CCU) of patients with AM1 was originally for dysrhythmia treatment and has evolved more recently to include interventions directed toward preserving myocardium (3). Although two British studies found no significant difference in mortality when patients with AM1 were randomized to home or hospital care, both studies were flawed by their small numbers of patients and exclusion of high risk patients (4,5). Admission to a monitored bed for intensive management of the complications of AM1 and possibly for treatment with thrombolytic therapy is generally accepted as improving outcomes and has become the standard of care in this country (6). Primary ventricular fibrillation is a treatable cause of early mortality and has an incidence of 2.8% to 4.5% (7-9). Clearly, the inappropriate discharge of the patient with AM1 from the emergency department may have serious consequences. In one study, among 35 patients discharged from the emergency department with AMI, the mortality at 72 hours was 26% compared to a mortality of 12% among a control group of 105 patients hospitalized with AM1 (10). The misdiagnosis of AM1 in the emergency department (ED) also presents a major medicolegal hazard (11). Data from the American College of
0 Keywords-myocardial infarction; chest pain; cardiac enzymes; electrocardiogram
INTRODUCTION
Cardiovascular disease remains the leading cause of mortality in this country, and an estimated 1.5 million people per year sustain a myocardial infarction (1). Patients with symptoms suggestive of acute myocardial infarction (AMI) present commonly to the emergency department. While the diagnosis of AM1 can almost always be reliably confirmed or excluded within the first 24 hours of hospital admission (2), diagnostic certainty in the emergency department has --___ =
. _ cardtology Commentary, a section devoted to topics in bedside cardiology and electrocardiography, is coordi-
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nated by Stephen R. Lowenstein, MD, MPH, University of Colorado Health SciencesCenter, Denver. RECEIVED: 2 July 1991; FINAL SUBMISSIONRECEIVED: 22 October 1991; 0736-4679/92 $5.00 + .OO ACCEPTED; 16 December 1991 455
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Emergency Physicians Insurance Committee indicate that nearly 20% of total dollar losses from malpractice claims settled between 1974 and 1983 was related to the misdiagnosis and substandard treatment of AM1 and amounted to 5.3 million dollars (12). Clearly, the emergency physician faces substantial malpractice risk for misdiagnosis of AMI. Given the potential medical complications and medicolegal consequences of erroneously discharging the patient with AM1 from the ED, physicians generally follow a liberal admission policy. There are an estimated 1.5 million CCU admissions annually in this country, and up to 70% of these admissions eventually rule out for AM1 (13-18). Rule-out rates may be somewhat higher at nonteaching as compared to teaching hospitals (19). Because of the substantial costs incurred by admission to a CCU bed, this high false-positive diagnostic rate has generated considerable interest regarding the issue of cost-effectiveness (20,21). The emergency physician, therefore, is confronted with the dilemma of avoiding underdiagnosis of AM1 with the concomitant increased risk of morbidity, mortality, and litigation, while at the same time avoiding over-diagnosis and the criticism of poor cost-containment. Studies addressing the physician’s diagnostic sensitivity for detecting AM1 in the ED report values ranging from approximately 90% to 97% (14-16,22) (Table 1). In the most recent and largest of these studies, physicians admitted 95.8% of patients with AMI, with 94.8% being admitted to monitored beds (16). Nearly the same sensitivity was attained in a large earlier study in which the diagnostic criteria also included new-onset or unstable angina (23). Tierney has stated that of all the clinical variables associated with the diagnosis of AMI, the physician’s estimate of probability is the single greatest predictor of AM1 (24). Nevertheless, at least 4% of patients presenting with AM1 are mistakenly discharged from the emergency department. In addition, studies of autopsyTable 1. Characteristics
Study (reference) (year) Schor et al (22) (1976) Hedges et al (14) (1967) Seiker et al (15) (1967) Goldman et al (16) (1966)
proven AM1 indicate that the correct antemortem diagnosis was made in only slightly more than 50% of the cases (25). The physician’s poorest diagnostic accuracy appears to occur with those cases where the estimated probability of AMI falls into the intermediate range (24). Part 1 of this series will review the literature regarding the role of the clinical presentation and electrocardiogram (ECG) interpretation in the evaluation of ED patients with possible AMI. Part 2 will examine the data on cardiac enzymes, predictive instruments, echocardiography, thallium scanning, and risk-based triage criteria.
RISK FACTORS Eliciting a thorough history from the patient with possible AM1 usually includes questioning the patient for possible cardiovascular risk factors. Classically, these factors include obesity, hypertension, smoking, hypercholesterolemia, diabetes, and a family history of cardiovascular disease (26). For the patient with a known history of angina or myocardial infarction who presents with a potentially new ischemic event, a history of risk factors has limited significance from a purely diagnostic perspective, since the presence of cardiovascular disease is a known fact. However, for the patient who presents with an atypical history or nondiagnostic ECG and no prior history of cardiac ischemia, the presence or absence of risk factors is usually considered important data that the physician integrates into the decision-making process to arrive at a probability prediction for AMI. Data from several large studies provide very little support for the diagnostic value of a history of risk factors. In three large studies that collectively have evaluated over 10,000 patients presenting to emergency departments with chest pain, no classical cardiac risk factor emerged as an independent predictor of AM1 (16,
and Triage of ED Patients with Symptoms
Suggestlve
of Myocardlai
Infarction
Number of ED Patients
Percent of Patients with AMI
Percent of Discharged Patients with AMI
Percent of AMis Discharged
Percent of Admissions with AMI
1,355’ nst 4,479$ 4,770t
33.9 6.6 16.4 12.1
5.6 1.0 2.0 1.1
7.6 9.6 2.9 4.2
58.5 15.6 24.3 21.7
AMI = acute myocardiai infarction. *Patients referred to ED with presumed AMI. +Patients age b 30 with chief complaint of chest pain. *Male patients age 230 and female patients 240 with chief complaint of chest pain, shortness of breath, or other symptoms suggestive of acute ischemic heart disease.
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Myocardial infarction
18,23). In each study a prior history of infarction or angina proved to be a significant independent variable. CLINICAL
PRESENTATION
The classical presentation of AM1 was described by Herrick as a severe pressure or tightness in the anterior chest and epigastrium with or without radiation and associated symptoms of nausea, vomiting, diaphoresis and dyspnea (27). Chest pain is regarded as the most common presenting complaint of the patient with AMI, but the limited sensitivity and specificity of this symptom has been recognized. The perception of cardiac pain is a complex process with modulation at several neurologic levels (28). Hence, chest pain is not the sole chief complaint, and when present its description has considerable variability. In Kinlen’s study (29) of 201 patients with AMI, pain was present in the chest or epigastrium in 82% of the cases and was described as crushing, constricting, or vicelike in 20%. More than 20% of the patients described a burning sensation or indigestion. Lee prospectively studied 596 patients presenting to an ED with a chief complaint of chest pain not explained by local trauma or chest x-ray abnormalities (30). Only 24% of the patients who described their pain as “pressure” were proven to have AMI. Of the 104 patients diagnosed with AMI, 59% described their pain as “pressure,” 10% as “aching,” 10% as “burning” or “indigestion,” and 8% as “sharp” or “stabbing.” In a recent study of 278 patients presenting to an ED with a chief complaint of chest pain (31), the most sensitive features were duration of pain greater than 60 minutes (88.8%), constriction or squeezing (78.6%), oppression (74.5%), and sudden onset (69.6%). However, the specificity for all of these descriptive characteristics ranged from 30% to 40070, and the highest positive predictive value was 42%. Part of the low specificity of the “typical” cardiac symptoms may be attributable to the ability of esophageal disorders to mimic the symptoms of cardiac ischemia (32,33). In one study, 32 of 55 patients discharged from a CCU after ruling out for AM1 demonstrated esophageal dysfunction by acid perfusion testing and manometry (34). It also appears that the chest pain experienced by outpatients with known coronary artery disease may frequently be caused by gastroesophageal reflux and esophageal motility disorders (35). In addition, the diagnostic specificity of symptom relief with sublingual nitroglycerin is lowered by the proven ability of nitroglycerin to relieve the symptoms of diffuse esophageal spasm (36). The classical presentation of AM1 includes associ-
ated symptoms of nausea, vomiting, diaphoresis, dyspnea, and radiation of pain. However, Ahnve reported (37) that the incidence of nausea, vomiting and dyspnea did not differ significantly among patients with and without AMI. In Kinlen’s study (29), diaphoresis was reported by 60% of the patients with AMI, and in Tierney’s derivation (18) of a logistic regression model, diaphoresis with chest pain emerged as a significant independent variable. The complaint of nausea had a sensitivity of 41% and a specificity of 84% in the most recent study of clinical presentation (31). In two large studies of ED patients with chest pain, nausea, vomiting, and diaphoresis did not have any significant predictive value (16,23). Pain radiation, on the other hand, may be a useful symptom in the evaluation of the patient with possible AMI. Ahnve reported (37) pain radiation in 67% of patients with AM1 compared with 46% of those patients who ruled out. Similar numbers were recorded in a study by Sawe (38) in which 71% of the cases with AM1 complained of radiation of pain into the neck or arms compared with 39% of the patients proven not to have AMI. In Berger and colleagues’ study (31) of 278 patients, left arm radiation of pain proved to have a sensitivity of 55% but a specificity of 76%. Most notably in that same study, radiation of pain into the right arm produced a sensitivity of 41% but a specificity of 94% and a positive predictive value of 80%. Finally, in Goldman and colleagues’ computer-derived protocol (16) for the prediction of AMI, the presence or absence of pain radiation to the neck or left arm or shoulder is one of nine significant clinical variables. Chest pain that is described as sharp or pleuritic is commonly assumed to originate from the chest wall and to be atypical of myocardial infarction. This is usually the case, but Hedges and Kobernick caution (39) that patients may commonly misinterpret the word “sharp” as meaning “severe” and that further clarification of this descriptive term should be sought. Tierney and colleagues reported (24) that 16% of the patients with infarction complained of sharp chest pain, and 15% had chest wall tenderness. Similarly, 8% of the patients with AM1 in Lee and colleagues’ study (30) described their chest pain as sharp or stabbing. In this latter study only a combination of sharp or stabbing pain and pain that was pleuritic, positional, or reproduced by palpation was sufficient to exclude AMI. In addition, it is possible for a patient to have both chest wall pain and pain of cardiac origin simultaneously. One study reported (40) that chest wall pain was present in 51% of patients with documented ischemic heart disease, but in only 23% of matched controls.
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Although most of the studies involving the diagnosis of AM1 have focused on the patient presenting with a chief complaint of acute chest pain, it is clear that myocardial infarction commonly occurs in the absence of chest pain. In fact, recent analysis of data from the Framingham Study (41) reveals that 25% of myocardial infarctions are clinically silent. In a study of 102 consecutive patients with proven AM1 who presented to the Boston City Hospital ED (42), 26 patients had no complaint of chest pain. Their primary complaints included dyspnea, abdominal pain, fatigue, left arm pain, cough, nausea and vomiting, and syncope. Most worrisome was the discovery that the mortality rate among the patients without chest pain was 50% as compared to 18% mortality in the group with chest pain. The higher rate of mortality among patients without chest pain was confirmed in a later report by Fesmire and Wears (43). Among 424 patients admitted from the ED with suspected myocardial infarction, the mortality rate was three times higher among those patients who never experienced chest pain as compared to those whose chest pain persisted or recurred in the ED, and 7.9 times higher compared to those whose chest pain resolved prior to arrival in the ED. It has been suggested that a history of prodromal symptoms could be helpful in the evaluation of the patient with possible AMI. An NIH study reported (44) that prodromal symptoms occurred in 70% of 160 patients hospitalized with myocardial infarction and in 64% of 138 patients who died from acute coronary disease out of hospital. The prodromata included chest pain, dyspnea, and arm pain, but also such symptoms as fatigue, malaise, weakness, dizziness, syncope, anorexia, nausea, and emotional changes. These symptoms preceded the acute event by days to weeks, and more than a quarter of the patients had consulted a physician at least once for these symptoms. However, a more recent study (45) of 276 CCU admissions found that other than angina, symptoms of stress, weakness, fatigue, or dyspnea during the 4 weeks prior to admission had no significant predictive value. The presentation of AM1 in the elderly is commonly nonclassical, and diagnosis is especially difficult. In one autopsy series (46) of 200 consecutive cases of AM1 in the elderly, the correct antemortem diagnosis was made only 43% of the time. The incidence of painless AM1 increases dramatically with age (47-49). More than 60% of myocardial infarctions in patients 85 or older will present without chest pain (47,49). In a study of 7,734 patients, Solomon found that for classical symptoms, the relative risk for AM1 was significantly lower in patients 65 or
Charles H. Herr
older when compared to the younger age group (50). A retrospective review of 777 cases of AM1 in patients age 60 to 100 demonstrated a decreased frequency of chest pain and diaphoresis with increasing age and an increased frequency of neurologic symptoms such as syncope, stroke, acute confusion, and weakness as the primary presenting complaint (47). In that same study the incidence of dyspnea and vomiting was not influenced by age. Several explanations are offered to account for the frequency of atypical presentations in the elderly. These include blunted autonomic responsiveness and a high incidence of coexistent disease. In addition, one author has demonstrated (51) a high correlation between atypical presentations of AM1 and poor performance on mental status testing.
DIAGNOSIS
BY ELECTROCARDIOGRAM
The electrocardiogram is the most commonly utilized diagnostic test in the evaluation of the patient with suspected myocardial ischemia or infarction. It is a quickly and easily obtainable test that is often reflexly ordered for the patient presenting with chest pain. It is also presently the major determinant of eligibility for thrombolytic therapy (52). Unfortunately, while the classic ECG changes of AM1 are highly specific, the initial ECG has proven to be a relatively insensitive test. Three previous studies that cumulatively evaluated over 1000 myocardial infarctions reported a sensitivity of the initial ECG that ranged from 43% to 65% (53-55). While the initial ECG demonstrates low sensitivity for AMI, the sensitivity of serial ECGs obtained after admission is considerably greater and in one study (54) was 83%. Clinicopathologic data correlating ECG findings with autopsy-proven AM1 is sparse, but tends to confirm the conclusions of the clinical studies. McQueen and colleagues reported (56) the initial ECG to be diagnostic in only 4 of 17 patients with proven AMI, but his ECG criteria were overly restrictive and excluded S-T segment depressions. In an autopsy study (25) of 100 consecutive acute myocardial infarctions, Zarling found that of the 85 cases for which an ECG was available, the ECG was diagnostic in only 25 cases and suggestive in 27 cases. However, the specific ECG criteria were not defined. The diagnostic inaccuracy of the initial ECG is in many cases attributable to baseline ECG abnormalities that make interpretation for ischemia or infarction difficult. Many cardiac conditions such as cardiomyopathy, left ventricular hypertrophy, and conduction abnormalities can either mimic or obscure the electro-
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cardiographic signs of infarction (57,58). One common abnormality that makes ECG interpretation for AM1 difficult, if not impossible, is the bundle branch block. However, it is sometimes possible using certain ECG criteria to diagnose acute infarction in the presence of bundle branch block (59,60). In many cases where the initial ECG findings are ambiguous or suggestive of ischemia or infarction, it would seem that the availability of a previous ECG for comparison would be an invaluable aid. However, one retrospective study (61) of 236 ED patients with chest pain concluded that the availability of a previous baseline ECG would have changed the physician’s decision to admit or discharge in only 17% of the cases. In a more recent prospective study (62) of 5,673 patients with chest pain, the availability of a prior ECG did not change the sensitivity for admission to the hospital or CCU of patients with AMI. However, non-AM1 patients with an available prior ECG were less likely to be admitted to the CCU than those non-AM1 patients without an old ECG, and this increased diagnostic specificity was most pronounced in those patients with ECG changes consistent with ischemia or infarction, Although most physicians consider the ECG to be an indispensable diagnostic aid, Hoffman and Igarashi showed (63) that the ECG may actually have very little influence on the physician’s decision-making process. In a study of 100 consecutive adult admissions to the ED with chest pain, the evaluating physician was asked to make the decision to admit or discharge the patient without having seen the ECG and then to re-evaluate this decision after reviewing the ECG. In only 4% of the cases did the physician reverse the original decision. Two recent large studies (64,65) have reported a surprisingly high sensitivity for the initial ECG. The first study (64) was derived from the Multicenter Investigation of the Limitation of Infarct Size (MILIS) and analyzed 3,697 CCU patients who presented with 30 minutes or more of pain thought to be ischemic. The ECG criteria included new Q waves (~30 ms wide and 10.20 mV deep), new S-T elevation or depression (10.10 mV), or complete left bundle branch block. Using these criteria, the sensitivity of the initial ECG was 8 1% and the specificity was 69%. Although this is the highest reported ECG sensitivity, these results are influenced by the patient population, which included only CCU patients. In addition, the study criteria eliminated from analysis and additional 2,158 patients admitted to the CCU for suspected MI during the same time period. The second study (65) is more recent, larger, and most importantly addresses an ED patient popula-
tion. The data from this study was obtained from 7,115 consecutive patients in the Multicenter Chest Pain Study, an analysis of patients aged 30 years or older presenting to the emergency departments of 7 institutions with a chief complaint of chest pain not explained by trauma or chest x-ray abnormalities. The following initial ECG criteria were considered highly suggestive of AMI: 1) 1 lmm S-T elevation or abnormal Q waves in ~2 leads; 2) 2 1 mm S-T depression in r2 leads; 3) other S-T or T wave changes of ischemia or strain including S-T depression < 1 mm and T wave inversions (all findings new or no old tracing available). The sensitivity of these criteria was 79%. Only 3% of patients with completely normal or nonspecific ECG changes subsequently proved to have AMI. Despite the fact that the ECG criteria were somewhat broad, the specificity of the initial ECG in this study was 83%. The interpretation of the initial ECG obtained in the ED also has important therapeutic implications. Large and well-designed clinical studies (66-68) have convincingly demonstrated substantial reductions in early mortality after AM1 when thrombolytic therapy is administered early. Since at present the benefits of thrombolysis apply mainly to those patients who demonstrate S-T segment elevation, careful interpretation of the initial ECG is critical in order that eligible patients are not denied potentially life-saving therapy. Given the limited sensitivity of the initial ECG, it is clear that substantial numbers of patients with AM1 will be denied thrombolytic therapy by present eligibility criteria. However, there is presently no convincing evidence that such therapy is beneficial to those patients without S-T segment elevations (52). It is also true, given the less than perfect specificity and positive predictive value of the initial ECG, that a significant number of patients who have the appropriate ECG criteria and who receive thrombolytic therapy will subsequently prove not to have AMI. By one estimate (69), using the present ECG criteria for treatment, for every 8 patients with proven AM1 who are treated, 1 to 2 patients with false positive ECGs will also be treated. Given the cost and complications of thrombolytic therapy, such a prediction has major implications regarding cost-effectiveness.
SUMMARY
Chest pain is the most common chief complaint of patients presenting to the ED with AMI. However, it is not the sole primary symptom of AMI, and there is evidence that the mortality may be higher among AM1 patients who do not complain of chest pain. In
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addition, chest pain has poor specificity for AMI, and the presence of esophageal motility disorders may account significantly for this low specificity. Although the chest pain of infarction is typically described as a pressure, crushing, or constricting sensation, there is considerable variation in the description of this complaint. In particular, a complaint of sharp pain should be interpreted with caution, and should not be taken as automatically excluding ischemia or infarction. Likewise, the presence of chest wall tenderness does not exclude concomitant acute coronary disease. Radiation of chest pain is an insensitive but moderately specific indicator of AMI. It should be considered an important historical feature that increases the possibility of AMI, particularly when pain radiates to the right arm. The associated symptoms of nausea, vomiting, diaphoresis, and dyspnea have relatively low sensitivity and specificity and do not emerge as significant independent predictors of AM1 in large prospective stud-
ies. Likewise, cardiac risk factors, typically used by the physician to formulate an initial baseline estimate of risk for coronary artery disease, have not been substantiated as important predictors of AM1 in large-scale studies of ED patients. Atypical presentation of AM1 is characteristic of the elderly. In particular, the incidence of chest pain and autonomic symptomatology decreases, and the incidence of primary neurologic complaints increases with advancing age. The diagnostic sensitivity of the initial ECG is generally considered to be quite low, approximately 50%. However, the study by Rouan and colleagues (65) stands in sharp contradistinction to this consensus. Employing rather liberal electrocardiographic criteria, the authors reported an initial ECG sensitivity for AM1 of 79% and a specificity of 83%. Because the study population included over 7,000 consecutive ED patients with chest pain at 3 university and 4 community hospitals, these findings may have considerable practical importance.
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12. Dunn J. Chest pain: foresight. Dallas: ACEP Publications; 1986:1-3. 13. Selker HP, Pozen MW, D’Agostino RB. Optimal identification of the patient with acute myocardial infarction in the emergency room. In: Califf RM, Wagner OS, eds. Acute coronary care: principles and practice. Boston: Martinus Nijhoff; 1985:289-98. 14. Hedges JR, Rouan GW, Toltzis R, Goldstein-Wayne B, Stein EA. Use of cardiac enzymes identifies patient with acute myocardial infarction otherwise unrecognized in the emergency department. Ann Emerg Med. 1987;16:248-52. 15. Selker HP, Griffith JL, Dorey FJ, D’Agostino RB. How do physicians adapt when the coronary care unit is full? a prosnective multicenter study. JAMA. 1987:257:1181-5. 16. Goldman L, Cook EF, Brand DA, et al:A computer protocol to predict myocardial infarction in emergency department patients with chest pain. N Engl J Med. 1988;318:797-803. 17. Fuchs R, Scheidt S. Improved criteria for admission to cardiac care units. JAMA. 1981;246:2037-41. 18. Tierney WM, Roth BJ, Psaty B, et al. Predictors of myocardial infarction in emergency room patients. Crit Care Med. 1985;13:526-31. 19. Bloom BS, Peterson OL. End results, cost and productivity of coronary care units. N Engl J Med. 1973;288:72-8. 20. Fineberg HV, Scadden D, Goldman L. Care of patients with a low probability of acute myocardial infarction: cost effectiveness of alternatives to coronary-care-unit admission. N Engl J Med. 1984;310:1301-7. 21. Wears RL, Li S, Hernandez JD, Luten RC, Vukich DJ. How many myocardial infarctions should we rule out? Ann Emerg Med. 1989;18:953-63. 22. Schor S, Behar S, Modan B, Bare11V, Drory J, Kariv I. Disposition of presumed coronary patients from an emergency room. JAMA. 1976;236:941-3. 23. Pozen MW. D’Aaostino RB. Selker HP. Svtkowski PA, Hood WB. A predictiv; instrument to improve-coronary care unit admission practices in acute ischemic heart disease: a prospective multicenter clinical trial. N Engl J Med. 1984;310:1273-8. 24. Tierney WM, Fitzgerald J, McHemy R, et al. Physician’s esti-
Myocardial Infarction mates of the probability of myocardial infarction in emergency room patients with chest pain. Med Decision Making. 1986;6: 12-17. 25. Zarling EJ, Sexton H, Milnor P. Failure to diagnose acute myocardial infarction: the clinicopathologic experience at a large community hospital. JAMA. 1983;250:1177-81. 26. Gotto AM, Farmer JA. Risk factors for coronary artery disease. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. 3rd ed. Philadelphia: WB Saunders; 1988: 1153-90. 27. Herrick JB. Clinical features of sudden obstruction of the coronary arteries. JAMA. 1912;59:2015-21. 28. Campbell S, Rocco MB, Nabel EG, et al. Factors determining the activity of ischemic heart disease. Am J Med. 1986; BO(Suppl4C):Y-17. 29. Kinlen LJ. Incidence and presentation of myocardial infarction in an English community. Br Heart J. 1973;35:616-22. 30. Lee TH, Cook EF, Weisberg M, Sargent RK, Wilson C, Goldman L. Acute chest pain in the emergency room: identification and examination of low risk patients. Arch Intern Med. 1985; 145:65-Y. 31. Berger JP, Buclin T, Halter E, Van Melle G, Yersin B. Right arm involvement and pain extension can help to differentiate coronary diseases from chest pain of other origin: a prospective emergency ward study of 278 consecutive patients admitted for chest pain. J Intern Med. 1990;227:165-72. 32. Brand DL, Martin D, Pope CE. Esophageal manometrics in patients with angina-like chest pain. Am J Dig Dis. 1977;22: 300-4. 33. Gravino FN, Perloff JK, Yeatman LA, Ippolitti AF. Coronary arterial spasm versus esophageal spasm: response to ergonovine. Am J Med. 1981;70:1293-6. 34. Areskog M, Tibbling L, Wranne B. Oesophageal dysfunction in non-infarction coronary care unit patients. Acta Med Stand. 1979;205:279-82. 35. Garcia-Pulido J, Pate1 PH, Hunter WC, Douglas JE, Thomas E. Esophageal contribution to chest pain in patients with coronary artery disease. Chest. lY90;98:806-10. 36. Orlando RC, Bozymski EM. Clinical and manometric effects of nitroglycerin in diffuse esophageal spasm. N Engl J Med. 1973;289:23-5. 37. Ahnve S. Noninfarction cases without previously known ischemic heart disease admitted to a coronary care unit. Eur J Cardiol. 1979;9:307-18. 38. Sawe U. Pain in acute myocardial infarction: a study of 137 patients in a coronary care unit. Acta Med Stand. 1971;lYO: 79-81. 39. Hedges JR, Kobernick MS. Detection of myocardial ischemia/ infarction in the emergency department patient with chest discomfort. Emerg Med Clin North Am. 1988;6:317-40. 40. McElroy JB. Angina pectoris with coexisting skeletal chest pain. Am Heart J. 1963;66:296-300. 41. Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction: an update on the Framingham Study. N Engl J Med. 1984;311:1144-7. 42. Uretsky BF, Farquhar DS, Berezin AF, Hood WB. Symptomatic myocardial infarction without chest pain: prevalence and clinical course. Am J Cardiol. 1977;40:498-503. 43. Fesmire FM, Wears RL. The utility of the presence or absence of chest pain in patients with suspected acute myocardial infarction. Am J Emerg Med. 1989;7:372-7. 44. Alonzo AA, Simon AB, Feinleib M. Prodromata of myocardial infarction and sudden death. Circulation. 1975;52:105662. 45. Klaeboe G, Otterstad JE, Winsnes T, Espeland N. Predictive value of prodromal symptoms in myocardial infarction. Acta Med Stand. 1987;222:27-30. 46. Cocchi A, Franceschini G, Incalzi RA, Farina G, Vecchio FM, Carbonin PU. Clinico-pathological correlations in the diagnosis of acute myocardial infarction in the elderly. Age Ageing. 1988;17:87-93.
461 47. Bayer AJ, Chadha JS, Farag RR, Pathy MS. Changing presentation of myocardial infarction with increasing old age. J Am Geriatr Sot. 1986;34:263-6. 48. Pathy MS. Clinical presentation of myocardial infarction in the elderly. Brit Heart J. lY67;29:1YO-9. 49. Muller RT. Gould LA. Betzu R. Vacek T. Pradeeo V. Painless myocardial infarction’in the elderly. Am Heart -J. lYYO;119: 202-4. 50. Solomon CG, Lee TH, Cook EF, et al. Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients: the multicenter chest pain study experience. Am J Cardiol. 1989;63:772-6. 5 1. Black DA. Mental state and presentation of myocardial infarction in the elderly. Age Ageing. 1987;16:125-7. 52. Muller DW, Top01 EJ. Selection of patients with acute myocardial infarction for thrombolytic therapy. Ann Intern Med. 1990;113:949-60. 53. Behar S, Shor S, Kariv I, Bare11 V, Modan B. Evaluation of electrocardiogram in emergency room as a decision-making tool. Chest. 1977;71:486-91. 54. McGuinness JB, Begg TB, Semple T. First electrocardiogram in recent myocardial infarction. Br Med J. 1976;2:449-51. 55. Short S. The earliest electrocardiographic evidence of myocardial infarction. Br Heart J. 1970;32:6-15. 56. McQueen MJ, Holder D, El-Maraghi NRH. Assessment of the accuracy of serial electrocardiograms in the diagnosis of myocardial infarction, Am Heart J. 1983;105:258-61. 57. Nowakowski JF. Use of cardiac enzymes in the evaluation of acute chest pain. Ann Emerg Med. 1986;15:354-60. 58. Clements SD. The role of the electrocardiogram in the diagnosis of myocardial infarction. Primary Care. 1981;8:355-70. 59. Hands ME, Cook EF, Stone PH, et al. Electrocardiographic diagnosis of myocardial infarction in the presence of complete left bundle branch block. Am Heart J. 1988;116:23-30. 60. Kuhn M. ECG diagnosis of acute myocardial infarction in patients with bundle branch block. Ann Emerg Med. 1988;17: 633-9. 61. Rubenstein LZ, Greenfield S. The baseline ECG in the evaluation of acute cardiac complaints. JAMA. 198&244:2536-Y. 62. Lee TH, Cook EF, Weisberg MC, Rouan CW, Brand DA, Goldman L. Impact of the availability of a prior electrocardiogram on the triage of the patient with acute chest pain. J Gen Intern Med. 1990;5:381-8. 63. Hoffman JR, Igarashi E. Influence of electrocardiographic findings on admission decisions in patients with acute chest pain. Am J Med. 1985;79:6YY-707. 64. Rude RE, Poole WK, Muller JE, et al. Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients. Am J Cardiol. 1983; 52:936-42. 65. Rouan GW, Lee TH, Cook EF, Brand DA, Weisberg MC, Goldman L. Clinical characteristics and outcome of acute myocardial infarction in patients with initially normal or nonspecific electrocardiograms (a report from the Multi-center Chest Pain Study). Am J Cardiol. 1989;64:1087-92. 66. ISIS-2 Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988;2:349-60. 67. Gruppo Italian0 per lo Studio della Streptochinasi nell ‘Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986; 1: 397-401. 68. Wilcox RG, Olsson CG, Skene AM, Von der Lippe G, Jensen G, Hampton JR. Trial of tissue plasminogen activator for mortality reduction in acute myocardial infarction. AngloScandinavian Study of Early Thrombolysis (ASSET). Lancet. 1988;2:525-30. 69. Lee TH, Weisberg MC, Brand DA, Rouan GW, Goldman L. Candidates for thrombolysis among emergency room patients with acute chest pain. Ann Intern Med. 1989;110:957-62.
Medicine,
Printed in the USA . Copyright 0 1992 Pergamon Press Ltd.
Vol 10, pp 455-461, 1992
THE DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION IN THE EMERGENCY DEPARTMENT; PART 1 Charles H. Herr, MD, FACEP Department of Medicine, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Reprint Address: Charles Herr, MD, Emergency Department, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756
0 Abstract-Despite major advances in treatment, the accurate diagnosis of acute myocardial infarction (AMI) in the emergency department (ED) remains a difficult clinical problem and is still mainly based on the history and interpretation of the electrocardiogram. Although the physician’s clinical impression is a highly sensitive indicator for AMI, at least 4% of patients presenting to the ED with AMI may be mistakenly sent home. Althoagh chest pain is the most common chief complaint, the clinical presentation can be extremely variable, particularly in the elderly. Complaints of sharp chest pain or chest wall tenderness should not be relied upon to exclude AMI. Radiation of chest pain is an important symptom. With careful analysis, the electrocardiogram may yield a higher diagnostic sensitivity than is commonly accepted.
remained an elusive goal. However, the accurate diagnosis of AM1 in the emergency department is important for reasons of morbidity and mortality prevention, cost-effectiveness, and liability. The rationale for admission to the coronary care unit (CCU) of patients with AM1 was originally for dysrhythmia treatment and has evolved more recently to include interventions directed toward preserving myocardium (3). Although two British studies found no significant difference in mortality when patients with AM1 were randomized to home or hospital care, both studies were flawed by their small numbers of patients and exclusion of high risk patients (4,5). Admission to a monitored bed for intensive management of the complications of AM1 and possibly for treatment with thrombolytic therapy is generally accepted as improving outcomes and has become the standard of care in this country (6). Primary ventricular fibrillation is a treatable cause of early mortality and has an incidence of 2.8% to 4.5% (7-9). Clearly, the inappropriate discharge of the patient with AM1 from the emergency department may have serious consequences. In one study, among 35 patients discharged from the emergency department with AMI, the mortality at 72 hours was 26% compared to a mortality of 12% among a control group of 105 patients hospitalized with AM1 (10). The misdiagnosis of AM1 in the emergency department (ED) also presents a major medicolegal hazard (11). Data from the American College of
0 Keywords-myocardial infarction; chest pain; cardiac enzymes; electrocardiogram
INTRODUCTION
Cardiovascular disease remains the leading cause of mortality in this country, and an estimated 1.5 million people per year sustain a myocardial infarction (1). Patients with symptoms suggestive of acute myocardial infarction (AMI) present commonly to the emergency department. While the diagnosis of AM1 can almost always be reliably confirmed or excluded within the first 24 hours of hospital admission (2), diagnostic certainty in the emergency department has --___ =
. _ cardtology Commentary, a section devoted to topics in bedside cardiology and electrocardiography, is coordi-
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nated by Stephen R. Lowenstein, MD, MPH, University of Colorado Health SciencesCenter, Denver. RECEIVED: 2 July 1991; FINAL SUBMISSIONRECEIVED: 22 October 1991; 0736-4679/92 $5.00 + .OO ACCEPTED; 16 December 1991 455
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Emergency Physicians Insurance Committee indicate that nearly 20% of total dollar losses from malpractice claims settled between 1974 and 1983 was related to the misdiagnosis and substandard treatment of AM1 and amounted to 5.3 million dollars (12). Clearly, the emergency physician faces substantial malpractice risk for misdiagnosis of AMI. Given the potential medical complications and medicolegal consequences of erroneously discharging the patient with AM1 from the ED, physicians generally follow a liberal admission policy. There are an estimated 1.5 million CCU admissions annually in this country, and up to 70% of these admissions eventually rule out for AM1 (13-18). Rule-out rates may be somewhat higher at nonteaching as compared to teaching hospitals (19). Because of the substantial costs incurred by admission to a CCU bed, this high false-positive diagnostic rate has generated considerable interest regarding the issue of cost-effectiveness (20,21). The emergency physician, therefore, is confronted with the dilemma of avoiding underdiagnosis of AM1 with the concomitant increased risk of morbidity, mortality, and litigation, while at the same time avoiding over-diagnosis and the criticism of poor cost-containment. Studies addressing the physician’s diagnostic sensitivity for detecting AM1 in the ED report values ranging from approximately 90% to 97% (14-16,22) (Table 1). In the most recent and largest of these studies, physicians admitted 95.8% of patients with AMI, with 94.8% being admitted to monitored beds (16). Nearly the same sensitivity was attained in a large earlier study in which the diagnostic criteria also included new-onset or unstable angina (23). Tierney has stated that of all the clinical variables associated with the diagnosis of AMI, the physician’s estimate of probability is the single greatest predictor of AM1 (24). Nevertheless, at least 4% of patients presenting with AM1 are mistakenly discharged from the emergency department. In addition, studies of autopsyTable 1. Characteristics
Study (reference) (year) Schor et al (22) (1976) Hedges et al (14) (1967) Seiker et al (15) (1967) Goldman et al (16) (1966)
proven AM1 indicate that the correct antemortem diagnosis was made in only slightly more than 50% of the cases (25). The physician’s poorest diagnostic accuracy appears to occur with those cases where the estimated probability of AMI falls into the intermediate range (24). Part 1 of this series will review the literature regarding the role of the clinical presentation and electrocardiogram (ECG) interpretation in the evaluation of ED patients with possible AMI. Part 2 will examine the data on cardiac enzymes, predictive instruments, echocardiography, thallium scanning, and risk-based triage criteria.
RISK FACTORS Eliciting a thorough history from the patient with possible AM1 usually includes questioning the patient for possible cardiovascular risk factors. Classically, these factors include obesity, hypertension, smoking, hypercholesterolemia, diabetes, and a family history of cardiovascular disease (26). For the patient with a known history of angina or myocardial infarction who presents with a potentially new ischemic event, a history of risk factors has limited significance from a purely diagnostic perspective, since the presence of cardiovascular disease is a known fact. However, for the patient who presents with an atypical history or nondiagnostic ECG and no prior history of cardiac ischemia, the presence or absence of risk factors is usually considered important data that the physician integrates into the decision-making process to arrive at a probability prediction for AMI. Data from several large studies provide very little support for the diagnostic value of a history of risk factors. In three large studies that collectively have evaluated over 10,000 patients presenting to emergency departments with chest pain, no classical cardiac risk factor emerged as an independent predictor of AM1 (16,
and Triage of ED Patients with Symptoms
Suggestlve
of Myocardlai
Infarction
Number of ED Patients
Percent of Patients with AMI
Percent of Discharged Patients with AMI
Percent of AMis Discharged
Percent of Admissions with AMI
1,355’ nst 4,479$ 4,770t
33.9 6.6 16.4 12.1
5.6 1.0 2.0 1.1
7.6 9.6 2.9 4.2
58.5 15.6 24.3 21.7
AMI = acute myocardiai infarction. *Patients referred to ED with presumed AMI. +Patients age b 30 with chief complaint of chest pain. *Male patients age 230 and female patients 240 with chief complaint of chest pain, shortness of breath, or other symptoms suggestive of acute ischemic heart disease.
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18,23). In each study a prior history of infarction or angina proved to be a significant independent variable. CLINICAL
PRESENTATION
The classical presentation of AM1 was described by Herrick as a severe pressure or tightness in the anterior chest and epigastrium with or without radiation and associated symptoms of nausea, vomiting, diaphoresis and dyspnea (27). Chest pain is regarded as the most common presenting complaint of the patient with AMI, but the limited sensitivity and specificity of this symptom has been recognized. The perception of cardiac pain is a complex process with modulation at several neurologic levels (28). Hence, chest pain is not the sole chief complaint, and when present its description has considerable variability. In Kinlen’s study (29) of 201 patients with AMI, pain was present in the chest or epigastrium in 82% of the cases and was described as crushing, constricting, or vicelike in 20%. More than 20% of the patients described a burning sensation or indigestion. Lee prospectively studied 596 patients presenting to an ED with a chief complaint of chest pain not explained by local trauma or chest x-ray abnormalities (30). Only 24% of the patients who described their pain as “pressure” were proven to have AMI. Of the 104 patients diagnosed with AMI, 59% described their pain as “pressure,” 10% as “aching,” 10% as “burning” or “indigestion,” and 8% as “sharp” or “stabbing.” In a recent study of 278 patients presenting to an ED with a chief complaint of chest pain (31), the most sensitive features were duration of pain greater than 60 minutes (88.8%), constriction or squeezing (78.6%), oppression (74.5%), and sudden onset (69.6%). However, the specificity for all of these descriptive characteristics ranged from 30% to 40070, and the highest positive predictive value was 42%. Part of the low specificity of the “typical” cardiac symptoms may be attributable to the ability of esophageal disorders to mimic the symptoms of cardiac ischemia (32,33). In one study, 32 of 55 patients discharged from a CCU after ruling out for AM1 demonstrated esophageal dysfunction by acid perfusion testing and manometry (34). It also appears that the chest pain experienced by outpatients with known coronary artery disease may frequently be caused by gastroesophageal reflux and esophageal motility disorders (35). In addition, the diagnostic specificity of symptom relief with sublingual nitroglycerin is lowered by the proven ability of nitroglycerin to relieve the symptoms of diffuse esophageal spasm (36). The classical presentation of AM1 includes associ-
ated symptoms of nausea, vomiting, diaphoresis, dyspnea, and radiation of pain. However, Ahnve reported (37) that the incidence of nausea, vomiting and dyspnea did not differ significantly among patients with and without AMI. In Kinlen’s study (29), diaphoresis was reported by 60% of the patients with AMI, and in Tierney’s derivation (18) of a logistic regression model, diaphoresis with chest pain emerged as a significant independent variable. The complaint of nausea had a sensitivity of 41% and a specificity of 84% in the most recent study of clinical presentation (31). In two large studies of ED patients with chest pain, nausea, vomiting, and diaphoresis did not have any significant predictive value (16,23). Pain radiation, on the other hand, may be a useful symptom in the evaluation of the patient with possible AMI. Ahnve reported (37) pain radiation in 67% of patients with AM1 compared with 46% of those patients who ruled out. Similar numbers were recorded in a study by Sawe (38) in which 71% of the cases with AM1 complained of radiation of pain into the neck or arms compared with 39% of the patients proven not to have AMI. In Berger and colleagues’ study (31) of 278 patients, left arm radiation of pain proved to have a sensitivity of 55% but a specificity of 76%. Most notably in that same study, radiation of pain into the right arm produced a sensitivity of 41% but a specificity of 94% and a positive predictive value of 80%. Finally, in Goldman and colleagues’ computer-derived protocol (16) for the prediction of AMI, the presence or absence of pain radiation to the neck or left arm or shoulder is one of nine significant clinical variables. Chest pain that is described as sharp or pleuritic is commonly assumed to originate from the chest wall and to be atypical of myocardial infarction. This is usually the case, but Hedges and Kobernick caution (39) that patients may commonly misinterpret the word “sharp” as meaning “severe” and that further clarification of this descriptive term should be sought. Tierney and colleagues reported (24) that 16% of the patients with infarction complained of sharp chest pain, and 15% had chest wall tenderness. Similarly, 8% of the patients with AM1 in Lee and colleagues’ study (30) described their chest pain as sharp or stabbing. In this latter study only a combination of sharp or stabbing pain and pain that was pleuritic, positional, or reproduced by palpation was sufficient to exclude AMI. In addition, it is possible for a patient to have both chest wall pain and pain of cardiac origin simultaneously. One study reported (40) that chest wall pain was present in 51% of patients with documented ischemic heart disease, but in only 23% of matched controls.
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Although most of the studies involving the diagnosis of AM1 have focused on the patient presenting with a chief complaint of acute chest pain, it is clear that myocardial infarction commonly occurs in the absence of chest pain. In fact, recent analysis of data from the Framingham Study (41) reveals that 25% of myocardial infarctions are clinically silent. In a study of 102 consecutive patients with proven AM1 who presented to the Boston City Hospital ED (42), 26 patients had no complaint of chest pain. Their primary complaints included dyspnea, abdominal pain, fatigue, left arm pain, cough, nausea and vomiting, and syncope. Most worrisome was the discovery that the mortality rate among the patients without chest pain was 50% as compared to 18% mortality in the group with chest pain. The higher rate of mortality among patients without chest pain was confirmed in a later report by Fesmire and Wears (43). Among 424 patients admitted from the ED with suspected myocardial infarction, the mortality rate was three times higher among those patients who never experienced chest pain as compared to those whose chest pain persisted or recurred in the ED, and 7.9 times higher compared to those whose chest pain resolved prior to arrival in the ED. It has been suggested that a history of prodromal symptoms could be helpful in the evaluation of the patient with possible AMI. An NIH study reported (44) that prodromal symptoms occurred in 70% of 160 patients hospitalized with myocardial infarction and in 64% of 138 patients who died from acute coronary disease out of hospital. The prodromata included chest pain, dyspnea, and arm pain, but also such symptoms as fatigue, malaise, weakness, dizziness, syncope, anorexia, nausea, and emotional changes. These symptoms preceded the acute event by days to weeks, and more than a quarter of the patients had consulted a physician at least once for these symptoms. However, a more recent study (45) of 276 CCU admissions found that other than angina, symptoms of stress, weakness, fatigue, or dyspnea during the 4 weeks prior to admission had no significant predictive value. The presentation of AM1 in the elderly is commonly nonclassical, and diagnosis is especially difficult. In one autopsy series (46) of 200 consecutive cases of AM1 in the elderly, the correct antemortem diagnosis was made only 43% of the time. The incidence of painless AM1 increases dramatically with age (47-49). More than 60% of myocardial infarctions in patients 85 or older will present without chest pain (47,49). In a study of 7,734 patients, Solomon found that for classical symptoms, the relative risk for AM1 was significantly lower in patients 65 or
Charles H. Herr
older when compared to the younger age group (50). A retrospective review of 777 cases of AM1 in patients age 60 to 100 demonstrated a decreased frequency of chest pain and diaphoresis with increasing age and an increased frequency of neurologic symptoms such as syncope, stroke, acute confusion, and weakness as the primary presenting complaint (47). In that same study the incidence of dyspnea and vomiting was not influenced by age. Several explanations are offered to account for the frequency of atypical presentations in the elderly. These include blunted autonomic responsiveness and a high incidence of coexistent disease. In addition, one author has demonstrated (51) a high correlation between atypical presentations of AM1 and poor performance on mental status testing.
DIAGNOSIS
BY ELECTROCARDIOGRAM
The electrocardiogram is the most commonly utilized diagnostic test in the evaluation of the patient with suspected myocardial ischemia or infarction. It is a quickly and easily obtainable test that is often reflexly ordered for the patient presenting with chest pain. It is also presently the major determinant of eligibility for thrombolytic therapy (52). Unfortunately, while the classic ECG changes of AM1 are highly specific, the initial ECG has proven to be a relatively insensitive test. Three previous studies that cumulatively evaluated over 1000 myocardial infarctions reported a sensitivity of the initial ECG that ranged from 43% to 65% (53-55). While the initial ECG demonstrates low sensitivity for AMI, the sensitivity of serial ECGs obtained after admission is considerably greater and in one study (54) was 83%. Clinicopathologic data correlating ECG findings with autopsy-proven AM1 is sparse, but tends to confirm the conclusions of the clinical studies. McQueen and colleagues reported (56) the initial ECG to be diagnostic in only 4 of 17 patients with proven AMI, but his ECG criteria were overly restrictive and excluded S-T segment depressions. In an autopsy study (25) of 100 consecutive acute myocardial infarctions, Zarling found that of the 85 cases for which an ECG was available, the ECG was diagnostic in only 25 cases and suggestive in 27 cases. However, the specific ECG criteria were not defined. The diagnostic inaccuracy of the initial ECG is in many cases attributable to baseline ECG abnormalities that make interpretation for ischemia or infarction difficult. Many cardiac conditions such as cardiomyopathy, left ventricular hypertrophy, and conduction abnormalities can either mimic or obscure the electro-
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cardiographic signs of infarction (57,58). One common abnormality that makes ECG interpretation for AM1 difficult, if not impossible, is the bundle branch block. However, it is sometimes possible using certain ECG criteria to diagnose acute infarction in the presence of bundle branch block (59,60). In many cases where the initial ECG findings are ambiguous or suggestive of ischemia or infarction, it would seem that the availability of a previous ECG for comparison would be an invaluable aid. However, one retrospective study (61) of 236 ED patients with chest pain concluded that the availability of a previous baseline ECG would have changed the physician’s decision to admit or discharge in only 17% of the cases. In a more recent prospective study (62) of 5,673 patients with chest pain, the availability of a prior ECG did not change the sensitivity for admission to the hospital or CCU of patients with AMI. However, non-AM1 patients with an available prior ECG were less likely to be admitted to the CCU than those non-AM1 patients without an old ECG, and this increased diagnostic specificity was most pronounced in those patients with ECG changes consistent with ischemia or infarction, Although most physicians consider the ECG to be an indispensable diagnostic aid, Hoffman and Igarashi showed (63) that the ECG may actually have very little influence on the physician’s decision-making process. In a study of 100 consecutive adult admissions to the ED with chest pain, the evaluating physician was asked to make the decision to admit or discharge the patient without having seen the ECG and then to re-evaluate this decision after reviewing the ECG. In only 4% of the cases did the physician reverse the original decision. Two recent large studies (64,65) have reported a surprisingly high sensitivity for the initial ECG. The first study (64) was derived from the Multicenter Investigation of the Limitation of Infarct Size (MILIS) and analyzed 3,697 CCU patients who presented with 30 minutes or more of pain thought to be ischemic. The ECG criteria included new Q waves (~30 ms wide and 10.20 mV deep), new S-T elevation or depression (10.10 mV), or complete left bundle branch block. Using these criteria, the sensitivity of the initial ECG was 8 1% and the specificity was 69%. Although this is the highest reported ECG sensitivity, these results are influenced by the patient population, which included only CCU patients. In addition, the study criteria eliminated from analysis and additional 2,158 patients admitted to the CCU for suspected MI during the same time period. The second study (65) is more recent, larger, and most importantly addresses an ED patient popula-
tion. The data from this study was obtained from 7,115 consecutive patients in the Multicenter Chest Pain Study, an analysis of patients aged 30 years or older presenting to the emergency departments of 7 institutions with a chief complaint of chest pain not explained by trauma or chest x-ray abnormalities. The following initial ECG criteria were considered highly suggestive of AMI: 1) 1 lmm S-T elevation or abnormal Q waves in ~2 leads; 2) 2 1 mm S-T depression in r2 leads; 3) other S-T or T wave changes of ischemia or strain including S-T depression < 1 mm and T wave inversions (all findings new or no old tracing available). The sensitivity of these criteria was 79%. Only 3% of patients with completely normal or nonspecific ECG changes subsequently proved to have AMI. Despite the fact that the ECG criteria were somewhat broad, the specificity of the initial ECG in this study was 83%. The interpretation of the initial ECG obtained in the ED also has important therapeutic implications. Large and well-designed clinical studies (66-68) have convincingly demonstrated substantial reductions in early mortality after AM1 when thrombolytic therapy is administered early. Since at present the benefits of thrombolysis apply mainly to those patients who demonstrate S-T segment elevation, careful interpretation of the initial ECG is critical in order that eligible patients are not denied potentially life-saving therapy. Given the limited sensitivity of the initial ECG, it is clear that substantial numbers of patients with AM1 will be denied thrombolytic therapy by present eligibility criteria. However, there is presently no convincing evidence that such therapy is beneficial to those patients without S-T segment elevations (52). It is also true, given the less than perfect specificity and positive predictive value of the initial ECG, that a significant number of patients who have the appropriate ECG criteria and who receive thrombolytic therapy will subsequently prove not to have AMI. By one estimate (69), using the present ECG criteria for treatment, for every 8 patients with proven AM1 who are treated, 1 to 2 patients with false positive ECGs will also be treated. Given the cost and complications of thrombolytic therapy, such a prediction has major implications regarding cost-effectiveness.
SUMMARY
Chest pain is the most common chief complaint of patients presenting to the ED with AMI. However, it is not the sole primary symptom of AMI, and there is evidence that the mortality may be higher among AM1 patients who do not complain of chest pain. In
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addition, chest pain has poor specificity for AMI, and the presence of esophageal motility disorders may account significantly for this low specificity. Although the chest pain of infarction is typically described as a pressure, crushing, or constricting sensation, there is considerable variation in the description of this complaint. In particular, a complaint of sharp pain should be interpreted with caution, and should not be taken as automatically excluding ischemia or infarction. Likewise, the presence of chest wall tenderness does not exclude concomitant acute coronary disease. Radiation of chest pain is an insensitive but moderately specific indicator of AMI. It should be considered an important historical feature that increases the possibility of AMI, particularly when pain radiates to the right arm. The associated symptoms of nausea, vomiting, diaphoresis, and dyspnea have relatively low sensitivity and specificity and do not emerge as significant independent predictors of AM1 in large prospective stud-
ies. Likewise, cardiac risk factors, typically used by the physician to formulate an initial baseline estimate of risk for coronary artery disease, have not been substantiated as important predictors of AM1 in large-scale studies of ED patients. Atypical presentation of AM1 is characteristic of the elderly. In particular, the incidence of chest pain and autonomic symptomatology decreases, and the incidence of primary neurologic complaints increases with advancing age. The diagnostic sensitivity of the initial ECG is generally considered to be quite low, approximately 50%. However, the study by Rouan and colleagues (65) stands in sharp contradistinction to this consensus. Employing rather liberal electrocardiographic criteria, the authors reported an initial ECG sensitivity for AM1 of 79% and a specificity of 83%. Because the study population included over 7,000 consecutive ED patients with chest pain at 3 university and 4 community hospitals, these findings may have considerable practical importance.
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