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Journal of Electrocardiology 44 (2011) 494.e1–494.e12www.jecgonline.com

ST elevation: differentiation between ST elevation myocardial infarctionand nonischemic ST elevation

Henry D. Huang, MD,a Yochai Birnbaum, MDa,b,⁎aThe Section of Cardiology, Baylor College of Medicine, Houston, TX, USAbTexas Heart Institute, St. Luke's Episcopal Hospital, Houston, TX, USA

Received 16 May 2011

Abstract It is well accepted that early reperfusion is beneficial in patients with acute myocardial infarction

⁎ Corresponding aMedicine, 1709Dryden

E-mail address: y

0022-0736/$ – see frodoi:10.1016/j.jelectroc

presenting with ST elevation (STE). Earlier studies suggested lack of beneficial effects in patientspresenting without STE and even with ST depression. Currently, time to reperfusion is considered tobe a quality of care measure, and the latest American College of Cardiology/American HeartAssociation guidelines for the treatment of STE acute myocardial infarction (STEMI) emphasize thatthe physician at the emergency department should make reperfusion decisions within 10 minutes ofperforming the initial electrocardiogram (ECG). However, not all ECGs with STE necessarily reflecttransmural infarction from acute thrombotic occlusion of an epicardial coronary artery, as a largenumber of patients presenting with compatible symptoms have baseline STE. In some cases a patternof benign nonischemic STE (NISTE) can be recognized fairly easily. Other times, differentiatingbetween true STEMI and NISTE may be difficult. It should be remembered that patients presentingwith chest pain and showing benign pattern of NISTE (eg, “early repolarization” or STE secondaryto left ventricular hypertrophy) may have true ischemic pain and non-STE myocardial infarction oreven STEMI on top of the baseline benign pattern. It seems that, in the “real world,” the ability ofphysicians to differentiate NISTE from STEMI based on the presenting ECG pattern widely variesand depends on the prevalence of baseline NISTE in the patient population. Further studies areneeded to assess the ability of various ECG criteria to accurately differentiate between STEMIand NISTE.© 2011 Elsevier Inc. All rights reserved.

Today, the electrocardiogram (ECG) still has a major rolein diagnosing and triage of patients presenting with chestpain. Patients with suspected acute ST elevation myocardialinfarction (STEMI) are immediately referred for reperfusiontherapy by either primary percutaneous coronary intervention(pPCI) or thrombolytic therapy, whereas those without STelevation (STE) are initially treated conservatively.1 Thecurrent American College of Cardiology/American HeartAssociation (ACC/AHA) guidelines for STEMI recommendthat patients with suggestive symptoms of myocardialischemia within the preceding 12 hours (even if symptomsare resolved) who have STE in 2 or more adjacent ECG leads(N0.1 mV at the J-point) should undergo immediatereperfusion therapy.1 The article “Universal Definition ofMyocardial Infarction” states that the cutoffs for STEMI areSTE at the J-point of N0.2 mV in men and N0.15 mV in

uthor. The Section of Cardiology, Baylor College ofRoad, Suite 9.32BCM620,Houston, TX77030,USA.

birnbau@bcm.edu

nt matter © 2011 Elsevier Inc. All rights reserved.ard.2011.06.002

women in leads V2-V3 and/or N0.1 mV in all other leads.2

The different criteria are a source of confusion andinconsistencies. Most probably, if the criteria of the“Universal Definition of Myocardial Infarction” are used,the reported prevalence of STE would be reduced. However,a large number of patients presenting with chest pain haveSTE of nonischemic etiology (NISTE) on their presentingECG.3-6 Further, older patients, women, and patients withdiabetes may present with atypical symptoms, making initialECG assessment even more important for decision-making inthese situations.7-9 Although troponin levels are useful in thediagnosis and management of non-STE myocardial infarc-tion (NSTEMI), they cannot be relied upon for diagnosis ofacute STEMI because serum levels may be undetectable forup to 6 hours after coronary artery occlusion, and decisionsconcerning urgent reperfusion therapy are usually madebefore troponin levels are detectable.

The ACC/AHA STEMI guidelines state that the physicianin the emergency department should make reperfusiondecisions within 10 minutes of performing the initial

Table 1Common patterns of NISTE

STE secondary to LVHSTE secondary to conduction defect (LBBB) and nonspecific IVCDEarly repolarization pattern (notched J-point mainly in anterolateral leads)Normal variant of STE (nonischemic STE mainly V2-V3)Concave STEOld myocardial infarction/ aneurysmSpontaneously reperfused myocardial infarctionPericarditisBrugada syndromeWolf-Parkinson-White syndrome (pre-excitation)Takotsubo syndrome (apical ballooning syndrome)HypercalcemiaHyperkalemia

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ECG.10 Thus, accurate, timely analysis of the presentingECG is crucial in the initial management of patientspresenting with chest pain.11 Several patterns of nonischemicSTE (NISTE) are common and can be easily identified by anastute physician and differentiated from STEMI. However,some patients with baseline NISTE (eg, left ventricularhypertrophy or early repolarization) may also present withconcurrent acute STEMI or NSTEMI; thus, a benign patternof NISTE does not exclude acute coronary syndrome. Otherpatients may have rare etiologies for STE that cannot beaccurately identified without further clinical information on-hand when triaging decisions must be made quickly.Obviously, the differential diagnosis of STE is broad,including conditions with comorbid ischemia (such as aorticdissection), baseline STE without ischemia, and conditionswith new STE and chest pain but without ischemia (ie,pericarditis or myocarditis). Understandably, given thecurrent emphasis on making diagnosis of acute STEMI intimely matter, the chances of overcalling “STEMI” andunnecessarily activating the catheterization laboratory orgiving thrombolytics may be higher now than before.

For the majority of healthy individuals, the ST segment isisoelectric (ie, it is more or less horizontal at the level of theadjacent T-P and/or P-R segments). ST-segment deviation

Fig. 1. Presenting ECG of a 49-year-old man presenting with chest pain. ECG shconcave configuration. Emergent coronary angiography revealed 99% occlusionprimary PCI. Echocardiogram showed apical akinesis and distal anterior hypokine

(elevation or depression) is typically considered to representmyocardial ischemia. However, there are reports suggestingthat NISTE is very common (as high as 15% in the generalpopulation). Hiss et al 12 reported that 91% of 6014 healthymen in the US Air Force who were between 16 and 58 yearsold had STE of 0.1 to 0.3 mV in N1 precordial leads (mostcommonly seen in lead V2). Surawicz and Parikh13 reportedthat the prevalence of STE N 0.1 mV in 1 or more leads in V1through V4 in 529 healthy men was 93% among those whowere between 17 and 24 years of age. The prevalencedeclined gradually with increasing age (30% in menN 76 years).13 Given that the majority of men have STEgreater than 1 mm, baseline STE is actually considered anormal finding rather than a variant and is often referred to asa male pattern. In contrast, approximately 20% of womenhad STE N0.1 mV, and this prevalence is not affected byage.13 These considerations are reflected in the article“Universal Definition of Myocardial Infarction” mentionedearlier, but perhaps confusingly, not the ACC/AHAguidelines for management of STEMI.

Henry et al14 reported that 14% of patients who weresuspected to have STEMI and referred for pPCI were foundto have no clear culprit lesions, indicating that they hadNISTE. In a recent study from Denmark, only 79% of thepatients who were referred for direct pPCI based onprehospital ECG showing STE had a final diagnosis ofSTEMI or died.15 Common causes of NISTE are shownin Table 1.

“Concave” versus “convex” pattern of STE

The ST segment reflects ventricular depolarization and isnormally isoelectric with the PR and TP segments. It iscommonly taught that STE in which the ST segmentmorphology is upwardly convex or straight is consistentwith STEMI compared with a concave morphology, which isassociated with NISTE. The ACC/AHA guidelines suggestthat it is less likely that STEMI is present if the upward-

ows sinus rhythm, minimal STE in inferior leads, and STE in V1-V3 withof his proximal left anterior descending coronary artery, and he underwensis. His cardiac markers were positive for acute STEMI.

t

Fig. 2. A presenting ECG of a 36-year-old woman with shortness of breath. ECG shows sinus rhythm with STE in leads I, aVL, II, V2-V6 with notched J-poincompatible with “early repolarization” pattern. Of note, ECG 4 days earlier did not show STE or notched J-points.

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directed ST-segment changes are concave rather thanconvex.1 However, Smith16 reported that 43% of patients(16/37) who underwent emergent pPCI of the left anteriordescending coronary artery had concave morphology of STEin the anterior leads, concluding that this feature was unableto exclude STEMI. Prominent T waves may hamperevaluation of the shape of the ST segment as T wave areconcave in morphology and it may be difficult to determineexact point where the ST segment ends and the T wavebegins. Fig. 1 shows a presenting ECG of a patient withanterior STEMI. There is mild concave STE in leads V2-V3.His cardiac markers were positive, and coronary angiogra-phy revealed 99% occlusion of his left anterior descendingcoronary artery.

Fig. 3. An ECG of a 41-year-old man presenting to the emergency department with confusion. His troponin I was 0.02; CK was 530 and CKMB was 12.8. ECGshows sinus bradycardia with prominent J-point notches in the inferior and precordial leads (V3-V6). The patient was found to be hypothermic. The ECGchanges resolved after warming the patient.

t

Early repolarization

The typical pattern of early repolarization NISTE showsSTE of 1-4 mm in the lateral leads (mainly V5-V6). It mayalso involve the inferior leads. There is a characteristic notchat the J-point (Fig. 2). The ST segment is usually concave,and tall, peaked T waves may be present. Early repolariza-tion NISTE is commonly seen in young males. In manycases, STE is transient and ameliorates or even disappearswith tachycardia and hyperventilation. Thus, dynamicchanges in the degree of STE are not always indicative ofischemia. At times T-wave inversions may also be noted inthe precordial leads, which are believed to be due to presenceof juvenile T waves in younger persons, and should not be

Fig. 4. A routine ECG of a 44-year-old African-American man showing typical “normal variant” of STE. There is concave-shaped STE in leads V1-V3. Thispatient has also T inversion in the lateral leads that is not typical for “normal variant” STE.

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mistaken for ischemia. This can be avoided by comparingprevious ECG tracings to see if pronounced T waveinversions are already present. There is a controversyregarding the underlying pathophysiology of “early repolar-ization” pattern, some have shown that this pattern is notassociated with early repolarization of the ventricle andsuggested that this term is misleading.17 For many years,early repolarization NISTE was thought to be a benignphenomenon and widely considered to be a normal variant,as this finding is represented in approximately 5% of thepopulation.18,19 However, more recently, it has beenassociated with arrhythmic cardiac death, especially ifthere is N0.2 mV STE.19-22

It should be remembered that hypothermia may causetransient prominent J-point notch (Osborne waves)23 (Fig. 3)that should not be mistaken for benign early repolarization.Often hypothermia is also associated with bradycardia andtremor. Osborne waves with STE may be seen also in severe

Fig. 5. An ECG of a 71-year-old African-American woman showing sinus rhythmdeviation, concave-shaped STE in leads V1-V3, and ST depression in leads I, Iventricular hypertrophy. It should be remembered that, according to the “Universalfor patients with LBBB or LVH.

hypercalcemia and nervous system disorders. althoughhypothermia may cause QT prolongation, hypercalcemia isusually associated with short QT interval.24 Hyperkalemia isa well-known cause of ST segment elevation but will alsousually present with QRS widening and changes to the PRsegment. Another phenomenon that can be confused withJ-point notching is the presence of epsilon waves that areseen in arrhythmogenic right ventricular dysplasia. Howev-er, in arrhythmogenic right ventricular dysplasia, epsilonwaves are seen in leads V1-V3.25

A “normal-variant” pattern of NISTE

A “normal-variant”STE isdefined asSTelevationmainly inleads V1-V3 (Fig. 4).5 It is common in young males, mainlyAfrican American and Hispanic. In contrast to the NISTE seeninpatientswith left ventricular hypertrophy (LVH), there are noQRS criteria for LVH present and there is no concomitant ST

, incomplete left bundle branch block, left ventricular hypertrophy, left axisI, aVL, and V5-V6 suggestive of repolarization changes secondary to leftDefinition of Myocardial Infarction” article,2 the cutoffs for STE do not apply

Fig. 6. Atypical patterns of STE due to LVH. (A) A patient with LVH, biatrial enlargement, left axis deviation. There is mild STE in the inferior leads and leadsV1-V5. There is mild ST depression in lead aVL. Cardiac markers were negative, and echocardiogram showed LVHwithout regional wall motion abnormalities(B) Sinus rhythm with left atrial enlargement. Voltage criteria for LVH. There are Q waves and STE in the inferior leads, ST depression in leads I and aVL, andmild STE in leads V1-V4. His cardiac markers were negative, and echocardiogram showed LVH without regional wall motion abnormalities. Again, it should beremembered that, according to the “Universal Definition of Myocardial Infarction” article,2 the cutoffs for STE do not apply for patients with LBBB or LVH(although it is unclear whether they refer to leads V2-V3 or all leads).

Fig. 7. A 53-year-old Hispanic woman with acute pericarditis 3 days after coronary artery bypass surgery. There is diffuse STE in all leads, except III, aVR, andV1. There is mild PR segment depression, best seen in leads I, II, and V6.

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.

Fig. 8. A patient with sinus rhythm, LBBB, STE in leads III, V1-V3, and ST depression in I, II, aVL, and V5-V6. This pattern is typical for STE secondary to LBBB.It should be remembered that, according to the “Universal Definition of Myocardial Infarction” article,2 the cutoffs for STE do not apply for patients with LBBB

Fig. 9. An 80-year-old white female with acute myelogenous leukemia presented with shortness of breath. (A) ECG shows sinus tachycardia with LBBB and STE inleadsV1-V3.PatienthasknowndilatedcardiomyopathywithLVEFof25%;however, therewerenoelevationsofcardiacmarkers.Hershortnessofbreathwasattributedto anemia and pleural effusion. Three days later, her condition has improved. (B) Repeat ECG shows sinus rhythm, incomplete LBBBwith less STE in leads V1-V3This patient demonstrates dynamic changes in the magnitude of STE secondary to changes in QRS width (QRS duration decreased from 124 to 102 milliseconds)It should be remembered that, according to the “Universal Definition ofMyocardial Infarction” document,2 the cutoffs for STE do not apply for patients with LBBB.

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.

.

.

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depression in the lateral leads. Some investigators do notdifferentiate between a “normal variant” pattern and “earlyrepolarization” pattern, lumping all together as “early repolar-ization.” Indeed, many patients have both “normal variant” and“early repolarization” patterns.

STE secondary to LVH

NISTE secondary to LVH is typically seen in leads V1-V3.Usually, there are QRS criteria for LVH and concomitant STdepression in the lateral leads V5-V6 (Fig. 5). In many cases,there is also STE in lead aVR. It is important not to confusethis pattern with the pattern reported to be related to left mainrelated or global ischemia (STE in leads aVR and V1 with STdepression in the inferior and anterolateral leads). It should beremembered that, according to the “Universal Definition ofMyocardial Infarction” article,2 the cutoffs for STE do notapply for patients with left bundle branch block (LBBB) orLVH. However, LVH may cause atypical patterns of STE(Fig. 6). Moreover, occasionally patients may have more than1 type of NISTE (LVH + early repolarization or LVH +nonspecific intraventricular conduction delay [IVCD]).

Acute pericarditis

The classical ECG pattern of acute pericarditis is diffuseSTE in all leads, except leads V1 and aVR, which instead mayshow ST depression (Fig. 7). Typically, the pattern of STE inpericarditis does not fit a single vascular territory. Depressionof the PR interval below the isoelectric line is commonly seenearly in the course of pericarditis. However, focal pericarditisafter STEMI or cardiac surgery may result in more localized

Fig. 10. ECG showing sinus tachycardia, biatrial enlargement, IVCD. There is STand V5.

and atypical forms of STE, which maymanifest ST depressionin leads other than aVR and V1, mimicking myocardialinfarction from an isolated coronary artery.

STE secondary to IVCD

LBBB is commonly associated with marked ST changes(Fig. 8). ST deviation is usually discordant to the direction ofthe major deflection of the QRS complex due to presence ofsecondary ST-T wave abnormalities. Acute myocardialinfarction, on the other hand, is more likely to present withprimary ST-T wave abnormalities (ie, deviation that isconcordant to the QRS complex.) Because patients withLBBB usually have negative QRS deflections in leads V1-V3, they usually display prominent STE in those leads.Sgarbossa and colleagues26,27 published criteria on how todifferentiate NISTE from STEMI in patients with LBBB.The 3 ECG criteria for STEMI in these patients re: STE N1mm that is concordant with the QRS complex; ST depressionN1 mm in lead V1, V2, or V3, and STE N5 mm that wasdisconcordant with the QRS complex. These criteria werevalidated by Al-Faleh et al28 However, these criteria cannotoften be relied upon as they have very low sensitivity(0%-16%) for identifying acute myocardial infarction inpatients with LBBB.29,30 It should be remembered that themagnitude of ST deviation in patients with LBBB is highlydependent on the degree of aberrancy and may change whenQRS duration or heart rate varies (Fig. 9). Also, the degree ofST deviation may differ among different tracing due todifferent positioning of the electrodes; this is especiallypronounced in the anterolateral precordial leads in patientswith left axis deviation.

E in leads aVR, V1 to V4. There is ST depression in leads I, II, aVF, III,

Fig. 11. STE secondary to pre-excitation (Wolf-Parkinson-White syndrome). There is short PR interval with delta waves in the inferolateral leads. There is STEin leads aVR and V1-V4 and ST depression in the inferior leads. According to the “Universal Definition of Myocardial Infarction” document, there is less than2 mm STE in leads V2 and V3. However, the magnitude of STE in leads V1 and V4 is more than 1 mm (but these leads are not contiguous, and therefore, thecriteria are not met).2

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Similar to LBBB, patients with nonspecific IVCD mayalso have NISTE secondary to repolarization changes(Fig. 10). The pattern of ST deviation in these patientsvaries, and accurate diagnosis can only be made bycomparing the presenting ECG to previous tracing orfollowing dynamic changes in subsequent tracings.

Right bundle branch block (RBBB) usually does notinterfere with interpretation of ST deviation. However,during tachycardia, patients with RBBB may display STdepression in the precordial leads V1-V3, which shouldnot be confused with true inferolateral (posterior) STEMI.Like in LBBB, concordant ST segment shifts with“flipping” of the ST segment and T waves in the samedirection as the major QRS deflection is highly suspiciousof transmural ischemia.

Wolf-Parkinson-White pattern may also cause NISTE dueto repolarization abnormalities. The degree of ST deviationis highly dependent on the degree of activation via the

Fig. 12. A 31-year-old man presented with chest pain. ECG shows sinus rhythm wiwith positive T wave. Emergent coronary angiography revealed normal coronary aarrhythmia, or syncope.

accessory pathway. Fig. 11 is an example of STE due toWolf-Parkinson-White pre-excitation.

Brugada syndrome

The Brugada pattern of NISTE shows an RBBB patternwith STE in the anterior leads.31,32 The Brugada syndrome isassociated with a high risk for ventricular tachyarrhythmia andsudden cardiac death. Type 1 Brugada is characterized by acoved STE N0.2 mV, followed by a negative T wave inN1 right precordial leads (V1-V3) in the presence or absence ofa sodium channel blocker and in conjunction with documentedventricular fibrillation, polymorphic ventricular tachycardia, afamily history of sudden cardiac death at age younger than45 years, similar ECG pattern in relatives, inducibility ofventricular tachycardia with programmed electrical stimula-tion, syncope, or nocturnal agonal respiration.33 Type 2 STE

th a type 2 Brugada pattern of STE. There is a saddle-shaped STE in lead V2rteries. There is no personal or family history of sudden death, palpitations,

Fig. 13. A presenting ECG of a 71-year-old woman with Takotsubo syndrome. ECG shows sinus tachycardia, STE in the inferior leads, and V3-V6 and STdepression in lead aVR.

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has a saddleback pattern with initial STE of N0.2 mV thatdecreases in the middle and distal portion with a positive orbiphasic T wave. Type 3 STE has either a saddleback or covedpattern of STE b0.1 mV. Type 2 and 3 patterns are notdiagnostic of the Brugada syndrome. The ECG changes of theBrugada syndrome are dynamic and may change over time,with different types of STE seen on different days.33 Fig. 12 isan example of Type 2 Brugada pattern of STE.

Takotsubo syndrome (apical ballooning syndrome)

Apical ballooning syndrome is more common in postmen-opausal women and classically occurs following acuteemotional or physiologic stress. Patients present with chestpain and/or shortness of breath, and their ECGmay show STE(81.6% of the patients, mainly in the precordial leads), T-waveabnormalities (64.3%) and Q waves (31.8%). Mild elevationof cardiac markers has been reported in 86.2% of thepatients.34 In many cases, the initial presentation is indistin-guishable from anterior STEMI, although evaluation of leftventricular function by echocardiogram may show apicaldistribution of regional wall motion abnormalities that is nottypical of STEMI. It has recently been suggested that at moreadvanced ECG stage, when T waves become negative in theprecordial leads, patients with Takotsubo have more oftenpositive T waves in lead aVR and no T wave inversion in leadV1.35 Patients with Takotsubo may also have more extensiveST segment deviation in lead aVR and less ST segmentdeviation in lead V1 compared with those with acute, anteriorSTEMI.36 Acute cerebral infarction (particularly with sub-arachnoid hemorrhage)37,38 and pheochromocytoma39,40 canpresent with similar ECG and echocardiographic findings asTakotsubo cardiomyopathy. Fig. 13 is an example of STE in apatient with Takotsubo syndrome.

Spontaneously reperfused STEMI

The current guidelines for STEMI recommend thatpatients with suggestive symptoms of myocardial ischemia

within the preceding 12 hours presenting with STE in ≥2adjacent ECG leads (N0.1 mV at the J-point) should undergoimmediate reperfusion therapy.1 The guidelines do notmention the entity of (spontaneously) reperfused STEMI atall, and they do not mention ongoing symptoms as aprerequisite for immediate reperfusion therapy. A largenumber of patients may have (partial) resolution ofsymptoms by the time they arrive to the hospital, especiallyif chewable aspirin was given earlier. In addition, their ECGmay show (partial) STE resolution with terminal T waveinversion if prehospital ECG is available as shown in Fig. 14.Although these patients are at risk of reocclusion, clinicaltrials have not addressed the role of reperfusion therapy(thrombolysis or pPCI) in these patients.

Left ventricular aneurysm

Left ventricular aneurysm is another diagnosis to beaware of as it may cause persistent STE after a previousmyocardial infarction that, at times, may be indistinguishablefrom acute STEMI. Diagnosis is especially difficult whenprevious ECG tracings are unavailable. At one hospital inMinnesota, a patient received systemic thrombolytics on 2separate occasions in the emergency room because ofchronic STE from a previous LV aneurysm after an old MI(http://hqmeded-ecg.blogspot.com/2008/11/65-yo-male-with-recent-rule-out.html). Usually, pathologic Q waves arepresent in the same leads as those with STE when LVaneurysm is present. Fig. 15 is an example of a patient withresidual STE 3 months after infarction.

Many patients show mixed patterns of STE that makesrapid and accurate differentiation between STEMI andNISTE difficult (Fig. 16). It should be remembered thatpatients with benign forms of NISTE may present with chestpain and end up having NSTEMI. This “pseudo”-STEMIshould not be confused with STEMI. Some types of NISTEmay be transient and fluctuate in magnitude (eg, earlyrepolarization, Brugada syndrome). These dynamic changesshould be differentiated from the typical ECG evolution of

Fig. 15. A 28-year-old African American woman presented in February 2011 with acute inferolateral STEMI (A) and underwent primary PCI. Repeat ECG inApril 2011 shows Q waves in the inferolateral leads, tall R waves in leads V1-V2, and residual STE with terminal T wave inversion in the inferior leads + V3-V6with mild ST depression in lead V2 (B). There was no evidence of acute infarction or ischemia, and this ECG most probably represents aneurysm. Without theprevious ECG this pattern could be interpreted as acute or recent STEMI.

Fig. 14. A 90-year-old woman with hypertension presented with substernal chest pain that started 12 hours earlier and subsided 1 hour before presentation. ECGshows sinus rhythm, Q waves in the inferolateral leads with STE, and terminal T wave inversion, suggestive of recent STEMI. Emergent coronary angiographyshowed 90% diameter stenosis of the right coronary artery and PCI was performed.

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,

Fig. 16. A 70-year-old white man with acute pericarditis 1 day after coronary artery bypass surgery. ECG shows sinus rhythm, STE with notched J-point in leadsI, II, aVL, V2-V6, and ST depression in leads III, aVR, and V1. The pattern is compatible with “early repolarization,” yet the magnitude of STE is relatively highfor “early repolarization.” There was no previous ECG in the chart.

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STEMI. The ACC/AHA STEMI guidelines state that thephysician at the emergency department should makereperfusion decisions within 10 minutes of performing theinitial ECG.1,10 This recommendation reflects that thebenefits of reperfusion therapy are time-dependent andrapid ECG interpretation is vital in strategies aimed to reducedoor-to-balloon times.41 In an effort to further reduce time toreperfusion, novel systematic strategies are currently beingcreated and evaluated. One such strategy is wireless pre-hospital transmission of ECGs by emergency medicalservices (EMS) to experienced on-call cardiologists.42 Thisstrategy has been shown to reduce door-to-balloon time43

and door-to-needle time.44 Systems have been developed inwhich the interpreting cardiologist communicates with thepatient and the EMS team via a mobile phone, in addition toreading the transmitted ECG.45 It has not yet beendetermined, however, if this approach improves the accuracyof pPCI activation decisions. However, in the United Statessuch systems have not been developed, and the electro-cardiographer is without the benefit of taking a patienthistory face-to-face, or being able to perform a physicalexamination, or review previous ECG's of the patients. Evenif previous ECGs are present in the medical record, duetoThe Health Insurance Portability and Accountability Actregulations, ECGs are transmitted without names or anyidentifier details. Therefore, the electrocardiographers can-not compare the transmitted ECG to the previous ones onfile. Although such strategy may improve the sensitivity ofdetecting STE, it is unclear how it will affect specificity andfalse activation of the catheterization laboratory, as thereaders may have the proclivity to overdiagnose STEMI. Tostudy the ability of experienced electrocardiographers todistinguish between STEMI to NISTE, 116 consecutiveECGs showing STE were sent to 15 experienced electro-cardiographers, asking whether they would activate thecatheterization laboratory for possible STEMI if patients hadcompatible symptoms.46 Only 8 patients (7%) had adjudi-cated STEMI and additional 8 patients had positive cardiactroponin without evidence of STEMI. The percentage of

ECGs for which pPCI was recommended for the patient bythe individual readers varied widely (7.8% to 33%). Thesensitivity and specificity of the individual readers rangedfrom 50% to 100%, (average 75%) and 73% to 97%,(average 85%), respectively. There were broad inconsis-tencies among the readers in the chosen reasons used toclassify NISTE, suggesting that completely different criteriawere used by the various readers.46 This study illustratesthe need for further research how to distinguish betweenSTEMI and NISTE in different populations and tostandardize the published criteria in order to improve theaccuracy of ECG reading.

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