Differentiating ST-Elevation Myocardial Infarction fromNonischemic ST-Elevation in Patients With Chest Pain
Viet Tran, MDa, Henry D. Huang, MDa, Jose G. Diez, MDa,b, Gerardo Kalife, MDb,Rajiv Goswami, MDa, David Paniagua, MDa, Hani Jneid, MDa, James M. Wilson, MDa,b,
Scott R. Sherron, MDb, and Yochai Birnbaum, MDa,b,*
Current guidelines for acute ST-segment elevation myo-cardial infarction (STEMI) emphasize the need for shorten-ing door-to-balloon times in patients presenting with symp-toms suggestive of myocardial ischemia and STE1–3 andencourage making triage decisions based on prehospital12-lead electrocardiographic (ECG) transmission.2,4,5 How-ver, although this approach has been shown to shortenimes to the catheterization laboratory, less is known abouthe accuracy of such an approach. In the absence of ECGigns of left ventricular hypertrophy (LVH) or left bundleranch block, guidelines define STE as new STE at the Joint in �2 contiguous leads with cut-off points of �0.2V in men and �0.15 mV in women in leads V2 and V3 or
�0.1 mV in other leads.6 However, nonischemic STE(NISTE) is found in �90% of healthy men.7,8 Up to 15%of patients presenting with chest pain have NISTE.9 –13 Inthe present study we assessed the ability of interventionalcardiologists to differentiate between STEMI and NISTEusing only electrocardiograms of consecutive patients forwhom the primary percutaneous coronary intervention(pPCI) protocol had been activated by emergency depart-ment physicians.
aDepartment of Medicine, Section of Cardiology, Baylor College ofMedicine, Houston, Texas; bTexas Heart Institute at St. Luke’s Episcopal
ospital, Houston, Texas. Manuscript received April 12, 2011; revisedanuscript received and accepted June 6, 2011.
A database of a large urban medical center containedrecords of 240 consecutive patients for whom the pPCIprotocol had been activated because of suspected acuteSTEMI from January 2008 through December 2008. Tworeaders (V.T. and H.D.H.) collected 84 electrocardiogramsshowing STE in �2 contiguous leads. Patients with leftbundle branch block or ventricular rhythms including elec-tronic ventricular pacing were excluded. We also excludedpatients whose patterns of STE did not meet guideline-based criteria for acute STEMI.
To confirm that ECG STE represented true acute STEMI,we performed detailed chart reviews that included finaldiagnoses from the in-hospital physician’s progress anddischarge notes and examined reports of in-hospital coro-nary angiograms and echocardiograms. We also indepen-dently confirmed that those cases diagnosed as acuteSTEMI demonstrated the typical increase and decrease incardiac marker levels (e.g., cardiac troponin I and crea-tine kinase-MB) consistent with STEMI and that subse-quent ECG tracings showed the typical evolution indic-ative of STEMI.
Seven experienced interventional cardiologists were thenasked to analyze the electrocardiograms after all identifyinginformation was removed and to decide whether they wouldsend these patients for pPCI based on ECG findings alone,assuming patients had appropriate corresponding symp-toms. Readers were blinded to clinical information for each
patient including age, ethnicity, and gender; types of symp-
1097Coronary Artery Disease/Ischemic Versus Nonischemic ST Elevation
toms; and the clinical setting in which pPCI was activated.If readers did not think ECG findings warranted pPCI pro-tocol activation, they were asked to code the electrocardio-gram as NISTE and then choose from a list of 12 possibleexplanations as to why STE was present. Readers wereallowed to code �1 reason to explain the cause of NISTEfor each case. Readers were then assessed for overall accu-racy, sensitivity, specificity, and positive and negative pre-dictive values in correctly identifying patients with adjudi-cated STEMI.
Results
Forty patients (48%) had adjudicated true STEMI and 44
Figure 1. Sensitivity, specificity, positive predictive value (PPV), and negatblack bars).
able 1ossible causes of nonischemic ST-segment elevation
patients (52%) had NISTE (13 of these patients [30%] had
positive cardiac markers suggestive of non-STEMI). Of the84 patients (59 men, average age 61 years, range 25 to 90),32 patients (38%) were white, 32 (38%) African-American,12 (14%) Hispanic, and 9 (10%) of other ethnicities. Of thepresenting symptoms, 62 patients (74%) had chest pain, 10(12%) had shortness of breath, 5 (6%) had weakness, and 7(8%) had other symptoms. With regard to risk factors, 57patients (68%) had a previous diagnosis of hypertension, 46patients (55%) had dyslipidemia, 30 patients (36%) haddiabetes mellitus, and 27 patients (32%) had previouslyestablished coronary artery disease.
Percent electrocardiograms for which pPCI was recom-mended varied widely among readers (33% to 75%), with
ictive value (NPV) of the 7 individual readers (gray bars) and the average
sensitivities ranging from 53% to 83% (mean 71%), speci-
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1098 The American Journal of Cardiology (www.ajconline.org)
ficities from 32% to 86% (mean 63%), positive predictivevalues from 52% to 79% (mean 66%), and negative predic-tive values from 67% to 79% (mean 71%; Figure 1). Evenwhen readers chose NISTE as the diagnosis, the causevaried (Table 1). LVH, which is commonly found in ourpatient population, was thought to be the cause of NISTE bythe individual readers in 6% to 31% of patients. Readerschose the option of old MI/aneurysm in 10% to 26% ofcases. Interestingly, STEMI with spontaneous reperfusionas an indication not to activate the catheterization laboratoryfor possible pPCI was the least frequent choice (0% to 5%)in all patients with suspected NISTE.
Discussion
We show that although 74% of patients presented withthe classic symptom of chest pain, 32% had known coronaryartery disease, only 48% had true STEMI. We found widevariance in the overall sensitivity and specificity of ourreaders in distinguishing between STEMI and NISTE. Our
Figure 2. (a) A 58-year-old man with human immunodeficiency virus had severeelevation in leads V1 to V5. Coronary angiogram showed a 99% thrombotic occlusiwas performed. Peak creatine kinase-MB level was 157.3 ng/ml. Transthoracic echakinesia. Therefore, this patient had a true ST-segment elevation myocardial infarheadache, chest pain, and blurred vision. Electrocardiogram shows left ventricular h
ith negative T waves in leads I, aVL, and V6. The interventional cardioloelectrocardiogram was comparable to previous tracings. The patient was observechocardiogram showed moderate left ventricular hypertrophy with a left ventricudetermined this patient had nonischemic ST-segment elevation.
results confirm that even in patients with corresponding
symptoms of STEMI and for whom the pPCI protocol wasactivated, it remains difficult for experienced interventionalcardiologists to determine by ECG criteria alone if patientshave true STEMI or if they have NISTE. In a previous studyusing electrocardiograms of consecutive patients showingSTE that were not necessarily recorded in the acute setting,we found a similarly wide discrepancy in the range ofsensitivity in experienced electrocardiographers.14
Figures 2 and 3 depict 4 representative cases. Figure 2hows a patient with adjudicated anterior STEMI; however,nly 3 readers chose STEMI, whereas the other 4 decidedhat the patient had NISTE; all marked the option “old
I/aneurysm without acute changes” and 1 added the op-ion “lack of reciprocal changes.” Figure 2 also shows a
patient with NISTE. Four readers thought that the patient hadSTEMI. Of the 3 readers who marked “NISTE,” 2 chose “earlyrepolarization pattern” as the cause and the other chose “STEsecondary to LVH.” Figure 3 shows a patient with adjudicatedSTEMI, but only 1 reader thought as such. Two readers chose
in for 2 hours. QS waves are present in leads V1 to V3 with concave ST-segmentin the left anterior descending coronary artery; percutaneous coronary interventionram on day 2 showed a left ventricular ejection fraction of 20% to 24% with apical) A 49-year-old man with a history of uncontrolled hypertension presented with
phy, concave ST-segment elevation in leads V1 to V5, and ST-segment depressionctivated the primary percutaneous coronary intervention protocol because thee chest pain unit and his cardiac marker levels did not increase. Transthoracicion fraction �60% and no regional wall motion abnormalities. Therefore, it was
chest pave lesionocardiogction. (bypertro
gist deaed in thlar eject
early repolarization pattern, 3 chose “pericarditis” (with 1
s
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1099Coronary Artery Disease/Ischemic Versus Nonischemic ST Elevation
reader adding “concave STE”), and 1 made a diagnosis ofNISTE because there were no reciprocal changes. The secondelectrocardiogram in Figure 3 shows NISTE. One readerthought that the patient had STEMI. Three readers decided thatthe patient had STE secondary to LVH, 2 readers chose oldMI/aneurysm without acute changes, and 1 decided that thepatient had NISTE because the STE was concave (Figures 2and 3, Table 1). Indeed, this patient has LVH criteria but STEecondary to LVH is typically seen in leads V1 to V3 and not
in the inferior leads. Moreover, this patient had narrow butdeep q waves in the inferior leads that 2 readers thought wererepresentative of an old MI or aneurysm. However, echocar-diogram revealed LVH without any regional wall motion ab-normalities.
Electrocardiograms recorded in the field by emergency
Figure 3. (a) A 55-year-old woman had chest pressure for 45 minutes. Ele
5 to V6. Coronary angiogram showed no significant narrowing. Laboratoryas 48.5 ng/ml, and there was a typical increase and decrease in cardiac
nferolateral segment with preserved left ventricular systolic function (ejlevation myocardial infarction. (b) A 52-year-old man with a history ofiscomfort and shortness of breath. Electrocardiogram showed left ventric
V4 and ST-segment depression in leads I and aVL. There was no previodeactivated the primary percutaneous coronary intervention protocol aftedynamic electrocardiographic changes and transthoracic echocardiogramfunction and no regional wall motion abnormalities. Coronary angiogramhad nonischemic ST-segment elevation.
medical service teams can be interpreted at the site or
electronically transmitted for interpretation at specializedcenters, local emergency departments, experienced electro-cardiographers, or on-call interventional cardiologists. Itshould be noted that in the United States, when prehospitalelectrocardiograms are transmitted, patients’ names andother identifying details must be omitted to comply withHealth Insurance Portability and Accountability Act(HIPPA) regulations. Therefore, even if previous electro-cardiograms exist in hospital medical records, readerswould have no access to these. This is not the case in othercountries, where the reader may have access to an electronicarchive of electrocardiograms. Systems have been devel-oped in which the interpreting physician communicates withthe patient and the emergency medical service team bymobile telephone in addition to reading the transmitted
iogram showed mild ST-segment elevation in the inferior leads and leadsshowed a positive result for cardiac troponin, her creatine kinase-MB levelr levels. Transthoracic echocardiogram showed hypokinesis of the distalraction 55% to 60%). It was determined this patient had a ST-segment
rolled hypertension and heavy alcohol consumption presented with chestpertrophy with ST-segment elevation in the inferior leads and leads V1 totrocardiogram on record for comparison. The interventional cardiologist
the patient at bedside. Cardiac markers were negative. There were nomild left ventricular hypertrophy with preserved left ventricular systolic3 showed no significant lesions. Therefore, it was determined this patient
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1100 The American Journal of Cardiology (www.ajconline.org)
approach improves the accuracy of pPCI activation com-pared to blind ECG interpretation.
The reported percent false activation of pPCI protocolsvaries from 5% to 25%.16–22 Results from a recent pooledanalysis of 10 prospective observational registries involving72 hospitals showed that pPCI was performed in only 76%of the 2,712 patients given a diagnosis of STEMI by thetransporting emergency medical service team.23 Previousstudies showed that wireless ECG transmission decreasesdoor-to-balloon times17,20,22,24,25; however, these studiesid not examine differences in clinical outcomes or costenefits.
The alternative of using automated ECG interpretive algo-ithms to speed decision making has been investigated20,24;
however, they showed lower sensitivity. Clark et al24
showed that despite increased specificity in 1 of 2 computeralgorithms compared to that of cardiologists, the cardiolo-gists had improved sensitivity (78% for the 2 algorithms vs85% for the cardiologists).24 It has been proposed that theate of inappropriate catheterization laboratory activationhould be �5%.18,26 It is assumed that cardiologists—es-ecially interventional cardiologists—would be more accu-ate than paramedics or emergency department physiciansn differentiating STEMI from NISTE. Rokos et al18 sug-
gested that the classification of appropriate versus inappro-priate activation of the pPCI protocol is strongly dependenton the interventional cardiologist, and when the pPCI pro-tocol is deactivated by an interventional cardiologist and noangiography is performed, the case can be classified asinappropriate activation.18 However, it would be incorrecto assume that the interventional cardiologist is always rightecause, as results of the present study show, the accuracyf off-line reading by experienced interventional cardiolo-ists is far from perfect.
As the population ages and the prevalence of baselineCG abnormalities increases, diagnosing STEMI in theresence of baseline STE caused by LVH, repolarizationbnormalities, or long-term infarction or aneurysm will be-ome only more challenging.14,24 As a result, if a wirelessriage method were to be implemented, it could furtherncrease false activations of the pPCI protocol when patientsresent with symptoms compatible with STEMI unless easyccess to a patient’s previous electrocardiograms is enabled.
Results of our study confirm that a diagnosis of STEMIrom the electrocardiogram alone can be challenging in aopulation with a high prevalence of abnormal baselinelectrocardiograms. Thus, from a cost–benefit and clinicalutcomes standpoint, there could be significant problems ifireless ECG transmission programs without access to pre-ious electrocardiograms and/or communication with a pa-ient were the only approach implemented. To our knowl-dge, there has been no study that proves this strategy aloneould lead to improved clinical outcomes in patients whoresent with chest pain.
cknowledgment: We thank Chrissie Chambers, MA, ELSor editorial assistance in the preparation of this report.
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