Posterior ECG Leads Improve the Detection of Left Circumflex Coronary Artery Occlusion

Abstract & commentary

By Andrew J. Boyle, MBBS, PhD

Source: Aqel RA, et al. Usefulness of three posterior chest leads for the detection of posterior wall acute myocardial infarction. Am J Cardiol. 2009;103:159-164.

Optimal management of transmural myocardial infarction (MI) depends on rapid reperfusion of the occluded infarct artery. Therefore, accurate early diagnosis is the cornerstone of initial patient assessment in the emergency department. It is recommended that a standard 12-lead electrocardiogram (ECG) be performed within 10 minutes of presentation to diagnose ST-elevation MI, but diagnosis of infarction in the left circumflex coronary artery (LCCA) territory remains difficult. In a significant number of patients with LCCA occlusion, the standard 12-lead ECG may show no ST-elevation at all, and these patients may, therefore, not be referred for urgent reperfusion.

Accordingly, Aqel et al performed a study to determine the utility of using three posterior chest leads to detect ischemia in the LCCA territory. They studied 53 consecutive patients undergoing clinically indicated percutaneous coronary intervention (PCI) of the LCCA. Standard 12-lead ECGs were performed, and they also recorded tracings from three posterior leads, V7, V8 and V9, in the left posterior axillary line at the 5th interspace, at the left midscapular line at the 5th interspace, and at the left paraspinal border at the 5th interspace, respectively. They excluded patients with ST-elevation MI, previous coronary artery bypass surgery, and uninterpretable baseline ECGs. After the baseline 15-lead ECG was recorded, the angioplasty balloon was inflated in the LCCA for 120 seconds. The 15-lead ECG was performed after balloon inflation and then every 30 seconds. ECGs were analyzed by two cardiologists. Because there is controversy regarding the cut-off for ST-elevation in the posterior leads, with some advocating 1 mm and others suggesting 0.5 mm; Aqel et al analyzed their data using both cutoffs.

Their patients were recruited at a Veterans Affairs Medical Center, were all male, 63 ± 9 years of age, 47% were diabetic, 34% had prior MI, and 47% had prior PCI. The procedural indication was stable angina in 43%, unstable angina in 43%, and non-ST-elevation MI in 13%. Importantly, there were no collaterals to the distal LCCA territory observed in any patient. The site of balloon occlusion was ostial or proximal in all patients. The posterior leads showed more ST elevation than any of the standard 12 leads (p < 0.0001). Using a cutoff of 1 mm S elevation in two contiguous leads, the use of posterior leads increased the detection of LCCA occlusion from 34% to 62%. Using a cutoff of 0.5 mm ST elevation in two contiguous leads, the use of posterior leads increased the detection of LCCA occlusion from 38% to 74%. If 0.5 mm is detected in any lead, the rate of detection of LCCA occlusion is increased from 47% to 77%. Aqel et al conclude that the 15-lead ECG identified more patients with posterior myocardial wall ischemia because of temporary balloon occlusion of the LCCA 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.


This study is consistent with previous studies that have shown very poor sensitivity of standard 12-lead ECGs in detecting posterior MI due to LCCA occlusion. The data suggest that addition of the posterior leads to the standard 12 leads results in an approximate doubling of the diagnosis of LCCA occlusion. This is a rapid and inexpensive test that can be easily performed in the emergency room, and may enhance diagnosis of posterior ischemia in patients with an otherwise normal ECG. This may, in turn, facilitate earlier reperfusion in this patient cohort. Thus, the presence of a normal 12-lead ECG in patients whose symptoms are very suggestive of MI should prompt further investigation with extra ECG leads, or even an echocardiogram.

Several limitations of this study should be noted. First, the patients were all male, VA patients, and were predominantly Caucasian. Therefore, the results may not be applicable to all patient subgroups. Second, the balloon inflations were all ostial or proximal and, therefore, the sensitivity for ischemia caused by more distal LCCA occlusion may be lower than seen in this study. Third, the duration of ischemia was short, only two minutes. Although ECG changes usually occur early within this time frame, differences from clinical thrombotic occlusion of the LCCA with thrombus propagation over time may not be appreciated in this type of study. Despite these limitations, this study serves as a reminder that the standard 12-lead ECG has poor sensitivity for detecting LCCA occlusion, and that posterior leads may approximately double this sensitivity.