CLINICAL STUDIES
Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the Myocardial Infarction Triage and Intervention (MITI) project
Peter J. Kudenchuk, MD, FACCa*,
Charles Maynard, PhDa*,
Leonard A. Cobb, MD, FACCa*,
Mark Wirkusa*,
Jenny S. Martin, RNa*,
J. Ward Kennedy, MD, FACCa*,
W. Douglas Weaver, MD, FACCa* for the MITI Investigators
a Department of Medicine, Division of Cardiology, University of Washington, Seattle, Washington, USA
* Henry Ford Hospital, Detroit, Michigan, USA
Manuscript received August 13, 1997;
revised manuscript received March 11, 1998,
accepted March 18, 1998.
Address for correspondence: Dr. Peter J. Kudenchuk, Division of Cardiology, Box 356422, University of Washington, Seattle, Washington 98195-6422
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Abstract
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Objectives. We sought to determine whether the prehospital electrocardiogram (ECG) improves the diagnosis of an acute coronary syndrome.
Background. The ECG is the most widely used screening test for evaluating patients with chest pain.
Methods. Prehospital and in-hospital ECGs were obtained in 3,027 consecutive patients with symptoms of suspected acute myocardial infarction, 362 of whom were randomized to prehospital versus hospital thrombolysis and 2,665 of whom did not participate in the randomized trial. Prehospital and hospital records were abstracted for clinical characteristics and diagnostic outcome.
Results. ST segment and T and Q wave abnormalities suggestive of myocardial ischemia or infarction were more common on both the prehospital and hospital ECGs of patients with as compared with those without acute coronary syndromes (p  0.00001). Those with prehospital thrombolysis were more likely to show resolution of ST segment elevation by the time of hospital admission (14% vs. 5% in patients treated in the hospital, p = 0.004). In patients not considered for prehospital thrombolysis, both persistent and transient ST segment and T or Q wave abnormalities discriminated those with from those without acute coronary ischemia or infarction. Compared with ST segment elevation on a single ECG, added consideration of dynamic changes in ST segment elevation between serial ECGs improved the sensitivity for an acute coronary syndrome from 34% to 46% and reduced specificity from 96% to 93% (both p < 0.00004). Overall, compared with abnormalities observed on a single ECG, consideration of serial evolution in ST segment, T or Q wave or left bundle branch block (LBBB) abnormalities between the prehospital and initial hospital ECG improved the diagnostic sensitivity for an acute coronary syndrome from 80% to 87%, with a fall in specificity from 60% to 50% (both p < 0.000006).
Conclusions. ECG abnormalities are an early manifestation of acute coronary syndromes and can be identified by the prehospital ECG. Compared with a single ECG, the additional effect of evolving ST segment, T or Q waves or LBBB between serially obtained prehospital and hospital ECGs enhanced the diagnosis of acute coronary syndromes, but with a fall in specificity.
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Abbreviations and Acronyms
| | AMI | = acute myocardial infarction | | ECG | = electrocardiogram, electrocardiographic | | LBBB | = left bundle branch block | | MITI | = Myocardial Infarction Triage and Intervention trial |
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Early diagnosis is pivotal in the contemporary management of patients with acute coronary syndromes and is an essential component of a rapid intervention strategy. Although newer enzymatic assays offer promise for earlier identification of patients with suspected acute myocardial infarction (AMI), the electrocardiogram (ECG) remains the most widely used initial screening test for evaluating patients with chest pain. Early electrocardiography may facilitate early intervention by identifying patients with true ischemic syndromes sooner. In contrast, if obtained too soon, patients with ECG abnormalities that are subtle or too nonspecific for definitive diagnosis may be misidentified and inappropriately treated. The purposes of this study were to characterize the frequency and serial evolution of very early ECG changes in patients with and without acute myocardial ischemia or infarction and to determine whether ECG screening before hospital admission improves the diagnosis of an acute coronary syndrome in patients with chest pain of suspected cardiac origin.
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Methods
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Patients.
The Myocardial Infarction Triage and Intervention (MITI) Project was a prospective, randomized trial comparing prehospital with in-hospital thrombolysis in patients with suspected AMI; the design and results of MITI have been reported previously (1). Briefly, consecutive patients with suspected symptoms of AMI and no clinical contraindications to thrombolytic therapy received a 12-lead prehospital ECG, which was interpreted by computer and transmitted by cellular telephone to a remote emergency department for review by a physician. During the treatment phase of the trial, patients whose ECG met criteria for acute epicardial injury were randomized to prehospital or in-hospital treatment with alteplase. Before and at the end of this treatment phase of the trial, prehospital ECGs continued to be obtained in all patients suspected of having an AMI, irrespective of their clinical eligibility for thrombolytic therapy. These patients did not receive thrombolytic therapy before hospital admission. In addition to the prehospital ECG, all patients received a second ECG immediately on hospital arrival.
Two groups of patients, those randomized to prehospital versus in-hospital thrombolysis, and those who did not participate in the randomized trial were the focus of this ECG study. This trial was conducted with the approval of the Human Subjects’ Review Committee at the University of Washington.
Electrocardiography.
Prehospital ECGs were obtained by a battery-powered, computer-integrated ECG system (Marquette Electronics). Prehospital and initial hospital ECGs were read independently by two experienced electrocardiographers who had no knowledge of the corresponding ECG, patient identity and outcome. Disagreements between readers regarding the presence or absence of acute epicardial injury were uncommon (<1% of tracings) and were resolved by consensus with a third electrocardiographer. ST segments were coded categorically as  1 mm, <1 mm or absent. ST segment elevation 1 mm in at least two contiguous ECG leads, in the absence of left bundle branch block (LBBB), ventricular pacing or an idioventricular rhythm, was defined as diagnostic of acute epicardial injury. In the presence of left ventricular hypertrophy, anterior ST segment elevation 4 mm in at least two contiguous leads was required for diagnosis of injury. Ischemic ST segment depression was defined as 1 mm horizontal or downsloping ST segment depression in two or more contiguous leads in the absence of LBBB or a ventricular rhythm. If accompanied by inferior ST segment elevation, ST segment depression in leads V2 and V3 was coded as indicative of probable posterior ST segment elevation. Pathologic Q waves were defined as an initial negative QRS deflection 40 ms in duration in at least two contiguous ECG leads in the absence of LBBB or a ventricular rhythm.
Diagnosis.
Prehospital and hospital records of all patients were abstracted for clinical characteristics and diagnostic outcome. Recognizing that the diagnosis of an acute coronary syndrome may be substantiated by a variety of means (characteristic symptoms, elevations in cardiac enzymes, cardiac catheterization or autopsy findings), the final hospital diagnosis was used to determine patients with acute myocardial ischemia or infarction (2).
Statistical analysis.
Differences between continuous and categoric variables were evaluated by using the two-tailed Student t test and the chi-square test (using the Yates correction as necessary), respectively. Sensitivity, specificity and predictive accuracy of a positive test were conventionally defined (3). The potential interaction between abnormalities observed on a single ECG and evolving abnormalities between serial ECGs on diagnosis was evaluated using a hierarchic log linear model. Statistical significance was defined as p 0.05 (two-tailed).
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Results
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Patients.
Between January 25, 1988 and February 28, 1993, 3,027 consecutive patients with symptoms of suspected AMI had prehospital electrocardiography performed by paramedics, and subsequently an in-hospital ECG. The clinical and ECG characteristics of these patients are shown in Table 1. Prehospital ECGs were obtained a mean of 91 ± 76 min after the onset of symptoms. In-hospital ECGs were obtained a mean of 24 ± 11 min after prehospital tracings. Either the prehospital or in-hospital ECG was technically uninterpretable in 10 patients (0.3%).
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Table 1 Clinical Characteristics and Prevalence of Electrocardiographic Abnormalities in All Patients Who Received a Prehospital and Initial Hospital Electrocardiogram for Evaluation of a Chest Pain Syndrome, in Those Who Were Randomized to Receive Prehospital Versus In-Hospital Thrombolysis and in Those Who Were Not Randomized to Receive Such Treatment
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Of these patients in whom a prehospital and in-hospital ECG were obtained for evaluation of suspected AMI, two groups were identified for further study: those who had been randomized to receive prehospital versus in-hospital thrombolysis and those who were not participants in the randomized treatment trial. The clinical and ECG characteristics of these patients are also shown in Table 1.
Effect of prehospital thrombolysis on the ECG in treated patients.
During the treatment phase of the MITI prehospital trial (November 2, 1988 to December 3, 1991), patients with suspected AMI, with no clinical contraindications to thrombolysis, and whose ECG met criteria for epicardial injury were eligible for randomization to prehospital or in-hospital treatment with alteplase. Results have been previously reported, based on intention to treat (1); they are presented here again based on actual treatment received. In this analysis, a total of 362 patients received prehospital (n = 173) or in-hospital thrombolytic therapy (n = 189) during the treatment phase of the trial. The clinical and ECG characteristics of these patients (based on actual treatment received) are described in Table 2. These patients differed in age and initial heart rate but were otherwise comparable in terms of gender, clinical and hemodynamic characteristics on presentation and incidence of AMI. Because of the study design, the group who received prehospital thrombolysis had an  15 min greater time interval between the prehospital and initial hospital ECG. In patients who had prehospital thrombolysis, the frequency of ST segment elevation on the prehospital ECG was insignificantly higher, whereas on the initial hospital ECG it tended to be lower than that in patients who had in-hospital thrombolysis (p = 0.07). Among all patients randomized to thrombolysis, the prevalence of ST segment elevation, ST segment depression or T wave inversion declined, whereas the prevalence of Q waves increased between the prehospital and initial hospital ECG (p < 0.005) (Table 1). These differences in the prevalence of ST segment and T or Q wave abnormalities between the prehospital and initial hospital ECG were more pronounced in those with prehospital versus in-hospital thrombolysis (Table 2), possibly owing to the effect of prehospital thrombolysis itself or to the different time intervals between ECGs in the two treatment groups.
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Table 2 Clinical and Electrocardiographic Characteristics of Patients Who Received Prehospital or In-Hospital Thrombolysis
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Table 3 describes the serial ECG changes between the prehospital and initial hospital ECG in those with prehospital thrombolysis and those in whom thrombolysis was delayed until after hospital admission. No overall differences were noted in the evolution of ECG abnormalities in the groups, with two notable exceptions. First, ST segment elevation was more likely to resolve completely by hospital admission in those with prehospital thrombolysis: 14% versus 5% of those treated before versus after hospital admission, respectively (p = 0.004). Second, patients who had thrombolysis in the hospital and who had ST segment elevations <1 mm on the prehospital ECG were more likely to progress in severity to 1 mm by hospital admission. Nondiagnostic ST segment elevation progressed to diagnostic proportions between the prehospital and initial hospital ECG in no patient who received prehospital thrombolysis compared with 3% of those who received thrombolysis after hospital admission (p = 0.02).
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Table 3 Serial Electrocardiographic Changes Between Prehospital and Initial Hospital Electrocardiogram in Patients With Prehospital Versus In-Hospital Thrombolysis (randomized patients)
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ECG changes in patients not evaluated for prehospital thrombolysis.
To avoid the confounding effect of thrombolysis on the ECG during the treatment phase of the MITI prehospital trial, serial changes in the prehospital and initial hospital ECG were evaluated strictly in the 2,665 patients with suspected AMI who were not participants in the randomized trial. The clinical characteristics and prevalence of ECG abnormalities in these patients are shown in Table 4.
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Table 4 Clinical Characteristics and Prevalence of Electrocardiographic Abnormalities in Patients With Suspected Acute Myocardial Infarction Who Were Not Randomized to Receive Prehospital Versus In-Hospital Thrombolysis
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Compared with patients whose chest pain was not determined to be related to ischemia or infarction, those with acute myocardial ischemia or infarction were older, more commonly male, more likely to have a previous cardiac history of infarction, angina or bypass surgery and had a higher incidence of ECG abnormalities suggestive of acute ischemia or infarction, but demonstrated a slower heart rate and lower blood pressure on presentation. The intervals between symptom onset and the prehospital and hospital ECG were similar between the two groups.
ST segment elevation or depression, T wave inversion and Q waves on both prehospital and hospital ECGs were more common in patients with acute coronary syndromes than in those without myocardial infarction or ischemia (Table 4). In patients with acute ischemia or infarction, Q waves were more prevalent on the initial hospital ECG than on the prehospital ECG (31% vs. 21%, p < 0.00001). Otherwise, the overall prevalence of ST segment elevation, ST segment depression, T wave inversion and LBBB did not differ on the prehospital versus initial hospital ECG in patients with and without documented acute myocardial ischemia or infarction (Table 4). In comparing prehospital with initial hospital ECGs, the identification of any abnormality in ST segment, T or Q wave or LBBB had a virtually identical sensitivity, specificity and positive predictive value for detecting acute myocardial ischemia or infarction—80%, 60% and 64%, respectively (Table 4).
Table 5 describes the serial ECG changes between the prehospital and initial hospital ECG in patients whose chest pain presentation was determined to be caused by acute myocardial ischemia or infarction as compared with those in whom it was not. The serial (dynamic) evolution of these changes between the prehospital and initial hospital ECG was an important discriminator between patients with and without acute coronary ischemia or infarction. In a total of 15% of patients with acute ischemia or infarction (as compared with 4% of those without an acute coronary syndrome), ST segment elevation evolved from or to diagnostic proportions between the prehospital and initial hospital ECG (p < 0.0000001). Representative changes are illustrated in Figures 1 to 3. In an additional 5% of patients with ischemia or infarction (as compared with 2% of those without), less pronounced but suggestive changes of injury were observed in ST segments between the two tracings (p < 0.0000001). That is, in addition to 26% of patients who had persistent ST segment elevation on both ECGs, an additional 20% of patients with subsequently documented myocardial ischemia or infarction could have been identified by evolutionary changes in ST segment elevation that transpired in the 30 min between their prehospital and initial hospital ECG evaluation. Compared with ST segment elevation on a single ECG (whether prehospital or initial hospital), persistent or dynamic changes in ST segment elevation between two serial ECGs improved the diagnostic sensitivity for acute myocardial ischemia or infarction from 34% to 46%, with only a modest reduction in specificity from 96% to 93% and in positive predictive value from 88% to 84% (all p < 0.00004) (Fig. 4).
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Table 5 Serial Electrocardiographic Changes in Patients With Suspected Acute Myocardial Infarction Who Were Not Receive Randomized to Prehospital Versus In-Hospital Thrombolysis
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Figure 1 Serial changes are depicted between the prehospital (left) and initial hospital (right) ECG in a patient with chest pain. The prehospital ECG depicts acute ST segment elevation in leads I, aVL and V4 to V6. On the initial hospital ECG, obtained 35 min after the prehospital tracing, ST segment elevation is more difficult to appreciate in leads I and aVL and deceptively masquerades as an apparent widening of the QRS complex in leads V4 to V6.
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Figure 2 Serial changes are depicted between the prehospital (left) and initial hospital (right) ECG in a patient with chest pain. The prehospital ECG shows ST segment elevation in leads V1 to V4, with ST segment sagging and T wave inversion in leads II, III and aVF. On the initial hospital ECG, obtained 23 min after the prehospital tracing, ST segment elevation has resolved and ST-T wave abnormalities are less pronounced in the inferior leads, whereas ST segment sagging is now evident in leads V4 and V5.
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Figure 3 Serial changes are depicted between the prehospital (left) and initial hospital (right) ECG in a patient with chest pain. The prehospital ECG shows subtle ST-T wave abnormalities that are nondiagnostic of myocardial ischemia. On the initial hospital ECG, obtained 36 min after the prehospital tracing, ST segment elevation is now evident in leads I, aVL and V2, with ST segment depression and T wave inversion in the inferior leads (II, III and aVF).
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Figure 4 The sensitivity, specificity and positive predictive value (PPV) of ST segment elevation or any ST segment T or Q wave or LBBB abnormality for acute myocardial ischemia or infarction are compared between the initial hospital ECG (open bars) and the initial ECG plus serial (prehospital and initial hospital) changes (solid bars). As compared with the initial hospital ECG alone, added consideration of serial changes between the prehospital and initial hospital ECG in these variables significantly improved the sensitivity for acute myocardial ischemia or infarction, at the expense of a reduction in specificity and positive predictive value. Data are shown for 1,254 patients with and 1,411 patients without acute myocardial ischemia or infarction.
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Changing ST segment depression, T wave inversion and diagnostic Q waves between the prehospital and initial hospital ECG were more common than ST segment elevation in patients with acute coronary ischemia or infarction. Between the 30 min that transpired between the prehospital and initial hospital ECG, transient ST segment depression, transient T wave inversion and newly developed Q waves were observed in 21%, 23% and 14%, respectively, of patients with an acute coronary syndrome, as compared with 7%, 15% and 6%, respectively, of those without ischemia or infarction (p < 0.0000001). In contrast, transient or persistent changes in LBBB were infrequent and similar in patients with and without acute coronary ischemia and infarction.
In all "evolving" changes in ST segment elevation or depression, T wave inversion, developing Q waves or LBBB between the prehospital and initial hospital ECG were observed in 57% of patients with acute myocardial ischemia or infarction as compared with 32% of patients without an acute coronary syndrome (Table 5) (p = 0.0000001). Taken by themselves, these serial changes were less sensitive but more specific for detecting acute myocardial ischemia or infarction than ST segment, T or Q wave or LBBB abnormalities observed on a single ECG (sensitivity 57% vs. 80%, specificity 68% vs. 60%, respectively, p = 0.0000001). However, compared with a single abnormal ECG, the presence or serial evolution of ST segment, T or Q waves or LBBB between the prehospital and initial hospital ECG improved the diagnostic sensitivity of the ECG for an acute coronary syndrome from 80% to 87%, with a decline in specificity from 60% to 50% and a decline in positive predictive value from 64% to 60% (all p < 0.000006) (Fig. 4). In a hierarchic log linear model, inclusion of serial abnormalities between the prehospital and initial hospital ECG enhanced the ability to predict the presence of an acute coronary syndrome over isolated findings on either ECG alone (p < 0.05).
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Discussion
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Electrocardiography has an established role in the evaluation of myocardial ischemia and is the most immediately available diagnostic modality for patients with suspected acute coronary syndromes. The relative ease of performing electrocardiography, together with development of portable, battery-operated electrocardiograph machines with land-based or cellular telephone transmission capabilities, and computer-facilitated interpretation of tracings have broadened the potential availability of this important tool to use outside the hospital or physician’s office (4,5).
Limited acceptance of prehospital electrocardiography.
Prehospital electrocardiography has been demonstrated to be a feasible and reliable method of screening patients with suspected AMI, particularly when thrombolytic therapy is contemplated (2,5). At present, however, it is infrequently used in the evaluation of patients with suspected AMI (6). In part, this may be related to the uncertain need for prehospital electrocardiography when prehospital thrombolytic therapy is not under consideration. In contrast, because of the relatively small number of patients found to be eligible for thrombolytic therapy in the prehospital setting, the wide deployment of prehospital electrocardiography may not be seen as justifiable (7).
A second problem relates to whether the prehospital ECG provides useful diagnostic information beyond an ECG obtained on hospital arrival. The interval over which such diagnostic changes make their ECG appearance is not precisely known. Most information used to make the ECG diagnosis of acute myocardial ischemia and infarction has stemmed from hospital evaluations of patients who have oftentimes presented many hours after symptom onset. It could be argued that if obtained too early, before ECG changes of myocardial ischemia become manifest, interpretation of the prehospital ECG could be misleading and result in the inappropriate triage of patients away from emergency coronary interventions.
Even if abnormalities are detected on the prehospital ECG, a third problem relates to the specificity of such findings. ST segment of acute epicardial injury can be mimicked by pericarditis or by chronic changes associated with left ventricular hypertrophy or aneurysm, intraventricular conduction abnormalities and early repolarization. Similarly, ST segment depression, T wave inversion and even Q waves may accompany conditions that are not necessarily associated with acute myocardial ischemia or infarction. In the presence of such abnormalities, it could be argued that prehospital electrocardiography offers no advantage over an ECG obtained on hospital arrival, or might even result in the overdiagnosis of acute coronary syndromes.
Study findings.
The findings of this study suggest that ECG abnormalities are an early manifestation of acute coronary ischemia and can be readily identified by prehospital electrocardiography. Such changes were commonly observed early (mean 60 to 90 min) after symptom onset in patients with acute myocardial ischemia or infarction.
During the treatment phase of the MITI prehospital trial (1), early electrocardiography did not hamper diagnosis in patients eligible for thrombolysis. In those with prehospital thrombolysis, the prehospital ECG was, as expected, more likely to be abnormal than their initial hospital ECG. Even in patients who were not allocated to receive thrombolysis until after hospital admission, the prevalence of ST segment elevation on the prehospital ECG was higher than that on the hospital ECG obtained 20 to 30 min later (p = 0.03) (Table 2). On the basis of serial changes, the vast majority of patients who were eligible for thrombolysis before hospital admission by clinical and ECG criteria remained so on hospital admission (Table 3). An added benefit was observed in 14% of those with prehospital thrombolytic therapy in whom ST segment elevation resolved by hospital arrival, suggesting that coronary reperfusion was successful (8,9) and that additional invasive interventions to restore infarct-related artery patency were not likely to be necessary.
Prehospital electrocardiography was also of value in patients with suspected pain of myocardial ischemia or infarction who might have become candidates for thrombolysis. On average, prehospital ECGs were obtained 20 min later after symptom onset in patients who were not considered for randomization compared with patients who were randomized to receive prehospital or in-hospital thrombolysis during the treatment phase of the trial (p = 0.0001). Persistent, dynamic or suggestive ST segment elevation of epicardial injury was observed in a total of 46% of these patients with subsequently documented acute myocardial ischemia or infarction, as compared with 7% of those without documented ischemia or infarction (p < 0.0000001) (Table 5). Compared with ST segment elevation on a single ECG, serial data improved the diagnostic sensitivity for an acute coronary syndrome potentially treatable with thrombolytic agents from 34% to 46%, with only a modest decline in specificity from 96% to 93% and in positive predictive value from 88% to 84% (all p < 0.00004) (Fig. 4).
An attribute of this study was the opportunity to compare and contrast prehospital ECG findings with those of the initial hospital ECG. Unlike patients without evidence of myocardial ischemia or infarction, ECG abnormalities (ST segment elevation, ST segment depression, T wave inversion and abnormal Q waves) were not only more prevalent in patients with confirmed unstable angina or infarction (Table 4), but were also more frequently dynamic (Table 5). When considered together, either an abnormal ECG or serial changes between the prehospital and initial hospital ECG significantly enhanced the diagnostic sensitivity for an acute coronary event, as compared with abnormalities observed on a single ECG.
Serial ECGs obtained in the hospital might have demonstrated the same diagnostic utility as those obtained in this study. However, obtaining a prehospital ECG utilized transport time efficiently, allowing for serial ECG changes to occur during otherwise "down time" while en route to the emergency department. Time to treatment could have been advanced by 30 min or more with prehospital electrocardiography, as compared with awaiting serial ECG evaluation in the hospital.
Clinical implications.
Previous studies have determined that diagnostic-quality prehospital 12-lead ECGs can be obtained with great success by paramedics (10), can enhance the sensitivity and specificity of the clinical diagnosis of acute myocardial ischemia and infarction (11), can shorten time to treatment after hospital admission (12) and can even potentially lower in-hospital mortality (6). To our knowledge, this is the first study to systematically evaluate the diagnostic utility of serial changes between the prehospital and hospital ECGs in patients with and without acute coronary syndromes, regardless of their candidacy for early thrombolysis. Although only a minority of patients with acute coronary syndromes are currently eligible for thrombolytic therapy (7), many more may be eligible for other effective early interventions (such as heparin) (13). Accordingly, prehospital electrocardiography appears to have potential utility for the screening and treatment of all patients with suspected cardiac chest pain.
Study limitations.
This was a retrospective study whose focus was on how serial prehospital and in-hospital electrocardiography in patients with suspected cardiac chest pain impacted the hospital diagnosis of ischemia or infarction. How the ECG ultimately impacted physician behavior, patient treatment, time to treatment or the economy of treatment were not evaluated. From the standpoint of these issues, wider use of the prehospital ECG merits further study. It is notable that findings from the National Registry of Myocardial Infarction have suggested that prehospital electrocardiography has the potential to favorably impact both more appropriate and more timely treatment in patients with AMI (6). The present study suggests that one mechanism by which prehospital electrocardiography may facilitate patient management is by improved diagnosis.
Interpretation of the ECG remains limited by the expertise of the reader (14). All ECGs in this study were interpreted by experienced electrocardiographers who may not be representative of other readers. In contrast, even among less experienced readers, changes between serial ECGs may be more easily identified than an isolated abnormality on a single tracing. Thus, it is possible that prehospital electrocardiography could even improve the accuracy of ECG interpretation on hospital admission by offering the opportunity to observe changes between tracings that might be more difficult to interpret individually (Fig. 1 to 3). However, some patients without documented acute ischemia or infarction manifested both persistent and transient ECG abnormalities. Hence, it is appropriate to be cautious about the absolute specificity of a single ECG or serial ECGs to discriminate chest pain that is of ischemic versus nonischemic origin. Indeed, in this study as well as others, increasing sensitivity for detecting acute ischemia or infarction resulted in some compromise of specificity (15,16).
Data from the National Registry of Myocardial Infarction suggest that patients who underwent prehospital electrocardiography had a longer delay to hospital admission (6). Such delays were not observed in the present study, except in patients who received prehospital thrombolysis. We observed that obtaining a prehospital ECG should add only a few minutes of time to the evaluation process (2). However, it is possible that the presence of abnormalities on the ECG could trigger other treatments before hospital admission, resulting in a longer delay to hospital admission. Thus, the deployment of any diagnostic or therapeutic maneuvers before hospital admission should be weighed against the potential harm of postponing hospital admission and the more definitive interventions available there.
Conclusions.
ECG abnormalities are an early manifestion of acute coronary syndromes and could be readily identified by prehospital electrocardiography. Taken by themselves, serial changes between early prehospital and in-hospital ECGs were less sensitive but more specific for acute ischemia or infarction than isolated abnormalities on a single ECG. Taken together, the presence or serial evolution of abnormalities between the prehospital and initial hospital ECG significantly enhanced the diagnostic sensitivity for an acute coronary event, at the expense of a decline in specificity, as compared with abnormalities observed on a single ECG.
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Footnotes
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This study was supported in part by Grant RO1HL38454 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and by unrestricted grants from Genentech Inc., South San Francisco, California; Marquette Electronics, Milwaukee, Wisconsin; and Pharmacia Deltec, St. Paul, Minnesota.
 A complete list of the MITI investigators appears in reference 2. 
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References
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1. Weaver WD, Cerqueira M, Hallstrom AP, et al. Prehospital-initiated vs hospital-initiated thrombolytic therapy: the Myocardial Infarction Triage and Intervention trial. JAMA. 1993;270:1211–1216[Abstract/Free Full Text]
2. Weaver WD, Eisenberg ME, Martin JS, et al. Myocardial Infarction Triage and Intervention Project, phase I: patient characteristics and feasibility of prehospital initiation of thrombolytic therapy. J Am Coll Cardiol. 1990;15:925–931[Abstract]
3. Peterson DR. Epidemiology and Clinical Problems. New York: MSS Information Corp; 1973. p. 9–68
4. Aufderheide TP, Hendley GE, Woo J, Lawrence S, Valley V, Teichman SL. A prospective evaluation of prehospital 12-lead ECG application in chest pain patients. J Electrocardiol. 1992;24(Suppl):8–13
5. Kudenchuk PJ, Ho MT, Weaver WD, et al. Accuracy of computer-interpreted electrocardiography in selecting patients for thrombolytic therapy. J Am Coll Cardiol. 1991;17:1486–1491[Abstract]
6. Canto JG, Rogers WJ, Bowlby LJ, French WJ, Pearce DJ, Weaver WD. The prehospital electrocardiogram in acute myocardial infarction: is its full potential being realized? J Am Coll Cardiol. 1997;29:498–505[Abstract]
7. Brugemann J, vanderMeer J, deGraeff PA, Takens LH, Lie KI. Logistical problems in prehospital thrombolysis. Eur Heart J. 1992;13:787–788[Abstract/Free Full Text]
8. Buszman P, Szafranek A, Kalarus Z, Gasior M. Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction. Eur Heart J. 1995;16:1207–1214[Abstract/Free Full Text]
9. Pepine CJ. Prognostic markers in thrombolytic therapy: looking beyond mortality. Am J Cardiol. 1996;78:24–27[CrossRef][Medline]
10. Aufderheide TP, Keelan MH, Hendley GE, et al. Milwaukee Prehospital Chest Pain Project, phase I: feasibility and accuracy of prehospital thrombolytic candidate selection. Am J Cardiol. 1992;69:991–996[CrossRef][Medline]
11. Aufderheide TP, Hendley GE, Thakur RK, et al. The diagnostic impact of prehospital 12-lead electrocardiography. Ann Emerg Med. 1990;11:1280–1287
12. Kereiakes DJ, Gibler WB, Martin LH, Pieper KS, Anderson LC. Relative importance of emergency medical transport and the prehospital electrocardiogram on reducing hospital time delay to therapy for acute myocardial infarction: a preliminary report from the Cincinnati Heart Project. Am Heart J. 1992;123:835–840[CrossRef][Medline]
13. Th’eroux P, Waters P, Qiu S, McCans J, deGuise P, Juneau M. Aspirin or heparin to prevent acute myocardial infarction during the acute phase of unstable angina. Circulation. 1993;88:2045–2048[Abstract/Free Full Text]
14. McCrea WA, Saltissi S. Electrocardiogram interpretation in general practice: relevance to prehospital thrombolysis. Br Heart J. 1993;70:219–225[Abstract/Free Full Text]
15. Elko PP, Weaver WD, Kudenchuk PJ, Rowlandson I. The dilemma of sensitivity versus specificity in computer-interpreted acute myocardial infarction. J Electrocardiol. 1992;24:2–7
16. Otto LA, Aufderheide TP. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis of acute myocardial infarction. Ann Emerg Med. 1994;23:17–24[Medline]
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J. L. Garvey, B. A. MacLeod, G. Sopko, M. M. Hand, and on behalf of the National Heart Attack Alert Progr
Pre-Hospital 12-Lead Electrocardiography Programs: A Call for Implementation by Emergency Medical Services Systems Providing Advanced Life Support--National Heart Attack Alert Program (NHAAP) Coordinating Committee; National Heart, Lung, and Blood Institute (NHLBI); National Institutes of Health
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C. Hanefeld, C. Sirtl, M. Spiecker, W. Bojara, P. H. Grewe, T. Lawo, and A. Mugge
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J. A. Spertus, M. J. Radford, N. R. Every, E. F. Ellerbeck, E. D. Peterson, and H. M. Krumholz
Challenges and opportunities in quantifying the quality of care for acute myocardial infarction: Summary from the acute myocardial infarction working group of the American heart association/American college of cardiology first scientific forum on quality of care and outcomes research in cardiovascular disease and stroke
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J. A. Spertus, M. J. Radford, N. R. Every, E. F. Ellerbeck, E. D. Peterson, and H. M. Krumholz
Challenges and Opportunities in Quantifying the Quality of Care for Acute Myocardial Infarction: Summary From the Acute Myocardial Infarction Working Group of the American Heart Association/American College of Cardiology First Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke
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H. P. Selker, J. R. Beshansky, J. L. Griffith, and for the TPI Trial Investigators*
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E. Braunwald, E. M. Antman, J. W. Beasley, R. M. Califf, M. D. Cheitlin, J. S. Hochman, R. H. Jones, D. Kereiakes, J. Kupersmith, T. N. Levin, et al.
ACC/AHA guidelines for the management of patients with unstable angina and non-st-segment elevation myocardial infarction: A report of the american college of cardiology/ american heart association task force on practice guidelines (committee on the management of patients with unstable angina)
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Prehospital ECGs Enhance Diagnosis of Acute Coronary Syndromes
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Abstract
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