a b s t r a c t

Background: ST-segment elevation due to inferior STE myocardial infarction (STEMI) may be misdiagnosed as pericarditis. Conversely, this less life-threatening etiology of ST elevation may be confused for inferior STEMI. We sought to determine if the presence of any ST-segment depression in Lead aVL would differentiate inferior STEMI from pericarditis.

Methods: Retrospective study of 3 populations. Cohort 1 included patients coded as inferior STEMI, cohort 2 in- cluded patients with a discharge diagnosis of pericarditis who presented with chest pain and at least 0.5 mm of ST elevation in at least 1 inferior lead. We analyzed the presenting electrocardiogram in both populations, with careful assessment of leads II, III, aVF, and aVL. In addition, we retrospectively studied a third cohort of pa- tients with subtle inferior STEMI (b 1-mm STE with occluded artery on catheterization) and assessed the sensi- tivity of ST depression in lead aVL for this group.

Results: Of 154 inferior STEMI patients, 154 had some amount of ST depression in lead aVL (100%; confidence in- terval, 98%-100%). Of the 49 electrocardiograms in the pericarditis group, all 49 had some inferior STE but none had any ST-segment depression in lead aVL (specificity, 100%; confidence interval, 91%-100%). In the third cohort, there were 272 inferior MIs with coronary occlusion, of which 54 were “subtle.” Of these, 49 had some ST depres- sion in lead aVL.

Conclusion: When there is inferior ST-segment elevation, the presence of any ST depression in lead aVL is highly sensitive for coronary occlusion in Inferior myocardial infarction and very specific for differentiating inferior myocardial infarction from pericarditis.

(C) 2015

Introduction

Background

Inferior acute myocardial infarction (AMI) due to occlusion of the infarct-related artery may manifest as diagnostic ST-segment elevation (STE) in 2 consecutive of “inferior” leads II, III, and aVF, or it may be elec- trocardiographically subtle, with lesser degrees of STE, or with Hyperacute T waves only. Emergency physicians must recognize such STE so that pa- tients with acute inferior myocardial infarction (MI) due to coronary oc- clusion rapidly undergo reperfusion therapy, and patients with benign

? No grants or external funding was used for this manuscript.

?? Abstract presented previously at: ACEP 2013; Denver, CO; October 9, 2013.

* Corresponding author: Johanna E. Bischof, MD, Department of Emergency Medicine, Hennepin County Medical Center, 701 Park Ave, Minneapolis, MN 55415.

E-mail addresses: [email protected] (J.E. Bischof), [email protected] (P. Thompson), [email protected] (D. Marti), [email protected] (S.W. Smith).

conditions are not unnecessarily subjected to undue risks or costs of thrombolytic therapy or cardiac catheterization. In order to do this, emer- gency providers must be able to differentiate STEMI from other entities that manifest ST elevation in the absence of MI. The most common of these entities are pericarditis, benign early repolarization (BER), left ven- tricular aneurysm, and left ventricular hypertrophy [1].

Strategies have been suggested to differentiate STEMI from other causes of STE, including a flat or convex morphology of the ST segment [1,2]. Brady [2] found that although a nonconcave morphology was quite specific for AMI (97%), it was only 77% sensitive. An electrocardio- gram (ECG) finding with high sensitivity and specificity for MI would be helpful for emergency physicians to quickly identify patients with infe- rior ST elevation who would benefit from PCI.

Differentiating patients with pericarditis from inferior STEMI thus can be both difficult and fraught with hazard. As discussed above, the ST elevation in inferior STEMI is typically in leads II, III, and aVF, but these are also the most common leads in which to see ST elevation in pericarditis. Spodick [3] evaluated 48 patients with pericarditis

http://dx.doi.org/10.1016/j.ajem.2015.09.035

0735-6757/(C) 2015

identified by the presence of a pericardial rub and found all 48 of these patients to have ST elevation in the limb leads. Inferolateral STEMI presents a particular diagnostic challenge as it often has diffuse ST ele- vation (leads I, II, III, aVF, V₅, V₆) which can easily be mistaken for peri- carditis. The differentiation between inferior STEMI and pericarditis is of particular clinical interest, as one entity benefits from anticoagulation/ Antiplatelet therapy and reperfusion (STEMI), whereas the same thera- py risks hemorrhagic pericardial effusion in the other (pericarditis).

The vector of ST elevation in inferior STEMI is generally between 60? and 120?(between leads II and III), which should result in some recipro- cal ST-segment depression in lead aVL (-30?), as the resulting ST vector angle is greater than 90? [4-6]. On the other hand, because pericarditis is a diffuse inflammation of the entire pericardium, the resulting ST axis should be at approximately 45?, toward the apex of the heart [7]. As 45? is at a 75? offset to aVL (-30?), this ST elevation would not man- ifest reciprocal ST depression in lead aVL. This is consistent with the findings of Spodick [3], who found that among 48 patients with pericar- ditis as proven by presence of a rub, no ECG had an ST vector greater than 60?; although this reported vector implies absence of ST depres- sion in lead aVL, he did not report specifically on lead aVL (Fig. 1).

Goals of this investigation

We propose that the presence of any ST depression in lead aVL would be both highly sensitive and specific for differentiating inferior STEMI from pericarditis. In addition, computerized Corrected QT interval (QTc; Bazett-corrected QT interval = QT in milliseconds divided by the square root of the preceding R-R interval) has proven valuable in differ- entiating benign causes of anterior ST elevation (anterior BER) from an- terior STEMI, and we hypothesized that it would have value in the interpretation of inferior ST elevation [8].

Methods

Research design and setting

We conducted a retrospective review of 2 cohorts to compare the ECGs of patients with inferior AMI with those who were diagnosed as having pericarditis. In addition, we retrospectively studied a third co- hort of consecutive patients with suspected coronary occlusion who were taken to angiography and found to have occlusion of the artery supplying the inferior wall, and we assessed the incidence of ST depres- sion in lead aVL in the subtle cases only, as defined by no STE N 1 mm in inferior leads.

ECG interpretation“>Fig. 1. Relative ST-segment vectors in inferior STEMI compared with pericarditis.

Inferior STEMI

For this group, we searched the catheterization laboratory database at Hennepin County Medical Center from January 2002 through March 2008 for patients coded by the catheterization laboratory as acute inferior STEMI. The ECGs, catheterization reports, and hospital records were reviewed to ensure accuracy of diagnosis. Patients were excluded for aberrant conduction (Left bundle-branch block, paced rhythm, Wolf- Parkinson-White syndrome), repeat encounters for in-stent thrombo- sis, if there was only a prehospital ECG used to make the diagnosis, and lack of ST elevation on presenting ECG. Fig. 2 is an example of an inferior STEMI ECG.

Subtle STEMI cohort

In addition, in order to evaluate our hypothesis in the setting of sub- tle inferior STEMI, a second STEMI cohort was reviewed, among which all patients who presented to the emergency department with suspicion for Acute coronary occlusion and any amount of STE were evaluated with emergent angiography [9]. From this cohort, we reviewed patients with occlusion of the artery supplying the inferior wall; among these cases, we only included patients with “subtle” occlusion, as defined by

<= 1-mm STE in inferior leads, because ECGs were available only for this

select group. These ECGs were scrutinized for the presence or absence of any ST depression in lead aVL to evaluate the sensitivity of this finding in the case of subtle MI.

Pericarditis

This group was identified by a discharge diagnosis of pericarditis (International Classification of Diseases, Ninth Revision [ICD-9] code 420.90) presenting to Hennepin County Medical Center between 1996 and 2012. Medical records of all patients were reviewed and cases were included if they presented with a complaint of chest pain and had at least 0.5-mm STE in 1 or more inferior leads. The medical records of these patients were scrutinized to ascertain the validity of the diagnosis. Most of these patients ruled out for MI with serial troponins, most had echocardiograms, and some had cardiac catheterization. The age of the patient and clinical presentation were taken into account to determine if serial troponins and/or catheterization was warranted. Patients were excluded if records were not complete enough to confirm the accuracy of diagnosis, or if there was an absence of ST elevation on the ECG. Be- cause pericarditis is strictly a clinical diagnosis for which there is no refer- ence standard or confirmatory test, we largely relied on the patient’s clinical diagnosis by the treating physicians if the documented history of presenting illness, physical exam, and above factors were consistent with the diagnosis. Fig. 3 is an example of a pericarditis ECG.

ECG interpretation

Electrocardiograms were obtained retrospectively from medical re- cord review, with the first diagnostic ECG used for analysis. ST segments were measured manually at the J point, to the nearest 0.25 mm in leads II, III, aVF, and aVL for STE or depression. Three authors (C.W., J.B., P.T.), blinded to outcome, measured the ST segments; each ECG was evaluat- ed by 2 individual authors, and discrepancies were determined by the second author (J.B.), who reviewed all ECGs. The authors agreed a priori that the ST segments would be measured at the J point relative to the PQ junction, and that any appreciable ST elevation or depression not meet- ing 0.5 mm would be coded as 0.25 mm. We have shown in the past that 0.5-mm measurements have good interrater reliability [10,11]. Lead aVL was particularly scrutinized for any ST depression (defined by

>= 0.25 mm) or T-wave inversion. Traditional “reperfusion criteria” were defined as at least 1-mm STE in at least 2 contiguous inferior leads (II, III, or aVF). For the inferior STEMI and pericarditis groups, it was noted whether the patients met our defined reperfusion criteria

Fig. 2. Example ECG of patient with subtle inferior STEMI, but evidence of ST depression in aVL which could help make this difficult diagnosis. This patient had acute 99% mid-RCA occlusion.

but did not affect inclusion. In addition, the ST elevation in leads II and III were directly compared for each patient, recorded as III N II, III b II, or equal. Lastly, the computer-measured QTc intervals were recorded for each ECG.

Outcomes

The primary outcome evaluated in our study was presence or ab- sence of any ST depression in lead aVL in patients with inferior STE due to STEMI vs pericarditis.

Secondary outcomes included the presence of T-wave inversion in aVL, comparisons of the relative ST elevation in leads II and III, and whether or not the ECG met the reperfusion criteria. In addition, the QTc interval was also measured as a secondary outcome because this has proven helpful in differentiating anterior STEMI from benign causes of STE (early repolarization) [8]. Furthermore, we sought to determine if the presence of concomitant lateral STEMI, as determined by at least 0.5-mm ST elevation in both leads V₅ and V₆, would negate reciprocal ST depression in lead aVL. Lastly, we sought to determine the sensitivity of any ST depression in aVL for inferior MI among those who do not meet the STEMI criteria.

Analysis

Statistics were by percentages with confidence intervals (CIs); groups were compared with Student t test (http://www.physics. csbsju.edu/stats/t-test.html).

Results

Inferior STEMI cohort

One hundred sixty patients were identified from catheterization lab- oratory records with a diagnosis of inferior STEMI. Six patients were ex- cluded for left bundle-branch block (1 patient), presence of only a prehospital ECG prior to catheterization (2 patients), anterior STEMI with incorrect coding (1 patient), repeat catheterization after in-Stent thrombosis (1 patient), and out-of-hospital cardiac arrest without ST elevation on ECG (1 patient). This left 154 patients for ECG analysis.

Of the 154 patients with catheterization laboratory diagnosis of infe- rior STEMI, 154 patients (sensitivity, 100%; CI, 98%-100%) had some de- gree of ST depression in lead aVL (at least 0.25 mm). In addition, all 154 patients demonstrated T-wave inversion in lead aVL (sensitivity, 100%; CI, 98%-100%). One hundred thirty-five patients had right coronary

Fig. 3. Example of ECG of patient with pericarditis. Although there is clear ST elevation in the inferior leads, lead aVL lacks ST depression.

artery (RCA) occlusion (88%), 17 had occlusion of the left circumflex ar- tery (11%), 2 had occlusion of the left anterior descending artery (1%), and 1 had occlusion of an obtuse marginal (1%). Thirty-five patients (23%) had ST elevation in leads V₅ and V₆ indicative of lateral involve- ment. Of these, 0 of 35 had ST elevation in lead aVL; in fact, all had some ST depression in aVL).

Considering patients who did or did not meet the reperfusion criteria (>= 1-mm STE in at least 2 inferior leads), 134 (87%) of 154 pa- tients (CI, 82%-92%) met these criteria; all 21 (100%) of 21 patients (CI, 85%-100%) who did not meet these “criteria” had some ST depres- sion in lead aVL (Fig. 4). In comparing ST elevation in lead II vs lead III, 136 (88%) of 154 (CI, 82%-93%) had ST elevation in lead III greater than lead II, the ST segments were equal in 13 (8%) of 154 (CI, 5%- 14%), and lead II was greater than lead III in 6 (4%) of 154 (CI, 2%-8%;

1

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0

ST Elevation Magnitude in lead III Compared with Lead II

Inferior STEMI (n = 155) Pericarditis (n = 49) STE III >II STE III = II STE III < II

Fig. 5). The mean QTc interval for the inferior MI group was 431.05, with an SD of 40.39.

Subtle STEMI cohort

In the cohort of patients who were taken for angiography for any amount of STE and suspicion of AMI, there were 272 inferior wall AMIs. Of these, 54 were subtle (again, defined as having <= 1 mm of ST el- evation) and 218 were obvious, having "marked STE," as defined by at least 1 mm of STE [9]. Unfortunately, only ECGs in the subtle group were available for measurement of lead aVL. Of these 54 subtle ECGs, 40 had obvious ST depression in aVL, 6 had some (though minimal) ST depression in aVL, and 5 had zero ST depression in aVL [9]. As we know that the diagnosis was unambiguous in the obvious cases, we can say that, of 272 inferior AMI, 267 had either an obvious diagnosis or some ST depression in lead aVL, for a sensitivity of 98.8% (95% CI, 97.3%-99.5%) [9].

Pericarditis cohort

A discharge diagnosis of pericarditis was found in 91 patients from our institution between 1996 and 2012. Of these, 42 patients were ex- cluded: 31 due to lack of ST elevation on ECG, 7 due to incomplete med- ical records, 2 due to alternate diagnoses, 1 due to a recent STEMI, and 1 due to a positive stress echocardiogram. This left 49 patients for analy- sis. Myocardial infarction was ruled out in all patients (either by nega- tive troponins or by absence of Clinical concern). Three patients had cardiac catheterization (all revealing no coronary disease), and 41 pa- tients had an echocardiogram with no focal wall motion abnormalities (which by itself rules out the presence of STEMI).

Of the 49 patients included in the study, zero (0%) had any ST-segment depression in lead aVL (CI, 0%-7%), and 7 (14%) of 49 (CI, 7%-27%) had T-wave inversion in aVL. Twenty (41%) of the 49 subjects (CI, 27%-56%) met our defined reperfusion criteria for

Reperfusion Criteria

100%

90%

80%

70%

60%

50%

40%

30%

20%

10%

0%

Inferior STEMI (n = 155) Pericarditis (n = 49) Meets reperfusion criteria Does not meet reperfusion criteria

Fig. 4. Percentage of patients from each cohort meeting our defined reperfusion criteria (N 1-mm ST elevation in N 1 inferior lead).

Fig. 5. Comparison of ST elevation magnitudes in lead III and II in each cohort of inferior STEMI, and pericarditis.

Catheterization laboratory activation (at least 1-mm STE in at least 2 consecutive leads). ST-segment elevation in II was >=STE in lead III in 49 (100%) of 49 patients (CI, 93%-100%; they were equal in 2/49 [4%]; CI, 1%-15%]). The mean QTc interval was 404.76, with an SD of 28.12.

QTc interval comparison

The mean QTc intervals of inferior STEMI group were significantly longer than in the pericarditis group (difference, 26.2 milliseconds, P b

.0001). Using a Bazett-corrected QTc value of greater than 450 millisec- onds provided good specificity but poor sensitivity for differentiating in- ferior STEMI from pericarditis. Forty-three of 154 inferior STEMI patients had QTc values greater than 450 milliseconds (sensitivity, 28%; CI, 21%-36%), whereas only 2 of 49 pericarditis patients had values greater than 450 milliseconds (specificity, 96%; CI, 85%-99%).

Limitations

This study has several important limitations. First, it was a retrospec- tive medical record review and we were limited by data recorded in pa- tient medical records. Our catheterization laboratory search for inferior MI was for inferior “STEMI” and thus may miss some AMI due to electro- cardiographically subtle coronary occlusion which was not diagnosed as STEMI. These patients would have been admitted to the hospital with- out emergent angiography and would have been diagnosed by bio- markers and undergone angiography under urgent, but not emergent, conditions. They would have received a diagnosis of non-STEMI. Thus, the true number of acute inferior MI may be underestimated and this may significantly affect the sensitivity of lead aVL for any inferior MI due to subtle occlusion. However, 21 (13%) of the 156 cases did not meet the STEMI criteria; all of them had some ST depression in lead aVL. The finding of ST depression in aVL in most patients in our subtle STEMI cohort counters this limitation.

In terms of our subtle STEMI cohort, the lack of data regarding ST de- pression in aVL in “obvious” STEMI is a limitation of the study. Despite this, we still felt that it was important to include this cohort as we hy- pothesized ST depression in lead aVL to be highly sensitive and specific for inferior STEMI. We feel that this finding, therefore, will be the most clinically useful in identifying subtle inferior STEMI and felt that it would be prudent to include such a cohort. Considering that our “inferi- or STEMI” group was identified by catheterization laboratory diagnosis of STEMI, we felt that the subtle STEMI data were especially important to ensure validation of our findings in subtle coronary occlusion.

The incidence of confirmed pericarditis at our institution was quite low, with the diagnosis often made without definitive proof. However, pericarditis is always a clinical diagnosis without any absolute reference standard. Patients without a clear clinical diagnosis were excluded, and these exclusions significantly limited the number of subjects included.

In addition, we relied on ICD-9 codes for identification of subjects. A lim- itation of the ICD-9 code is that we may have missed cases of clinical pericarditis not coded as such. Lastly, because those included were not consecutive emergency department patients, we could not calculate the positive and negative predictive values (PPV and NPV).

Discussion

Inferior ST elevation in patients presenting with Ischemic symptoms may or may not be due to STEMI. The differentiation of STEMI from more benign etiologies of STE is important to physicians evaluating for the presence of AMI. In our study, we found that ST depression of at least 0.25 mm in lead aVL is 100% (CI, 98%-100%) sensitive and 100% (CI, 91%-100%) specific for inferior STEMI compared with pericarditis. Our third data set slightly tempers these data: combining both AMI groups, the finding of either obvious ST elevation or some ST depression in aVL had a sensitivity of 97.3%, with a lower limit of CI.

Although lateral STEMI presents with ST elevation in lead aVL, we found that all patients with inferolateral MI (as defined by >= 0.5-mm ST elevation in both of leads V₅ and V₆) still had ST depression in lead aVL despite lateral involvement. This is because leads V₅ and V₆ are sig- nificantly inferior in location to aVL.

T-wave inversion was also 100% sensitive for inferior STEMI and 86% specific. A reperfusion criterion of at least 1 mm in 2 or more consecu- tive leads was less sensitive than any ST depression in aVL, identifying 87% of patients with inferior STEMI. ST-segment elevation in lead III greater than lead II was 88% sensitive and 100% specific for inferior MI when compared with pericarditis. We retrospectively evaluated QTc duration and found that it is indeed significantly different in the 2 pop- ulations, but it is not clinically useful, as a cutoff of 450 milliseconds at which an ECG was more likely to represent AMI rather than pericarditis was only 28% sensitive (and 96% specific) for inferior STEMI.

Methods evaluating ST-segment morphology [2,12] and STE magni-

tude [13] have shown poor accuracy in the selection of patients who will benefit from emergent cardiac catheterization. Birnbaum et al [14], however, found that only 3% of patients with evolving inferior MI did not have any ST depression in aVL; they also found that 8% of patients presenting with inferior STEMI had ST depression in lead aVL as the sole ECG finding of infarction. For these reasons, we studied reciprocal ST depression in aVL as a means to differentiate inferior STEMI from pericarditis as a benign cause of ST elevation.

In our inferior STEMI data set, most patients had RCA occlusion as well as ST elevation greater in lead III than in lead II. Hurst et al [5] de- scribe the STE axis closest to lead III (+120?) in RCA occlusion, which is 150? opposite to aVL (-30?). In left circumflex artery occlusion, how- ever, the axis of ST elevation is closest to aVF and tends to be equal in leads II and III. Thus, this criterion of lead III STE N lead II STE is unlikely to differentiate inferior AMI due to circumflex occlusion from pericardi- tis. However, because the ST-segment vector in both RCA and left cir- cumflex occlusions is between 60? and 120?, there should be some amount of ST depression in aVL in inferior MI due to either of these cul- prit arteries. This is consistent with our findings above.

Our data for pericarditis demonstrated that 96% of ECGs had STE in

lead II greater than lead III and were equal in 4%. This has been sug- gested previously by several authors [1,3,15,16]. Previous literature doc- uments the axis of inferior ST elevation in pericarditis around 45? to 60? (close to lead II), which explains why one would expect to see no recip- rocal ST depression in aVL [1]. In one published abstract, lead II N III did not help to distinguish pericarditis from inferior STEMI; this contradic- tory finding is probably due to diagnostic confusion between pericardi- tis and BER, and also to the complicating factor discussed above that circumflex occlusion may also result in lead II STE N lead III STE [17].

The mechanistic explanation for the direction of the ST vector is as follows: pericarditis is usually diffuse, involving all myocardial walls, with each part of the wall having an endocardial to epicardial ST vector. Because the base of the heart (right-posterior-superior) does not have a

ventricular wall, the sum of all ST vectors must be toward the apex, to- ward leads II and V₅. The exception is regional (localized) pericarditis, in which isolated inferior ST elevation is possible; in this setting, even in the absence of MI, there may be reciprocal ST depression in lead aVL. Re- gional pericarditis is a comparatively Rare condition, however, and we did not have any such patients in our study. In this way, our findings of high sensitivity and specificity of ST depression in aVL are consistent with known mechanisms and prior literature.

In addition to differentiating STEMI from pericarditis, our findings will also be useful for identifying subtle inferior STEMI-in which the STE in the inferior leads is not large enough to meet traditional criteria (>= 1 mm in 2 contiguous leads). Our data demonstrate that any ST de- pression in aVL is highly sensitive and specific for myocardial ischemia and should at least prompt the recording of serial ECGs and perfor- mance of emergent echocardiography, or possibly justify activation of the catheterization laboratory, especially if the ischemic symptoms are refractory to medical anti-ischemic therapy. These data were corrobo- rated by the findings of our second cohort. When all the data are com- bined, ST depression in lead aVL had 98.8% sensitivity (95% CI, 97.3%- 99.5%) and 100% specificity (95% CI, 93%-100%) for differentiating infe- rior STEMI from pericarditis [9].

We recommend scrutiny of lead aVL in patients with suspicion of acute inferior MI. Those with any ST depression in aVL may have subtle coronary occlusion and should be intensively evaluated with serial ECGs, immediate formal echocardiography, or angiography, instead of a more relaxed approach in which MI is only ruled out by biomarkers. If there is absence of reciprocal STD in aVL and resources for interven- tion are limited, then a non-AMI diagnosis might be entertained and a more judicious approach to catheterization laboratory activation may be undertaken, which may also include serial ECGs and echocardiogra- phy. Finally, our data do not allow for calculation of PPV and NPV; be- cause inferior AMI is far more common than pericarditis, it is likely that the high sensitivity of ST depression in lead aVL translates into an even higher PPV, and the high specificity of its absence translates into an NPV that is not as favorable.

Conclusion

In the presence of even minimal inferior STE and even when there is ST elevation in leads V₅ and V₆, the presence of any ST depression in lead aVL is highly sensitive and specific for differentiating inferior myocardi- al MI due to coronary occlusion from pericarditis.

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