The Journal of Emergency Medicine, Vol 10, pp 591-599,

1992

Printed in the USA

Cardioiogy

THE DIAGNOSIS OF ACUTE MYOCARDIAL IN THE EMERGENCY DEPARTMENT; Charles H. Herr,

MD,

Copyright 0 1992 Pergamon Press Ltd.

Commentary

INFARCTION PART 2

FACEP

Department of Medicine, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire ReprintAddress: Charles Herr, MD, Emergency Department, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756

? ?Abstract -At present, routine use of cardiac enzymes in the emergency department (ED) cannot be justified, except possibly as a final screen prior to discharge. Computerderived predictive instruments do not surpass the physician’s diagnostic sensitivity for acute myocardial infarction (AMI), but do demonstrate significantly higher specificity. Limited data exist on the utllity of echocardiography and thallium scanning in the ED. Methods of trlaglng patients on the basis of prognosis are well supported in the literature. The physician’s high diagnostic sensitivity is maintained at the cost of significant numbers of admissions who subsequently rule out for AMI. No single clinical variable or combination of clinical variables can reliably confirm or exclude AMI in the ED. Ultimately, the physician’s clinical assessment must remain the final determinant of the necessity for admission. However, judicious use of prediction rules and prognostic indicators should improve resource utilization.

CARDIAC

Since the 1950s serum enzymes have played a pivotal role in the diagnosis of AMI. Initially the diagnosis was based on the characteristic rise and fall of creatine kinase (CK), lactic dehydrogenase (LDH), and aspartate aminotransferase (AST) (2,3). However, these enzymes lack specificity and, more recently, the isoenzymes of CK (CK-MB) and LDH (LDH-1) have become the diagnostic tests of choice (2-6). The elevation of LDH-1, although highly specific for AMI, is limited in utility because of its delayed appearance and has more diagnostic value in patients who present after a significant time interval from the onset of symptoms (2,4,6). CK-MB, with its earlier onset of elevation, has become the most widely utilized confirmatory test for AMI. When measured on presentation and at 12-hour intervals for 24 hours after the onset of symptoms, it approaches a sensitivity and specificity of nearly 100% (5,6). While serial cardiac enzymes have become the gold standard for diagnosing AM1 in CCU patients, their ability to detect AM1 in the ED population of patients presenting with acute chest pain has been disappointing. This early diagnostic inaccuracy can in large part be explained by the characteristic enzyme kinetics with resulting substantial time delays between the onset of symptoms and the earliest detectable rise in serum enzyme levels (Table 1). This variation in kinetics is a function of molecular

0 Keywords - myocardlal infarction; chest pain; cardiac enzymes; electrocardiogram

INTRODUCTION

In Part 1, the contributions of the clinical presentation and electrocardiogram (ECG) to the diagnosis of acute myocardial infarction (AMI) in the emergency department (ED) were reviewed (1). In this part, the role of cardiac enzymes, mathematical predictive instruments, echocardiography, thallium scanning, and risk-based triage will be examined. =

=

ENZYMES

Cardiology Commentary, a section devoted to topics in bedside cardiology and electrocardiography, is coordinated by Stephen R. Lowenstein, MD, MPH, University of Colorado Health Sciences Center, Denver.

RECEIVED: 2 July 1991; FINALSUBMISSIONRECEIVED: 12October ACCEPTED: 16 December 1991 591

1991;

0736-4679/92 $5.00 + .OO

Charles H. Herr

592 Table 1. Time Course of Cardiac Enzymes Onset of rise (h)

Peak(h)

4-8 4-8 8-12 8-12

12-24 12-20 72-l 44 18-36

Z-MB LDH AST

Based on data presented by Lee and Goldman (6).

weight, regional blood and lymphatic flow, and clearance rates (6). Because of their earlier appearance in the serum, CK and CK-MB have been the main focus of attention as potential early markers of AMI. In a study of 80 ED patients with chest pain, Eisenberg reported that reliance on an initial total CK drawn at the time of presentation would have prevented the release of only one patient with AMI, but would also have resulted in 11 more inappropriate admissions and the discharge of 5 patients with AM1 (7). Seager found total CK to be of no diagnostic value in the assessment of 250 ED patients with chest pain (8). One study of 252 ED patients reported that the total CK had a diagnostic sensitivity of 9% if measured within 4 hours of the onset of symptoms, but increased to 63% if measured more than 4 hours after the onset of symptoms (9). The data addressing the diagnostic accuracy of CK-MB have not been much more encouraging than the studies of total CK. In one of the earliest prospective evaluations of CK-MB, Blomberg found the initial CK-MB to be elevated in fewer than 50% of 47 patients with AM1 (10). In a large prospective study, Lee evaluated CK and CK-MB in 639 patients age 30 or older who presented to an ED with chest pain unexplained by trauma or chest x-ray findings (11). The overall sensitivity of CK-MB was 34% with a specificity of 88%. Sensitivity was only 18% if the patient presented within 4 hours of the onset of symptoms, but rose to only 57% after more than 12 hours (Table 2). Positive predictive value did not increase significantly with increasing time after onset of symptoms because of the decreased prevalence of AM1 among the patients who presented later. AlTable 2. Sensitivity, Specificity and Predictive Value of CK-MB > 5% of total CK Time after onset of symptoms (h) 12 >o

Sensitivity (%)

Specificity (%)

Positive Predictive Value (%)

18 50 57 34

91 84 89 88

36 42 32 36

Based on data presented by Lee et al. (11).

though this is an important study, it can be criticized on two counts. First, of a total enrollment of 1,055 patients, 411 patients were excluded from analysis because of insufficient data. Second, since CK-MB was assayed only if total CK was elevated, the overall sensitivity of CK-MB may have been underestimated (12). Clearly, the diagnostic accuracy of CK or CK-MB is insufficient for either test to stand alone as a sole criterion for determining admission or discharge from the ED of the patient with suspected AMI. One alternative is to integrate the enzyme assays into the total context of the clinical and ECG evaluation. Hedges studied 773 patients who presented to a university hospital with a chief complaint of chest pain (13). Patient disposition was made on the basis of the physician’s clinical and ECG assessment, but enzymes were drawn at the time of presentation. Using a CK-MB cutoff of 12 IU/L (immunoinhibition assay), Hedges reported that if the isoenzyme had been measured on each of the 482 discharged patients, 3 of 5 inappropriately discharged AMIs could have been prevented at a cost of only two additional false-positive admissions. His conclusion was that CK-MB may best be utilized as a final screening test in those patients whom the ED physician intends to release on clinical grounds. Most recently, attention has been directed to rapid immunochemical assays for early detection of AM1 in the ED. In 183 ED patients, Gibler evaluated four immunochemical methods of measuring CK-MB (14). Levels measured at the time of presentation produced sensitivities ranging from 50% to 62% with specificities of 84% to 97%. However, at 3 hours after presentation, sensitivity of these tests rose to an impressive 92% to 97% with specificities of 83% to 96%. This trial has served as a pilot study for an ongoing multicenter investigation designed to assess the diagnostic value of CK-MB measured by an immunochemical technique at 0, 1,2, and 3 hours after presentation. Such data may also have significant implications regarding eligibility criteria for the administration of thrombolytic therapy. In addition to cardiac enzymes, serum myoglobin has been extensively examined as a method for early detection of AMI. Its potential diagnostic value derives from its low molecular weight of 17,000, which is responsible for its rapid diffusion from injured cells and the resultant serum elevation within 1 to 2 hours after the onset of infarction (15-18). Its utility in the ED was initially limited by the time-consuming radio-immunoassay methods (19), but this problem has been overcome with the introduction of more rapid radio-immunoassays and latex agglutination

Myocardial Infarction

testing (20-24). The other limitation of serum myoglobin has been its predictable lack of specificity due to its elevation with conditions other than AM1 (15,17). In one study of 136 CCU patients, the sensitivity of the initial myoglobin level was 94070, but specificity was only 33% (20). Most myoglobin studies to date have been limited by their retrospective design or their restriction to a CCU patient population (16,20,22-24). However, two reports involving a combined total of almost 400 ED patients with suspected AM1 have yielded somewhat encouraging results (15,21). In one study of 73 ED patients, the initial myoglobin level on presentation was 62% sensitive for AMI, but rose to 100% sensitivity 3 hours later with a specificity of 76% (15). In the larger study of 305 ED patients, the sensitivity climbed from 72% on admission to 98% 4 hours after presentation with a constant specificity of 83% (21). Hence, the implications are that myoglobin has potential value if the patient can be held in the ED for 3 to 4 hours or if it is utilized to revise the triage decision after initial admission to the CCU.

PREDICTIVE INSTRUMENTS Rather than focusing on a single diagnostic test to facilitate the decision making process, some investigators have attempted to derive mathematical predictive models based on a number of historical and clinical variables (25-30). All of these models are designed to supplement and not to substitute for the physician’s clinical judgment. None of them reliably improve on the physician’s unaided sensitivity in detecting AMI, but some are able to demonstrate a statistically significant increase in specificity. In one of the earliest attempts to create a predictive instrument, Sawe derived a diagnostic index from discriminant function analysis (30). The index was based on 9 variables, 6 historical and 3 clinical. When applied prospectively to 191 CCU admissions, the model functioned with a sensitivity for AMI of lOO%, but any practical value was negated by its specificity of 16%. Tierney’s attempt at producing a decision rule focused on an ED population of 540 patients whose chief complaint was chest pain (26). He randomly selected one-half of the patients to serve as the derivation set. Multivariate analysis of data from these patients produced only four clinical variables, two electrocardiographic and two historical, that had independent predictive value. Validation of the predictive rule on the remaining patients demonstrated a disappointing sensitivity for AM1 of only 81% as

593

opposed to the physician’s sensitivity of 87%. Tierney concluded that despite the low sensitivity, if the decision rule were used in conjunction with the physician’s judgment, overall sensitivity would have increased to 95% without a significant sacrifice of specificity. The first large-scale trial aimed at creating a mathematical predictive tool was reported by Pozen and colleagues in 1980 (29). His focus was to predict the more general diagnosis of acute ischemic heart disease rather than just acute infarction. He also expanded the eligibility criteria to include patients with one or more of nine clinical symptoms suggestive of acute ischemia. The prediction rule was derived from 925 ED patients at Boston City Hospital. Data for 105 variables were collected on each patient and subjected to cluster and logistic regression analysis. The resulting probability function was based on 9 independent predictors, 5 historical and 4 electrocardiographic. Subsequently, the prediction rule was tested in a prospective trial of 856 patients who presented to the same hospital ED. The design of this trial was such that during odd-numbered (experimental) months, the ED physician was allowed to see the calculated probability and during even numbered (control) months, the probability value was withheld from the physician. Sensitivity for detection of acute ischemia was slightly lower during experimental months (86.4% vs. 89.9%), but specificity was significantly better (91.6% vs. 80.1%). Encouraged by the results of this pilot study, Pozen and colleagues then expanded their study to a more generalized population that included 6 hospitals, 2 of which were rural, nonteaching hospitals (27). Entry criteria included age of 30 or more for men and 40 or more for women and a chief complaint of chest pain, jaw or left arm pain, shortness of breath, or a changed pattern of angina. A total of 59 clinical features of 2,801 patients were evaluated by stepwise regression analysis to produce an equation that provided a probability estimate for acute ischemia based on seven variables (Table 3). The prospective trial to validate the predictive instrument Table 3. Clinical Variables for Calculation of the Probability of Acute lschemla Pain in chest or left arm Pressure, pain, or discomfort in chest is most important symptom History of heart attack History of nitroglycerin use for chest pain S-T segment elevation or depression t 1 mm S-T segment straightening T wave peaking or inversion 2 1 mm Adapted from Pozen et al. (27).

Charles H. Herr

594

was conducted on 2,320 patients at the same six hospitals and followed the same design as the pilot study. Sensitivity for acute ischemia did not differ significantly between experimental and control groups (94.5% compared with 95.3%), but the variation in specificity was statistically significant (78.1% compared with 73.2%, P = 0.002). Pozen and colleagues concluded that use of this mathematical predictive model would have reduced inappropriate CCU admissions from 44% to 33 % . The instrument seemed most helpful when the probability of acute ischemia was less than 50% and, if utilized in those cases, would have produced a 22% reduction in the false-positive diagnostic rate. The multicenter Chest Pain Study contains the largest data base for construction and testing of a prediction model (25,28). The study now involves seven hospitals and includes ED patients age 30 or older who present with a chief complaint of chest pain not explained by trauma or chest x-ray findings. The preliminary study to develop a computer-derived protocol was published in’ 1982 and was conducted in two phases (28). During the first phase, extensive historical and clinical data were collected on 482 eligible patients in the ED of the Yale-New Haven Hospital. Using recursive partitioning analysis, a decision tree was constructed based on nine clinical parameters. In the second phase the algorithm was prospectively evaluated on 468 patients at Brigham and Women’s Hospital (Boston). Sensitivity for detection of AM1 was identical for physicians and the algorithm, but specificity was somewhat better for the algorithm (70% compared with 67%, P c 0.01). This preliminary study was subsequently expanded to include a training set of 1,379 patients for derivation of a computer protocol followed by a prospective evaluation of the protocol with 4,770 patients at six hospitals, including four community hospitals (25). The algorithm was derived from recursive partitioning analysis of 50 potential variables. The resultant decision tree was constructed of 9 clinical and 2 ECG factors and contained 14 terminal subgroups, 6 of which had a probability for AM1 of greater than 7% (Table 4). When tested prospectively, the algorithm demonstrated a sensitivity nearly identical to that of the physician’s, but a specificity that was significantly higher than the physician’s (74% compared with 71%, P < 0.00001). Use of the computer protocol would have reduced false-positive CCU admissions by 11.5%. However, the protocol made a number of diagnostic predictive errors that an experienced clinician could easily avoid, and the authors conclude that the physician’s judgment should always supervene. The authors also state that the optimal

Table 4. Clinical Variables for Construction of a Computer Protocol To Predict Myocardial Infarction S-T segment elevation or Q waves in 2 or more leads, not known to be old Onset of chest pain 248 hours ago Prior history of angina or MI ST-T changes of ischemia or strain, not known to be old Longest pain episode tone hour Pain worse than prior angina or the same as a prior MI Pain radiates to neck, left shoulder, or left arm Age 240 Chest pain reproduced by palpation Pain radiates to back abdomen or legs Chest pain is “stabbing” Adapted from Goldman et al. (25).

of the algorithm may be to direct admissions to an intermediate-care bed rather than a CCU bed in those cases in which the physician decides that admission is necessary but the protocol does not predict AMI. utilization

ECHOCARDIOGRAPHY An immediate consequence of myocardial ischemia or infarction is abnormal ventricular wall motion. The ability of echocardiography to detect regional wall motion abnormalities (RWMA) in AM1 is well established (31). Two studies have examined echocardiography as a tool for establishing the early diagnosis of AM1 among patients with chest pain (32,33). Horowitz and colleagues performed M-mode and two-dimensional echocardiography within 8 hours of admission on 80 consecutive patients admitted with a chief complaint of chest pain (32). Among the 36 patients who demonstrated RWMA, there were 31 with myocardial infarction, and among the 29 patients without definite RWMA, 2 patients developed myocardial infarction. The resulting diagnostic sensitivity and specificity were 94% and 84%, respectively, and the positive predictive value was 86%. However, the study population included only CCU patients. Extrapolating these results to an ED population of patients with chest pain, among whom the prevalence of AM1 is significantly lower, would markedly diminish the predictive value of this test. In addition, 15 (18%) of the patients in this study had technically unsatisfactory echocardiograms and were excluded from data analysis. Of those 15 patients, 8 were subsequently proven to have an acute infarction. The second study examined 46 patients presenting to an emergency department with chest pain and with a normal or nondiagnostic ECG (33). Of the 15 patients diagnosed with AMI, 14 had evidence of

Myocardial

Infarction

RWMA on echocardiogram. In addition, the authors note that the presence of wall motion abnormality was a good indicator of significant coronary artery disease in non-AM1 patients if the echocardiogram was performed during chest pain, but lacked sensitivity if performed after the resolution of chest pain. The role of echocardiography in evaluating the patient with chest pain is not clearly delineated by these two studies. The number of subjects is small, and only the second report deals with emergency department patients. Factors that would seem to limit the utility of echocardiography are the presence of valvular heart disease, previous myocardial infarction or cardiomyopathy, technical difficulties, and the requirement that someone skilled in the performance and interpretation of the test be present.

595

in the emergency department has potential usefulness in evaluating those patients with positive ECG findings and no chest pain, or those with chest pain but normal or nondiagnostic ECGs. Clearly, more prospective data will be necessary in order to firmly establish thallium imaging as a useful and cost-effective diagnostic tool in the emergency department. While thallium scanning may have potential value in selective cases, the cost of the procedure, including radiopharmaceutical, the inability to distinguish fresh from old infarction, and the requirement for 24-hour availability of special technical expertise, may limit its practical applicability.

ADMISSION TRIAGE THALLIUM SCINTOGRAPHY The sensitivity of thallium scanning for detecting acute myocardial infarction is time-dependent and is highest within the first 6 hours after the onset of symptoms (34). The specificity of this imaging procedure is limited by the inability of a single study to distinguish between acute infarction, unstable angina, and previous infarction (35). Wackers performed thallium scintography within 10 hours of admission on 203 CCU patients with atypical presentations and nondiagnostic ECGs (35). Among the 34 patients with AMI, there were 30 positive scans and 4 equivocal scans. Overall sensitivity and specificity for AM1 was 88070,and the positive predictive value was 61%. If all equivocal scans were counted as positive tests, the sensitivity increased to 100070,but specificity and predictive value decreased to 63% and 35%, respectively. Only one author has addressed the diagnostic value of thallium imaging in the emergency department (36). Mace performed portable thallium scintography in the ED on 20 consecutive patients presenting with chest pain, 12 of whom had atypical presentations and equivocal ECGs and 8 of whom had classic presentations (36). If the initial scan was abnormal, an additional scan was performed one hour later. All 3 patients with scans indicative of AM1 received a final diagnosis of AMI, and all 3 had atypical presentations. Three patients had sequential scans consistent with ischemia, and each one had documented significant coronary artery disease. There were no myocardial infarctions among the 14 patients with negative imaging studies. However, discharged patients were apparently not followed up. The author concludes that portable thallium imaging

Most of the research regarding the disposition of patients presenting to the emergency department with suspected myocardial infarction has focused on reducing the number of unnecessary hospitalizations. An alternative approach to improving diagnostic accuracy is to utilize data collected in the emergency department evaluation to predict prognosis. Since the coronary care unit is an expensive facility designed to manage the acute complications of myocardial infarction, its resources should be allocated to those admissions with a high probability of developing lifethreatening complications. Patients with a lower risk of developing complications could be triaged to an intermediate care unit, a less costly alternative to the CCU that would still provide centralized monitoring and personnel experienced in recognizing and treating life-threatening dysrhythmias. One of the early studies addressing the issue of admission triage based on prognosis examined the incidence of significant interventions required for 414 CCU admissions (37). Significant interventions were defined as administration of lidocaine, atropine sulfate, sodium nitroprusside or vasopressors, electroshock, and insertion of a Swan-Ganz catheter or a temporary pacemaker. The patients were divided into high-risk and low-risk groups based on the presence or absence of pulmonary rales, ongoing chest pain, or the presence of one or more premature ventricular contractions (PVCs) on a 12-lead ECG. Among the 306 patients in the high-risk group, 126 required at least one intervention and 11 died in the CCU. Only 6 low-risk patients required an intervention, and 3 of these interventions were deemed unnecessary in retrospect. There were no CCU deaths among this group. The authors conclude that patients without pulmonary rales, ongoing chest pain,

Charles H. Herr

596

or PVCs do not require the use of a CCU and can be safely admitted to intermediate care beds. According to a report by Fesmire, the presence or absence of chest pain is an important prognosticator (38). Among 424 patients admitted from their ED with suspected AMI, those patients whose chest pain persisted or recurred in the ED had a 3.8 times greater risk of life-threatening complications than those patients whose chest pain resolved prior to arrival in the ED and did not recur in the ED. The worst prognosis occurred in the patients who never experienced chest pain. Their risk of life-threatening complications was 5.2 times greater and their risk of death was 7.9 times greater, compared with patients who had chest pain that resolved prior to arrival in the ED. A number of investigators have focused their attention on the initial ECG as an important prognostic indicator (39-43). Among 475 patients admitted to rule out myocardial infarction, Yusuf found that the presence of S-T segment elevation (~1 mm) identified patients at greater risk for heart failure, dysrhythmias, cardiac arrest, and death (39). Slater finds that the initial ECG is an accurate predictor of the likelihood of 8 serious complications (infarct extension, cardiac arrest, sustained hypotension, ventricular fibrillation, ventricular tachycardia, second or third-degree heart block, Killip class 3 or higher, or death) (40). In a study of 775 CCU admissions with a chief complaint of chest pain, serious complications evolved in 4% of patients with an initial ECG that was normal, in 11% with an ECG demonstrating nonspecific S-T segment or T-wave changes, and in 25% with an initial diagnostic ECG. In addition, only 5 of the 180 patients (2.8%) without distinctly abnormal ECG findings developed complications that warranted treatment in a CCU. In a study conducted at two university hospitals, Brush and colleagues assessed the prognostic value of the initial ECG in 469 patients admitted from the ED to the CCU with a chief complaint of chest pain (41). For this study a negative ECG was defined as being normal, showing nonspecific S-T segment Twave changes, or being unchanged from a previous ECG available at the time of admission. A positive ECG required the presence of one or more of the following: pathologic Q- waves, S-T segment elevation or depression, or T-wave inversion consistent with infarction, ischemia, or strain; left ventricular hypertrophy; left bundle branch block; or paced rhythm. Of the 167 patients with a negative ECG, the incidence of life-threatening complications (ventricular fibrillation, sustained ventricular tachycardia, heart block) was 0.6% as compared to 14%

among the 302 patients with a positive ECG. Hence, the risk of immediate life-threatening complications was 23 times higher for patients with a positive initial ECG. In addition, for all other individual complications of AM1 and for major interventions, the risk for patients with a positive initial ECG was significantly higher than for patients with a negative ECG. The authors conclude that patients with an initial ECG that is normal, nonspecific, or unchanged form a group that is at low risk and can safely be admitted to an intermediate care unit. Adherence to the proposed ECG criteria for triage would have reduced CCU admissions by 36% in this study. Although a subsequent retrospective study reported a much smaller increase in relative risk associated with a positive ECG (44), the results of Brush and colleagues’ investigation have now been confirmed by two subsequent prospective studies that followed the same basic methodology (Table 5) (42,43). Recent data from the multicenter Chest Pain Study suggest that there is no compromise in care or outcome for chest pain patients who are initially admitted to a step-down unit because of a predicted low probability of AM1 and who subsequently rule in for AM1 (45).

SUMMARY Substantial data suggest that traditional measurements of cardiac enzymes and isoenzymes have very little utility in the diagnostic evaluation of the patient with potential AM1 in the emergency department. However, there is some limited evidence to support the selective ordering of CK-MB isoenzymes as a final screening test for those patients whom the physician plans to discharge from the ED. Using this format, it may be possible to prevent some inappropriate discharges with a minimal sacrifice in diagnostic specificity. Preliminary data on the use of the rapid, more sensitive immunochemical CK-MB assays are encouraging. If the usefulness of these assays is confirmed in larger studies of ED patients, the utility of isoenzymes in the ED may be substantially revised. Although serum myoglobin rises earlier in AM1 than cardiac enzymes measured by electrophoresis, its sensitivity is, nevertheless, significantly timedependent, and its specificity is low. At present, there are insufficient data to support the routine use of serum myoglobin in the emergency department. Echocardiograph and thallium scanning have been studied only in small numbers of ED patients, but may be helpful in the evaluation of those cases in

Myocardial

Infarction

Table 5. Complications

597 and Mortality among CCU Admissions as a Function of the initial ECG Negative ECG ?? Number of patients

Brush et al (41) Zalenski et al (42) Stark and Vacek (43)

469 211 221

Complications* (W 0.6 0 1.3

Mortality (O/o) 0.6 0 0.6

Positive ECGT Complications* (W 14 14.6 11.1

Mortality (%) 9.9 6.3 6.3

“Negative ECG = normal, nonspecific S-T segment of T-wave changes or unchanged from previous ECG. TPositive ECG = pathologic Q waves, S-T segment elevation or depression or T-wave inversion consistent with infarction, ischemia, or strain; left ventricular hypertrophy; left bundle branch block; paced rhythm. *Complications = ventricular fibrillation, sustained ventricular tachycardia, heart block (Brush et al [41], Stark et al [43]) or ventricular fibrillation, sustained ventricular tachycardia, 2nd or 3rd degree heart block requiring a pacemaker, shock (BP < 90 torr and use of pressors), or death (Zaienski et al [42]).

which the history and ECG findings are equivocal. The ability of these tests to detect unstable ischemia may be advantageous, since most of these patients will also require hospital admission. However, technical and practical considerations seem likely to limit the usefulness of these diagnostic techniques in most hospitals. The mathematical predictive instruments deserve the clinician’s particular attention. They were derived by computer analysis of large data bases, and were prospectively validated on large numbers of emergency department patients. Although these decision rules do not improve on the physician’s diagnostic sensitivity for AMI, they may be valuable in reducing false positive admissions or at least in decreasing inappropriate CCU admissions. Despite the proven efficacy of the computer models, they have not achieved widespread use. The reason for this is not entirely clear. Use of the computer models does not require excessive time or any special computer expertise. The data required are the typical clinical and historical data that a physician would obtain in the evaluation of any patient with potential AMI. Subsequently, the physician either enters 7 variables into a programmable calculator (taking less than 20 seconds) to obtain a probability estimate, or simply applies 11 variables to a decision tree (25,27). It is possible that part of the physician’s reluctance to utilize the protocols stems from an inherent conviction that no computer-derived model can take into account all the subtle variations of clinical presentation. Certainly the applicability of the predictive instruments is limited by their inclusion criteria. The prediction rule developed by Goldman and colleagues applies only to patients presenting with a chief complaint of chest pain, thereby missing the atypical presentations of AM1 (25). The probability formula reported by Pozen and colleagues is based on broader inclusion criteria that include chest, jaw, or left arm pain; dyspnea; or a changed pattern of

angina, but would still exclude many atypical presentations (27). But pressure is mounting to provide more costeffective care, and the nearly 70% rule-out rate among CCU admissions provides an obvious target. The computer-derived predictive instruments, although diagnosis- rather than outcome-oriented, and although diminished somewhat by inclusion bias, do increase diagnostic specificity without sacrificing sensitivity. It may be wise for physicians to integrate these instruments into the regular diagnostic assessment of the ED patient with possible AMI. The prediction provided by the mathematical model could be used as an adjunct to, rather than as a substitute for, the physician’s clinical intuition. The calculated prediction could be used as a final check prior to the discharge of a patient, or perhaps more appropriately, as an indicator to admit to an intermediatecare bed if the physician believes admission is necessary but the calculated probability is low. One advantage of Pozen and colleagues’ computer model as compared to Goldman’s is that Pozen includes unstable angina along with AM1 as a diagnostic endpoint. The Goldman model does not discern which of the patients at low risk for AM1 have unstable angina. Patients presenting with chest pain form a continuum extending from atypical, noncardiac chest pain to new-onset or unstable angina, to non-Q wave infarction, and finally, to transmural infarction. During the brief patient encounter in the ED, with limited diagnostic tools, it is difficult for the physician to determine where to place a particular patient in this clinical spectrum. Unstable angina and AM1 have a very similar pathogenesis and clinical presentation (46,47). In addition, unstable angina may deserve diagnostic and therapeutic attention equal to that accorded AMI. Indeed, patients admitted to the hospital who rule out for AMI, but who have unstable angina, have a long-term prognosis similar to patients with AM1 (48-50). Hospitalization

Charles H. Herr

598

of patients with unstable angina for diagnosis and stabilization is the standard of care, including intensive medical therapy, definition of coronary anatomy, and revascularization procedures (46,47,51). Hence, probability estimatts of AM1 should not be allowed to deny hospital admission to patients who may have unstable angina. The concept of admission triage based on early risk stratification acknowledges the reality of diagnostic ambiguity in the ED. This concept focuses on outcomes rather than diagnoses. It assumes that a substantial number of false-positive admissions is unavoidable, but attempts to improve resource utilization. Risk-based admission triage is now a concept that is well supported in the literature. Using one criterion, patients with chest pain that has resolved and does not recur in the ED have a low risk of significant complications and can be safely admitted to a step-down bed (38). The best supported method uses the ECG as a prognosticator (41-43). If the initial ECG lacks pathologic Q waves, S-T or T-wave changes consistent with infarction, ischemia, or strain, left ventricular hypertrophy, left bundle branch block, or a paced rhythm; the patient can be safely triaged to an intermediate care bed. To summarize, it is helpful to divide the physician’s role regarding patients with possible AM1 into two fundamental tasks: first, deciding if hospital admission is indicated, and second, if admission is necessary, selecting the appropriate triage site. For now, the physician’s clinical judgment should remain the ultimate determinant of the need for admission. The bed assignment may be aided by triage and prediction rules. Both processes must acknowledge that distinguishing between unstable angina and AM1 in the ED may be impossible, but that patients with either disease state require admission. A minority of patients with AM1 will present with classic histories and ECG changes. Such patients do

not present a major diagnostic dilemma. For these patients the physician must immediately address the issue of eligibility for thrombolytic therapy, recognizing that by current ECG criteria up to 20% of treated patients will rule out for AMI. In assessing the large number of patients who present with equivocal histories and ECG findings, the emphasis of several points may help to avoid inappropriate discharges. First, the cardiac risk profile, although not substantiated as an independent indicator of AMI, should nevertheless be used to formulate a baseline probability estimate for coronary artery disease. Second, sharp chest pain or chest wall tenderness does not exclude AMI. Third, radiation of chest pain, especially to the right arm, increases the possibility of AMI. Fourth, atypical presentation of AM1 in the elderly is common. Specifically, the likelihood of chest pain and autonomic symptoms decreases, and the likelihood of primary neurologic complaints increases with advancing age. Fifth, careful and detailed ECG interpretation may have a higher yield than traditionally accepted. Sensitive and specific criteria would include S-T elevations or depressions 11 mm in two or more leads, and other S-T or T-wave changes consistent with ischemia or strain, including S-T depression r 1 mm and T-wave inversions (all findings new or no tracing available). Finally, measurement of CK-MB or calculation of the probability of AM1 from a computer protocol may be useful as a final check prior to patient discharge from the ED. Once the decision has been made for admission, prognostic criteria or prediction rules can be utilized to maximize cost-effective resource allocation. The patient whose chest pain has resolved and whose ECG lacks specific risk criteria can be admitted to an intermediate care bed. Alternatively, a patient with a low calculated probability of AM1 can also be triaged to an intermediate-care bed.

REFERENCES 1. Herr CH. The diagnosis of acute myocardial infarction in the emergency department; part 1. J Emerg Med. 1992;10:455-61. 2. Nowakowski JF. Use of cardiac enzymes in the evaluation of acute chest pain. Ann Emerg Med. 1986;15:354-60. 3. Johnston CC, Bolton EC. Cardiac enzymes. Ann Emerg Med. 1982;11:27-35. 4. Lott JA, Stang JM. Serum enzymes and isoenzymes in the diagnosis and differential diagnosis of myocardial ischemia and necrosis. Clin Chem. 1980;26:1241-50. 5. Irvin RG, Cobb FR, Roe CR. Acute myocardial infarction and MB creatine phosphokinase. Relationship between onset of symptoms of infarction and appearance and disappearance of enzyme. Arch Intern Med. 1980;140:329-34. 6. Lee TH, Goldman L. Serum enzyme assays in the diagnosis of acute myocardial infarction. Ann Intern Med. 1986;105:22133.

7. Eisenberg JM, Horowitz LN, Busch R, Arvan D, Rawnsley H. Diagnosis of acute myocardial infarction in the emergency room: a prospective assessment of clinical decision-making and the usefulness of immediate cardiac enzyme determination. J Community Health. 1979;4:190-8. 8. Seager SB. Cardiac enzymes in the evaluation of chest pain. Ann Emerg Med. 1980;9:346-9. 9. Viskin S, Heller K, Gheva D, et al. The importance of creatine kinase determination in identifying acute myocardial infarction among patients complaining of chest pain in an emergency room. Cardiology. 1987;74:100-10. 10. Blomberg DJ, Kimber WD, Burke MD. Creatine kinase isoenzymes: predictive value in the early diagnosis of acute myocardial infarction. Am J Med. 1975;59:464-9. 11. Lee TH, Weisberg MC, Cook EF, Daley K, Brand DA, Goldman L. Evaluation of creatine kinase and creatine kinase-MB

Myocardial Infarction for diagnosing myocardial infarction: clinical impact in the emergency room. Arch Intern Med. 1987; 147: 115-21. 12. Yusuf S, Collins R, Lin L, Sterry H, Pearson M, Sleight P. Significance of elevated MB isoenzyme with normal creatine kinase in acute myocardial infarction. Am J Cardiol. 1987;59: 245-50. 13. Hedges JR, Rouan GW, Toltzis R, Goldstein-Wayne B, Stein EA. Use of cardiac enzymes identifies patients with acute myocardial infarction otherwise unrecognized in the emergency department. Ann Emerg Med. 1987;16:248-52. 14. Gibler WB, Lewis LM, Erb RE, et al. Early detection of acute myocardial infarction in patients presenting with chest pain and non-diagnostic EC&: serial CK-MB sampling in the emergency department. Ann Emerg Med. 1990;19:1359-66. 15. Gibler WB, Gibler CD, Weinshenker E, et al. Myoglobin as an early indicator of acute myocardial infarction. Ann Emerg Med. 1987;16:851-6. 16. Drexel H, Dworzak E, Kirchmair W, Milz MM, Puschendorf B, Dienstl F. Myoglobinemia in the early phase of acute myocardial infarction. Am Heart J. 1983;105:642-51. 17. Stein EA, Kaplan LA. Serum enzymes, isoenzymes, myoglobin, and contractile proteins in acute myocardial infarction. Cardiovasc Clin. 1983;13:355-69. 18. Grenadier E, Keidar S, Kahana L, Alpan G, Marmur A, Palant A. The roles of serum myoglobin, total CPK, and CK-MB isoenzyme in the acute phase of myocardial infarction. Am Heart J. 1983;105:408-16. 19. Gilkeson G, Stone MJ, Waterman M, et al. Detection of myoglobin by radioimmunoassay in human sera: its usefulness and limitations as an emergency room screening test for acute myocardial infarction. Am Heart J. 1978;95:70-7. 20. Schultz A, Larsen CE, Kristensen SD, Schmidt EB, Astrup G. Serum myoglobin measured by latex agglutination: rapid test for exclusion of acute myocardial infarction. Am Heart J. 1986;112:609-10. 21. Roxin L-E, Cullhed I, Groth T, Hallgren T, Venge P. The value of serum myoglobin determinations in the early diagnosis of acute myocardial infarction. Acta Med Stand. 1984;215: 417-25. 22. Pang S-C, Chiang C-W, Fu M, et al. Early diagnosis of acute myocardial infarction by myoglobin latex agglutination test. Jpn Heart J. 1988;29:631-8. 23. Norregaard-Hansen K, Hangaard J, Norgaard-Pedersen B. A rapid latex agglutination test for detection of elevated levels of myoglobin in serum and its value in the early diagnosis of acute myocardial infarction. Stand J Clin Lab Invest. 1984; 44:99-103. 24. Norregaard-Hansen K, Lindo KE, Ludrigsen CV, NorgaardPedersen B. Serum myoglobin compared with creatine kinase in patients with acute myocardial infarction. Acta Med Stand. 1980;207:265-70. 25. 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. 26. Tierney WM, Roth BJ, Psaty B, et al. Predictors of myocardial infarction in emergency room patients. Crit Care Med. 1985;13:526-31. 27. Pozen MW, D’Agostino RB, Selker HP, Sytkowski PA, Hood WB. A predictive 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. 28. Goldman L, Weinberg M, Weisberg M, et al. A computerderived protocol to aid in the diagnosis of emergency room patients with acute chest pain. N Engl J Med. 1982;307:58896. 29. Pozen MW, D’Agostino RB, Mitchell JB, et al. The usefulness of a predictive instrument to reduce inappropriate admissions to the coronary care unit. Ann Intern Med. 1980;92:238-42. 30. Sawe U. Early diagnosis of acute myocardial infarction with special reference to the diagnosis of the intermediate coronary syndrome: a clinical study. Acta Med Stand (Suppl). 1972; 545:1-76.

599 31. Kolter MN, Goldman AP, Parry WR. Acute consequences and chronic complications of acute myocardial infarction. In: Kerber RE, ed. Echocardiography in coronary artery disease. Mount Kisco, New York: Futura; 1988:17-51. 32. Horowitz RS, Morganroth J, Parrotto C, Chen CC, Soffer J, Pauletto FJ. Immediate diagnosis of acute myocardial infarction by two-dimensional echocardiography. Circulation. 1982; 65:323-g. 33. Sasaki H, Charuzi Y, Beeder C, Sugiki Y, Lew AS. Utility of echocardiography for the early assessment of patients with non-diagnostic chest pain. Am Heart J. 1986;112:494-7. 34. Wackers FJTh, Sokole EB, Samson G, et al. Value and limitations of thallium-201 scintigraphy in the acute phase of myocardial infarction. N Engl J Med. 1976;295:1-5. 35. Wackers FJTh, Lie KI, Liem KL, et al. Potential value of thallium-201 scintigraphy as a means of selecting patients for thecoronarycareunit. BrHeart J. 1979;41:111-17. 36. Mace SE. Thallium myocardial scanning in the emergency department evaluation of chest pain. Am J Emerg Med. 1989;7: 321-8. 37. Fuchs R, Scheidt S. Improved criteria for admission to cardiac care units. JAMA. 1981;246:2037-41. 38. 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. 39. Yusuf S, Pearson M, Sterry H, et al. The entry ECG in the early diagnosis and prognostic stratification of patients with suspected acute myocardial infarction. Eur Heart J. 1984;5: 690-6. 40. Slater DK, Hlatky MA, Mark DB, Harrell FE, Pryor DB, Califf RM. Outcome in suspected acute myocardial infarction with normal or minimally abnormal admission electrocardiographic findings. Am J Cardiol. 1987;60:766-70. 41. Brush JE. Brand DA. Acamnora D. Chalmer B. Wackers FJ. Use of the initial electrocardibgram to predict i&hospital complications of acute myocardial infarction. N Engl J Med. 1985; 312:1137-41. 42. Zalenski RJ, Sloan EP, Chen EH, Hayden RF, Gold IW, Cooke D. The emergency department ECG and immediately life-threatening complications in initially uncomplicated suspected myocardial ischemia. Ann Emerg Med. 1988;17:221-6. 43. Stark ME, Vacek JL. The initial electrocardiogram during admission for myocardial infarction. Arch Intern Med. 1987; 147:843-6. 44. Young MJ, McMahon LT, Stross JK. Prediction rules for patients with suspected myocardial infarction. Arch Intern Med. 1987;147:1219-22. 45. Fiebach NH, Cook EF, Lee TH, et al. Outcomes in patients with myocardial infarction who are initially admitted to stepdown units: data from the Multicenter Chest Pain Study. Am J Med. 1990;89:15-20. 46. Rutherford JD, Braunwald E, Cohn PF. Chronic ischemic heart disease. In: Braunwald E, ed. Heart disease: a text book of cardiovascular medicine. 3rd ed. Philadelphia: WB Saunders; 1988:1314-78. 47. Munger TM, Oh JK. Unstable angina. Mayo Clin Proc. 1990; 65:384-406. 48. Schroeder JS, Lamb IH, Hu M. Do patients in whom myocardial infarction has been ruled out have a better prognosis after hospitalization than those surviving infarction? N Engl J Med. 1980;303:1-5. 49. Krauss KR, Hutter AM, DeSanctis RW. Acute coronary insufficiency: course and follow-up. Arch Intern Med. 1972;129: 808-13. 50. Mulcahy R, Awadhi AHA, de Buitleor M, Tobin G, Johnson H, Contoy R. Natural history and prognosis of unstable angina. Am Heart J. 1985;109:753-8. 51. Parisi AF, Khuri S, Deupree RH, Sharma GVRK, Scott SM, Luchi RJ. Medical compared with surgical management of unstable angina: 5-year mortality and morbidity in the Veteran’s Administration Study. Circulation. 1989;80:1176-89.

The diagnosis of acute myocardial infarction in the emergency department; Part 2.

At present, routine use of cardiac enzymes in the emergency department (ED) cannot be justified, except possibly as a final screen prior to discharge...
1MB Sizes 0 Downloads 0 Views