Usefulness of Three Posterior Chest Leads for the Detection of Posterior Wall Acute Myocardial Infarction
Article Outline
A significant proportion of patients with myocardial infarction are missed upon initial presentation to the emergency department. The 12-lead electrocardiogram (ECG) has a low sensitivity for the detection of acute myocardial infarction, especially if the culprit lesion is in the left circumflex artery (LCA). This study was designed to evaluate the benefit of adding 3 posterior chest leads on top of the 12-lead ECG to detect ischemia resulting from LC disease, using a model of temporary balloon occlusion to produce ischemia. We studied 53 consecutive patients who underwent clinically indicated coronary interventions. At the time of coronary angiography, the balloon was inflated to produce complete occlusion of the proximal LCA. We recorded and analyzed the changes noted on the 15-lead ECG, which included 3 posterior leads in addition to the standard 12 leads. In response to acute occlusion of the LCA, the posterior chest leads showed more ST elevation than the other leads, and more patients had ST elevation in the posterior leads than in any other lead. The 15-lead ECG was able to detect ≥0.5 mm (74% vs 38%, p <0.0001) and ≥1 mm (62% vs 34%, p <0.0001) ST elevation in any 2 contiguous leads more frequently than the 12-lead ECG. In conclusion, the 15-lead ECG identified more patients with posterior myocardial wall ischemia because of temporary balloon occlusion of the LC than the 12-lead ECG. This information may enhance the detection of posterior MI in the emergency department and potentially facilitate early institution of reperfusion therapy.
The diagnosis of acute myocardial infarction (MI) is missed in a significant proportion of patients presenting with chest pain syndromes to the emergency department (ED).1, 2 The 12-lead electrocardiogram (ECG) is the most valuable initial test for risk stratification and, in patients with chest pain, ideally should be performed and interpreted within 10 minutes of arrival to the ED.3, 4 The latest American College of Cardiology and American Heart Association guidelines indicate that if the initial 12-lead ECG is not diagnostic and high clinical suspicion for acute coronary syndrome exists, serial ECGs should be done and it is reasonable to obtain additional posterior chest leads (V7 to V9) to detect MI resulting from left circumflex coronary artery (LCCA) occlusion.5 In a recent internet-based survey, more than 20% of ED physicians did not request posterior chest leads in patients with isolated posterior MI and the corresponding percentage for posterior plus inferior MI increased to 40%.6 The value of adding the 3 posterior leads to the routine 12-lead ECG is still uncertain. The aim of this study is to examine the benefit of adding 3 posterior chest leads to the standard 12-lead ECG for diagnosing ST-segment elevation MI (STEMI) caused by acute occlusion of the LCCA using a model of temporary balloon occlusion to produce ischemia in the catheterization laboratory.
Methods
This study included 53 consecutive patients who underwent clinically indicated percutaneous coronary interventions of proximal LCCA lesions (ostial or proximal) at a tertiary Veterans Affairs catheterization laboratory. Patients who presented with STEMI, had left bundle branch block or ventricular pacing on their ECGs, or had undergone coronary artery bypass grafting were excluded. Baseline characteristics were recorded. A 15-lead ECG (standard 12 leads plus V7 to V9) was performed on arrival to the catheterization laboratory and before any coronary intervention. Lead V7 was placed at the left posterior axillary line at the 5th interspace, V8 at the left midscapular line at the 5th interspace, and V9 at the left paraspinal border at the 5th interspace.
Left-sided heart catheterization and coronary angiography were performed using standard techniques. A balloon was then inflated in the LCCA at the site of stenosis to fully occlude the artery, and inflation pressure was routinely maintained for 120 seconds. The balloon was deflated earlier if symptoms or severe ECG abnormalities developed (<10% of patients). After balloon inflation, iodinated contrast was injected in the LCCA to confirm complete occlusion, and no flow was seen beyond the balloon in any of the patients. During the procedure, 15-lead ECG was continuously monitored, and an ECG was recorded immediately after balloon inflation and at every 30 seconds thereafter. Additional ECGs were recorded if symptoms were reported or if more severe ECG changes were noted on the continuous monitor. ECGs were recorded using a calibration of 10 mm/mV and a paper speed of 25 mm/second. The ECGs were quantitatively analyzed for ST segment deviation. ST segment deviation was measured at 80 milliseconds after the J point using the TP segment as the isoelectric reference in accordance with accepted guidelines.7 All ECGs were read separately by 2 experienced electrophysiologists and, in cases of disagreement, adjudication was done by a third expert observer (<10% of ECGs). ST-segment deviation was measured at baseline and at peak ST change after balloon inflation. Both the absolute postballoon inflation ST shift and the ST-segment change (ST deviation at peak – ST deviation at baseline) were determined; but because the results were comparable, only ST-segment deviations at peak are reported here to correspond to the ED scenario of a presenting ECG with STEMI in which a baseline ECG is frequently not available. Previous work by Wung et al8 suggested that a new criterion of 0.5 mm rather than the standard 1.0 mm ST-segment elevation should be used in the posterior leads. In this study, we report the frequency of both the 0.5 mm and the 1.0 mm ST-segment elevations but use the same cut-offs for all 15 leads to avoid bias favoring the posterior leads.
All statistical analyses were performed using the SPSS version 11.5 for Windows (SPSS Inc., Chicago, Ilinois). Categorical data were presented as frequencies, and continuous variables were presented as means ± SD. Categorical variables were compared using the chi-square test. Continuous variables were compared using t test or 1-way ANOVA as appropriate. When odds ratios are reported, these are followed by the 95% confidence intervals in brackets. Factors associated with ST elevations on the ECG were determined using univariate and multivariate logistic regression analysis. All p values reported were 2 sided. Statistical significance was defined as a p value <0.05. The Institutional Review Board for Human Research at the Birmingham Veterans Affairs Hospital approved the study. There were no complications from this study.
Results
The mean age of the patients was 63 ± 9 years. All 53 patients were men. Most of the patients carried a diagnosis of coronary artery disease (81%) or had multiple coronary risk factors. The baseline characteristics are listed in Table 1. No collaterals to the LCCA were evident on angiography. There were no significant flow-limiting stenoses (diameter narrowing >75%) of the left anterior descending or the right coronary arteries. Left ventricular function was normal in 43 patients (81%), and the remaining patients had a left ventricular ejection fraction of 43 ± 7%. Balloons with diameters larger than 3.0 mm were used in 62% of the patients. Two-thirds of the patients reported having symptoms during balloon inflation. The characteristics of the intervention are listed in Table 2.
Table 1. Baseline characteristics
| Variable | Number (%) (n = 53) |
|---|---|
| Male | 53 (100%) |
| Caucasian | 47(89%) |
| Hypertension | 45(85%) |
| Diabetes mellitus | 25(47%) |
| Hyperlipidemia⁎ | 41(77%) |
| Peripheral vascular disease | 8(15%) |
| Chronic kidney disease | 5(9%) |
| Previous myocardial infarction | 18(34%) |
| Anterior | 4(22%) |
| Inferior | 7(39%) |
| Lateral | 2(11%) |
| Unknown | 5(28%) |
| Previous percutaneous coronary intervention | 25(47%) |
| Left main | 0(0%) |
| Left anterior descending | 10(19%) |
| Left circumflex | 8(15%) |
| Right | 7(13%) |
| Heart failure | 9(17%) |
| Depressed left ventricular function | 10(19%) |
| Tobacco use | |
| Active | 12(23%) |
| Past use | 34(64%) |
| Smokeless tobacco | 1(2%) |
| Never | 6(11%) |
| Reason for percutaneous coronary intervention | |
| Stable angina | 23(43%) |
| Unstable angina | 23(43%) |
| Non-ST segment elevation myocardial infarction | 7(13%) |
| Medications | |
| Aspirin† | 35(66%) |
| Clopidogrel | 20(38%) |
| β blockers | 36(68%) |
| Nitrates | 31(59%) |
⁎Patient is considered to have hyperlipidemia if prescribed medications to control cholesterol or triglyceride levels. |
†These data are for prescription aspirin and do not account for over-the-counter use. |
Table 2. Left circumflex artery balloon inflation
| Variable | Number (%) (n = 53) |
|---|---|
| Site of balloon inflation | |
| Ostial | 9(17%) |
| Proximal | 45(85%) |
| Left dominant circulation⁎ | 7(13%) |
| Collaterals to the LCA | 0(0%) |
| Symptoms during balloon inflation | 35(66%) |
| Duration of balloon inflation(seconds)† | 120 |
| Balloon diameter(mm) | |
| 2.0 | 2(4%) |
| 2.5 | 16(30%) |
| 2.8 | 2(4%) |
| 3.0 | 15(28%) |
| 3.5 | 16(30%) |
| 4.0 | 2(4%) |
| Heart rate before inflation (beats/min) | 63 ± 31 |
| Heart rate after inflation (beats/min) | 62 ± 29 |
| Blood pressure before inflation (mm Hg) | 114 ± 59/78 ± 40 |
| Blood pressure after inflation (mm Hg) | 112 ± 59/70 ± 34 |
⁎Left dominant circulation is defined by the origin of the posterior descending artery from the LCA. |
†Balloon was deflated earlier in case of symptom development. |
During and after balloon inflation, ST elevation was present in the inferior (I, III, aVF) and posterior (V7 to V9) leads and ST depression in the lateral leads (I, aVL) and V2 to V5. No ST deviation was seen in aVR and V1. A representative ECG tracing is shown in Figure 1. The posterior leads showed more ST elevation than the other leads (Figure 2; p <0.005). In addition, more patients had ST elevation in the posterior leads than in any other lead (Figure 3; p <0.0001). A 15-lead ECG was able to detect the presence of ST elevation (≥0.5 mm) more often than a 12-lead ECG (odds ratio 2.6 [1.8 to 3.8]). It was also able to detect ≥0.5 mm (odds ratio 2.2 [1.5 to 3.0]) and ≥1 mm (odds ratio 2.2 [1.5 to 3.2]) ST elevation in any 2 contiguous leads more effectively than the 12-lead ECG (Table 3, Table 4).
Figure 1.
A 15-lead electrocardiogram in response to LC occlusion. A representative electrocardiographic tracing from a patient at baseline (A) and during fully occlusive balloon inflation in the proximal LC artery (B). ST-segment elevation is evident in the posterior leads (V7 to V9) despite no significant ST elevation in the standard 12 leads.
Figure 2.
ST deviation. Maximum ST deviation for all 15 leads during and after balloon inflation in the left circumflex artery. Error bars = the SD around the mean.
Figure 3.
ST elevation. Percentage of patients showing ST elevation in each of the 15 leads after balloon inflation in the LC artery.
Table 3. Electrocardiographic changes in response to left circumflex artery occlusion
| Variable⁎ | Number (%) n = 53 |
|---|---|
| ≥0.5 mm ST elevation in a posterior lead | 33(62%) |
| ≥1 mm ST elevation in a posterior lead | 28(53%) |
| ≥1 mm ST depression in an anterior lead | 17(32%) |
| ≥1 mm ST elevation in a posterior lead with no ST elevation ≥1 mm in any other lead | 14(26%) |
| ≥1 mm ST elevation in a posterior lead with no ST depression ≥1 mm in an anterior lead | 16(30%) |
| ≥1 mm ST elevation in a posterior lead with no ST elevation or depression in any other lead | 6(11%) |
| ≥1 mm ST elevation in 2 contiguous leads on the 12-lead ECG | 18(34%) |
| ≥1 mm ST elevation in 2 contiguous leads on the 15-lead ECG | 33(62%) |
| ≥1 mm ST elevation in 2 contiguous posterior leads with no ST elevation ≥1 mm in any other 2 contiguous leads | 15(28%) |
| ≥0.5 mm ST elevation in 2 contiguous leads on the 12-lead ECG | 21(40%) |
| ≥0.5 mm ST elevation in 2 contiguous leads on the 15-lead ECG | 39(74%) |
⁎Posterior leads = V7, V8, and V9. Anterior leads = V1, V2, and V3. |
Table 4. ST elevation after balloon occlusion of the left circumflex artery
| Variable | 12-Lead ECG (n = 58) | 15-Lead ECG (n = 58) | Odds Ratio | 95% Confidence Interval |
|---|---|---|---|---|
| ≥1 mm ST elevation in 2 contiguous leads⁎ | 18(34%) | 33(62%) | 2.2 | 1.5to3.2 |
| ≥0.5 mm ST elevation in 2 contiguous leads | 21(38%) | 39(74%) | 2.2 | 1.5to3.0 |
| ≥0.5 mm ST elevation in any lead | 25(47%) | 44(77%) | 2.6 | 1.8to3.8 |
⁎Accepted criteria for administering fibrinolytics in ST-elevation myocardial infarction. |
Of the patients with ST elevation (≥0.5 mm) in any 2 contiguous leads on their 15-lead ECG, 24 (62%) had symptoms during balloon occlusion compared with 11 (79%) of those without ST changes (p = 0.2). Using univariate and multivariate analysis, only vessel diameter was associated with ≥1 mm ST elevation in 2 contiguous leads on the 15-lead ECG (Table 5).
Table 5. Multivariate analysis for factors associated with 1 mm ST elevation in 2 contiguous leads on the 15-lead ECG
| Variable | Univariate Odds Ratio | Multivariate Odds Ratio |
|---|---|---|
| Large vessel† | 4.69[1.42to15.53]⁎ | 5.95[1.53to23.20]⁎ |
| Left dominant circulation‡ | 1.61[0.28to9.19] | 1.84[0.27to12.39] |
| Symptoms§ | 0.51[0.15to1.75] | 0.46[0.12to1.77] |
| Acute coronary syndrome∥ | 1.11[0.36to3.40] | 1.75[0.48to6.35] |
| Diabetes mellitus | 1.15[0.38to3.51] | 0.65[0.18to2.42] |
⁎p <0.05, confidence intervals listed between brackets. |
†Large vessel is defined by balloon inflation with a diameter ≥3.0 mm. |
‡Left dominant circulation is defined by the origin of the posterior descending artery from the left circumflex artery. |
§Development of symptoms during balloon inflation. |
∥Acute coronary syndrome on presentation (unstable angina or myocardial infarction versus stable angina). |
Discussion
The major finding of this study is that during acute occlusion of the LCCA, the addition of 3 posterior leads (V7 to V9) to the 12-lead ECG allows for the detection of ST elevation in more patients than the standard 12-lead ECG. Because the cornerstone of management of STEMI is early coronary reperfusion, these findings may enhance the detection of posterior MI in the ED and potentially facilitate early institution of reperfusion therapy, thus shortening door-to-reperfusion time—a measure that has been correlated with mortality and infarct size after STEMI and is used to gauge quality of care delivered in hospitals.9, 10, 11 The current preferred strategy for reperfusion during STEMI is primary percutaneous coronary intervention if available in a timely fashion.12 If this strategy is utilized as an initial approach for managing STEMI patients, it will be indicated in patients suspected of having a true posterior MI.3 However, because 60% to70% of patients present initially to hospitals without capability to perform primary percutaneous coronary interventions, they would not receive timely reperfusion.13 Current guidelines reserve fibrinolytic therapy to patients with ≥1.0 mm ST elevation in at least 2 contiguous precordial leads or 2 adjacent limb leads.3 In our balloon occlusion model, only 34% of patients met these criteria. An additional 28% were identified when the 3 posterior chest leads were included, thus raising the percentage of theoretically eligible patients for fibrinolytic therapy to 62%. Posterior myocardial wall infarctions constitute around 15% to 20% of all MIs. Although traditionally these infarcts were thought to occur mostly in the setting of inferior or lateral MIs, isolated posterior MIs are currently thought to account for as much as 11% of all MIs.14
It has long been demonstrated that the 12-lead ECG has a very low sensitivity for the detection of acute MI, especially if the culprit lesion is in the LCCA.15, 16 Because there are no leads corresponding to the posterior portion (inferobasal, according to the new nomenclature) of the left ventricle, precordial ST-segment depression on the 12-lead ECG has been used as a surrogate for the identification of patients with acute posterior MI.17, 18 These changes, however, could also indicate anterior wall ischemia and thus are nondiagnostic. Several groups have demonstrated that the addition of posterior leads was helpful in identifying patients with posterior wall infarction and suggested that they may benefit from fibrinolytic therapy.19, 20, 21, 22 In this study, the posterior leads showed the greatest absolute ST-segment deviation after LCCA occlusion, with a mean of 0.736 mm for lead V8. Furthermore, 62% of patients demonstrated ST-segment elevation in either V7 or V8, more than in any other lead. Consistent with previous studies,14, 20 ST depression in the anterior leads was absent in a significant number of patients who had ST elevation in the posterior leads and in the majority of patients who had LCCA occlusion. Some patients with ST elevation in the posterior leads had no ST deviation (ST elevation or depression) in any other lead on the 12-lead ECG (Table 3).
In an earlier balloon occlusion study, Kulkarni et al23 showed that none of the patients with right coronary artery occlusions developed isolated ST elevations in the posterior leads although all patients with LCCA occlusion and ST elevations had ST elevations in those leads. Analogous to our findings, 68% of LCCA occlusions were accompanied by ST elevations in the posterior leads, with 7% having isolated changes in these leads. Wung et al8 reported that the addition of the 3 posterior leads improved the sensitivity of identifying LCCA occlusion—from 49% to 58%—when a criterion of ≥1 mm ST-segment elevation from baseline in the posterior lead was used on top of the 12-lead ECG, but their results did not reach statistical significance until they lowered the threshold for the posterior leads to ≥0.5 mm.8 The discrepancy in results could be the result of the low number of patients in their study with ST elevation in a posterior lead with no ST elevation in any other lead on the 12-lead ECG (5% compared with 26% in the present study). Schmitt et al.24 studied 36 patients who had an MI involving an occlusion of the LCCA diagnosed by coronary angiography and showed that the addition of posterior leads to the 12-lead ECG in the ED improved the detection rate of ST elevations from 50% to 61%. It is important to note that the findings from all these studies point toward the low sensitivity of the standard 12-lead ECG for the detection of LCCA occlusion and suggest an improvement with the addition of the posterior leads. Whereas these findings are consistent with our own, the present study further showed that the sensitivity of the 12-lead ECG for the detection of LCCA occlusion using criteria for fibrinolytic therapy was low and that the addition of the posterior leads improved it by 2-fold (Table 4). Furthermore, 11% of the patients with LCCA occlusion had ST elevation in a posterior lead with no ST deviations ≥1 mm (elevation or depression) in any other leads. Although the occurrence of ST deviations in other leads might alert the physician and lead to the performance of a 15-lead ECG, this approach might delay the diagnosis and, in the setting of an STEMI, prolong the door-to-reperfusion time.
Interestingly, the diameter of the LCCA, as assessed by the size of the balloon inflated in the vessel, was associated with the presence of 1-mm ST-segment elevation in 2 contiguous leads on the 15-lead ECG but the presence of symptoms was not. Patients with vessel diameter larger than 3.0 mm had a five- to sixfold higher chance of having significant ST elevation with total occlusion of their LCCA than patients with smaller vessels. The extent of ST-segment elevation has been correlated with infarct size on perfusion imaging as well as with the proximity of the lesion in the coronary artery.25, 26 Furthermore, in the study by Schmitt et al.24 discussed above, there was a trend toward an increase in the infarct size (as assessed by creatine kinase levels) in patients with ST elevation in a posterior lead on top of the 12-lead ECG. It is reassuring that the absence of significant ST-segment elevation to satisfy fibrinolysis criteria in the setting of LCCA occlusion was correlated with small coronary vessel diameter, suggesting a small area of myocardium at risk.
This study suffers from several limitations. The balloon occlusion model may differ from acute MI but, in previous studies, has provided a wealth of information on coronary physiology, collateral flow, and ischemic burden. We do not have data on the right and left anterior descending coronary arteries balloon occlusions to determine the specificity of ST elevation in these leads but based on available literature, isolated ST elevations in the posterior leads seem to be specific for posterior MI and, in particular, LCCA occlusion.20 Our population consisted of veterans, all men and most Caucasian, which might limit the generalization of the findings to other populations.
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PII: S0002-9149(08)01513-0
doi:10.1016/j.amjcard.2008.09.008
© 2009 Elsevier Inc. All rights reserved.
