The standard 12-lead ECG is our essential diagnostic tool in the evaluation of patients with suspected cardiac pathology, including myocardial infarction and dysrhythmias. Myocardial infarction due to acute coronary occlusion, however, may occur without ST-segment elevation on 12-lead ECG . 20 - 27% of patients diagnosed with NSTEMI who subsequently undergo angiography are found to have a completely occluded culprit vessel [2-4]. In some situations, alternate acquisition strategies, such as modified lead placement or recording speed, can increase its diagnostic yield, a few of which we will discuss through this post.
Posterior Leads (V7 – V9)
ST-segment elevation is particularly insensitive as a marker for occlusion of the posterior coronary circulation, and specifically the left circumflex artery [5,6]. The standard 12-lead ECG does not directly assess the posterior wall of the left ventricle, and while posterior MI most commonly occurs with concomitant inferior or lateral infarct, isolated posterior MI may occur in up to 8% of acute circumflex occlusions . The predominant 12-lead finding in isolated posterior MI is ST-segment depression ≥0.5 mm in leads V1-V3 . The addition of posterior leads V7-V9 (Figure 1) increases ECG sensitivity for posterior MI [1,8], and current guidelines consider ST-segment elevation ≥0.5 mm in V7-V9 (≥1 mm for men under age 40) to be diagnostic (Table 1) [9,10]. Per both the AHA/ACC and ESC Guidelines, however, isolated anterior ST-segment depression alone is an indication for emergent cardiac catheterization [10,11]. Leads V7-V9 may therefore have the greatest utility in patients with clinically-suspected MI but non-diagnostic 12-lead ECGs by providing an objective finding to expedite emergent intervention. Notably, concern for ongoing ischemia – as in a patient with refractory angina despite maximal medical therapy – should also prompt immediate catheterization, even with a normal ECG [10,11]. Thus, while the presence of ST-segment elevation in V7-V9 warrants emergent intervention, its absence should not necessarily preclude it.
Right-Sided Leads (V1R – V6R)
Right ventricular infarction (RVI) typically occurs with concomitant inferior wall MI, most often due to occlusion of the right coronary artery proximal to the acute marginal branch . Autopsy data suggests isolated RVI is both rare and non-fatal . On a standard 12-lead ECG, RVI may present with ST-segment elevation in the right precordial leads, most prominent in V1, typically with concurrent inferior ST-segment elevation; in the setting of associated posterior MI, however, elevation in V1 may be attenuated or absent due to superimposed ST-segment depression . Right-sided chest leads V1R-V6R (Figure 2) can be used to improve diagnostic accuracy for RVI, and ST-segment elevation in V4R ≥0.5 mm is roughly 80% sensitive and specific . Current ESC/ACC/AHA/WHF guidelines define this as the appropriate diagnostic cutoff, except in men under age 30, for whom 1 mm should be used (Table 2) . RVI may result in right ventricular dysfunction, compromising left ventricular filling and cardiac output. Adequate right ventricular preload is essential to maintaining LV function and systemic perfusion, and medications that decrease venous return and RV filling, such as nitrates, should be avoided in RVI [10,16]. That said, there is no long-term mortality benefit to nitrate administration in STEMI , and current ESC guidelines recommend against the routine use of nitrates, even without RV involvement, except in the setting of hypertension or heart failure .
15-lead ECG (V4R, V8, V9)
So why aren’t these leads in our default ECG acquisition? The overwhelming majority of studies regarding both the diagnostic and prognostic utility of adding posterior and right-sided leads date from the late 1970s to early 2000s; that is, a time when thrombolysis was the mainstay of reperfusion therapy, with diagnostic ST-elevation as a nearly-universal prerequisite for intervention. In the context of current interventional guidelines, however, the additive benefit of extended-lead ECG is unlikely to affect recommended patient management in the majority of cases. Extended leads are easy to obtain and may provide additional evidence to justify emergent catheterization, however their acquisition should not delay or deter intervention that is otherwise indicated. Current ESC guidelines state right-sided and posterior leads “should be considered” in cases of inferior and suspected posterior MI, respectively (Class IIa recommendation, level of evidence B) . AHA/ACC guidelines consider it “reasonable” to obtain leads V7-V9 in patients with a non-diagnostic ECG and high risk of ACS (Class IIa recommendation, level of evidence B) .
Lewis Lead (S5)
Evidence of atrioventricular dissociation on ECG in the setting of a wide-complex tachycardia is extremely specific for a ventricular origin, but is relatively insensitive . The Lewis lead (Figure 3) is a modified limb lead configuration that accentuates atrial activity, originally developed to assess atrial fibrillation . In the context of an undifferentiated wide-complex tachycardia, the Lewis lead can aid in recognition of AV dissociation that is not apparent on a standard 12-lead ECG, confirming a diagnosis of ventricular tachycardia [20-25]. Though not well-described in the literature, the Lewis lead has anecdotal utility in other situations where the identification of atrial activity has diagnostic and therapeutic implications (e.g. differentiating complete heart block from junctional bradycardia, atrial fibrillation from atrial flutter from multifocal atrial tachycardia, or SVT from sinus tachycardia).
In tachycardic patients, particularly those with very high heart rates, narrow intervals on the ECG tracing may make subtle findings difficult to appreciate. Increasing the paper speed from the standard 25 mm/s – where 1 small box is 0.04 s and 1 large box is 0.2 s – to 50 mm/s artificially elongates the intervals, making findings such as flutter waves or slight irregularity easier to recognize .
The value of alternate ECGs ultimately depends on the extent to which they influence patient management. Posterior and right ventricular leads may improve the characterization of infarct territories, but likely have minimal impact on clinical decision-making outside select cases (e.g. a patient with isolated posterior MI and no ischemic changes on 12-lead), and intervention that is otherwise indicated should not be delayed to facilitate their acquisition. The Lewis lead and double-speed ECG have the potential to alter management decisions, again in select cases by aiding in the diagnosis of arrhythmias.
Abbreviations: AHA – American Heart Association, ACC – American College of Cardiology, ESC – European Society of Cardiology, WHF – World Heart Federation
Post by Kate Connelly, MD
Dr. Connelly @kmconnel78 is a PGY-1 Emergency Medicine Resident at the University of Cincinnati
Peer Review by Robert whitford, MD and Ryan LaFollette, MD
Schmitt C, Lehman G, Schmeider S, et al. Diagnosis of acute myocardial infarction in angiographically documented occluded infarct vessel: limitations of ST-segment elevation in standard and extended ECG leads. Chest. 2001;120(5):1540-1546.
Wang TY, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. 2009;157(4):716-723.
Warren J, Mehran R, Yu J, et al. Incidence and impact of totally occluded culprit coronary arteries in patients presenting with non-ST-segment elevation myocardial infarction. Am J Cardiol. 2015;115:238-433.
Khan AR, Golwala H, Tripatha A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38:3082-3089.
Krishnaswamy A, Lincoff AM, and Menon V. Magnitude and consequences of missing the acute infarct-related circumflex artery. Am Heart J. 2009;158(5):706-712.
From AM, Best PJM, Lennon RJ, et al. Acute myocardial infarction due to left circumflex artery occlusion and significance of ST-segment elevation. Am J Cardiol. 2010;106:1081-1085.
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J. 2010;160:995-1003.
Agarwal JB, Khaw K, Aurignac F, et al. Importance of posterior chest leads in patients with suspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram. Am J Cardiol. 1999;83:323-326.
Thygesen K, Alport J, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Circulation. 2018;138:e618-e651.
Ibanez B, James S, Agewall S, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39:119-177.
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64:e139-e228.
Ondrus T, Kanovsky J, Novotny T, et al. Right ventricular myocardial infarction: from pathophysiology to prognosis. Exp Clin Cardiol. 2013;18(1):27-30.
Andersen HR, Falk E, and Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol. 1987;10(6):1223-1232.
Moye S, Carney MF, Holstege C, et al. The electrocardiogram in right ventricular myocardial infarction. Am J Emerg Med. 2005;23:793-799.
Haji SA and Movahed A. Right ventricular infarction – diagnosis and treatment. Clin Cardiol. 2000;23:473-482.
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol. 2013;61(4):e78-e140.
ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet. 1995;345(8951):669-685.
Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1981;83(5):1649-1659.
Lewis T. Auricular fibrillation. In: Clinical Electrocardiography. 5th ed. London, UK: Shaw and Sons; 1931.
Bakker ALM, Nijkerk G, Groenenmeijer BE, et al. The Lewis lead: making recognition of P-waves easy during wide complex QRS tachycardia. Circulation. 2009;119:e592-e593.
Holanda-Miranda WR, Furtado FM, Luciano PM, et al. Lewis lead enhances atrial activity detection in wide QRS tachycardia. J Emerg Med. 2012;43(2):e97-99.
Mizuno A, Masuda K, and Niwa K. Usefulness of Lewis lead for visualizing P-wave. Circ J. 2014;78:2774-2775.
Aksu U, Kalkan K, Gulgu O, et al. Comparison of standard and Lewis ECG in detection of atrioventricular dissociation in patients with wide QRS tachycardia. Int J Cardiol. 2016;225:4-8.
Huemer M, Meloh H, Attanasio P, et al. The Lewis lead for detection of ventriculoatrial conduction type. Clin Cardiol. 2016;39(2):126-131.
Ali H, Epicoco G, Ambroggi G, et al. A narrow QRS tachycardia and Cannon A waves: what is the mechanism? Ann Noninvasive Electrocardiol. 2017;22:e12423.
Accardi A, Miller R, and Holmes J. Enhanced diagnosis of narrow complex tachycardias with increased electrocardiograph speed. J Emerg Med. 2002;22(2):123-126.