The Lonely Lead

Author: Philippe Ayres, MD

Editor: Esteban Davila, MD

Case:

A 65-year-old male with a past medical history of hypertension, insulin-dependent diabetes, hyperlipidemia, and coronary artery disease was brought to the ED by EMS as a “STEMI notification”. He reported 5 days of malaise, myalgias, fevers, chills and two days of epigastric and midline pressure-like chest pain and full body pain. The patient’s vital signs were temperature 102.2 F, pulse 125/min, systolic blood pressure 160 mm Hg, respiratory rate 24/min, and pulse oximetry 93% on room air. He received supplemental oxygen, aspirin 324 mg, and nitroglycerin 0.4 mg SL x 2 from EMS. Physical exam was significant for epigastric and suprapubic tenderness. 

The initial ECG had ST-elevation in aVR with diffuse ST-depressions:

Given the history and exam, the ED team canceled the catheterization lab activation and managed the patient as a sepsis case. Initial lab results were significant for troponin 0.29 mmol/L, lactate 2.2 mmol/L, beta-hydroxybutyrate 1.99 mmol/L, anion gap 16, pH 7.4, bicarbonate 18 mmol/L, CO2 29 mm Hg, blood glucose 416 mg/dL and ketonuria. Bedside ultrasonography identified diffuse B-lines over the left lower lung. The patient was treated for sepsis secondary to pneumonia with azithromycin, ceftriaxone, acetaminophen, normal saline 2L bolus, ketorolac, and insulin. There was persistent tachycardia of 111/min. The patient was admitted to medicine for further sepsis management.

Eight hours after being admitted, the patient complained of pleuritic chest pain. A repeat ECG at this time was unchanged, and a repeat troponin had increased to 12 mmol/L. The medicine team initiated management for “NSTEMI” with ticagrelor 180 mg and heparin drip. Cardiology was consulted stat!

Questions to Consider:

Did the EM team miss a diagnosis of occlusion myocardial infarction (OMI)? What is the differential diagnosis for an ECG with ST-segment elevation in aVR with diffuse ST-depressions?

Introduction:

Lead aVR is one of three augmented leads created by Goldberger who used Einthoven’s triangle as the basis for calculating aVR, aVL, and aVF. The purpose of lead aVR was to obtain specific information from the right upper side of the heart such as the right ventricular outflow tract and basal part of the septum.[1] This area of the heart is supplied either by the large first septal branch (S1) of the left anterior descending artery alone or the large conus branch of the right coronary artery, and transmural ischemia of these regions results in ST-elevation in aVR.[2][3]

Figure 1: Anatomical correlation of each lead. Note that although V1 is the most rightward precordial lead, it is commonly interpreted as a septal lead, leaving only aVR as the sole lead representing the right upper heart.[4][5]

Table 1: The sensitivity and specificity of lead aVR for LMCA occlusion. ST-elevation > 0.05 mV in aVR has an overall sensitivity of 68% to 91% and specificity of 73% to 80% in predicting LMCA occlusion.[7[8]

Table 2: ST-elevation in lead aVR predicts clinical outcome. ST-elevation in lead aVR has increased mortality versus no ST-elevation in lead aVR.[9][10]

Not Just Occlusion Myocardial Infarction:

With all the attention placed on STEMI and STEMI equivalents, ST-elevation in aVR has unintentionally shifted the focus away from the diffuse ST-depressions seen in the other leads. This pattern is not unique to OMI. Among 133 ECGs showing ST-elevation in aVR with diffuse ST-depression in > 7 leads (excluding left bundle branch block, QRS > 130 msec, ventricular rhythm, or ventricular paced rhythm), 47 (35%) patients were diagnosed with tachydysrhythmias, 49 (37%) patients were diagnosed with non-cardiac shock states (such as septic shock, hemorrhagic shock, dissection, and pulmonary embolism), and 37 (28%) patients were diagnosed with acute coronary syndrome (ACS).[13] The study concluded that the AHA/ACCF/HRS classification of ST-elevation in aVR with diffuse ST-depressions as STEMI equivalent is not supported, and “circumferential subendocardial ischemia” is a more accurate reflection of the underlying pathophysiology.[13] What is circumferential subendocardial ischemia, you ask? In general, it is recognized that transmural infarcts extend into the outer half of the myocardium while subendocardial infarcts involve only the inner half of the myocardium. If the subendocardial ischemia is circumferential, it occurs in the distribution of all three major coronary arteries and thus is a result of global ischemia.

Another study showed that even baseline LV enlargement, repolarization abnormalities (LBBB), metabolic/toxic etiologies (hypokalemia or digoxin toxicity), demand ischemia secondary to supraventricular tachycardia or other causes, and aortic stenosis can also all lead to > 1 mm ST-elevation in aVR.[14] 

You may be asking yourself, “Okay, maybe not every ST-elevation in aVR with diffuse ST-depressions is OMI, but shouldn’t we just be on the safe side and activate the cath lab and let cardiology decide?” To this, I urge you to remember that coronary angiography is not a benign procedure. Also, remember that heparinizing a patient in hemorrhagic shock/dissection or even a subacute bleed could be devastating.

Table 3: Post-coronary angiography complications. [15]

Figure 2: This patient presented with chest pain and shortness of breath. There are diffuse ST-depressions and T wave inversions with ST-elevation in aVR. The patient was taken for emergent cardiac catheterization which did not reveal an occlusion. This pattern was secondary to hypertrophic cardiomyopathy.[16]

Figure 3: This patient presented with weakness and vomiting. Again we see diffuse ST-depression with ST-elevation in aVR, and there are U waves seen most notably in the inferior leads. Appropriately, the ED physicians did not activate the cath lab and lab tests revealed hypokalemia.[16]

Figure 4: This patient presented with fever, hypotension, and tachycardia. There are diffuse ST-depressions and reciprocal ST-elevation in aVR along with lateral T wave inversions. The patient was treated for sepsis with crystalloid, vasopressors, and antibiotics. Repeat ECGs showed resolution of the ST/T wave changes.[16]

What to Make of aVR:

As with all things in medicine, nothing lives within a vacuum. The ECG is an invaluable tool, but we cannot rely solely on a single ECG to decide upon cath lab activation. We should always consider symptom patterns consistent with myocardial ischemia such as active retrosternal chest discomfort, diaphoresis, emesis, and pain radiation along with dynamic ECG changes and bedside echocardiography (http://blog.clinicalmonster.com/2021/09/16/regional-wall-motion-abnormalities/). 

Yes, ST-elevation in aVR with diffuse ST-depressions can be due to OMI, but it is also caused by a myriad of other pathologies as we have discussed. If you do see ST-elevation in aVR, know that there may be underlying non-cardiac pathology that requires more investigation and therapy. Don’t stop at ACS – consider PE, acute/subacute hemorrhage, sepsis, myopericarditis, and electrolyte abnormalities. 

TLDR:

1) ST-elevation in aVR with diffuse ST-depressions is more appropriately classified as circumferential subendocardial ischemia instead of “STEMI equivalent”

2) The differential for ST-elevation in aVR with diffuse ST-depression includes tachydysrhythmias and non-cardiac shock states such as shock, subacute hemorrhage, aortic dissection, and pulmonary embolism; also hypokalemia or digoxin toxicity and repolarization abnormality secondary to LV enlargement or LBBB

3) An ischemic symptom pattern is required for OMI diagnosis and should be idenitified prior to activating the catheterization lab

4) Obtaining serial ECG may be helpful as treatment of the underlying pathology will eventually show resolution of the ST-elevation in aVR with diffuse ST-depressions

5) Coronary angiography is not without risk of complication 

References:

1) Gorgels A, Engelen D, Wellens H, et al. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography*. J Am Coll Cardiol. 2001 Nov, 38 (5) 1355–1356.

2) K. Williamson, A. Mattu, C.U. Plautz, A. Binder, W.J. Brady Electrocardiographic applications of lead aVRAm J Emerg Med, 24 (2006), pp. 864-874

3) J. Eichhöfer, N. Curzen, Unexpected profound transient anterior ST elevation after occlusion of the conal branch of the right coronary artery during angioplasty Circulation, 111 (2005), p. 113

4) Randazzo, Andrew. “Guide to 12-Lead ECG Placement.” Prime Medical Training, 2 Jan. 2023, https://www.primemedicaltraining.com/12-lead-ecg-placement/. 

5) “The ECG Leads: Electrodes, Limb Leads, Chest (Precordial) Leads, 12-Lead ECG (EKG).” ECG & ECHO, 28 Feb. 2023, 

6) Yamaji H, Iwasaki K, Kusachi S, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol. 2001;38(5):1348-1354.

7) Salim Rezaie, MD. “Lead AVR: The Forgotten 12th Lead.” ALiEM, 10 Sept. 2019, https://www.aliem.com/avr-the-forgotten-12th-lead/. 

8) Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-STsegment elevation acute coronary syndrome. Am J Cardiol. 2011;107(4):495-500.

9) Barrabés J, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation. 2003;108(7):814-819. 

10) Abbase AH, ALjubawii AA. The Significance of ST Segment Elevation in Lead aVR in Acute Anterior Myocardial Infarction. Medical Journal of Babylon. 2011;8(4):490-496. http://www.iasj.net/iasj?func=fulltext&aId=32167. 

11) O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation 2013, 61(4): 378-140

12) Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Eur Heart J 2019, 40: 237-269

13) Knotts RJ, WIlson JM, Kim E, et al. Diffuse ST depression with ST elevation in aVR: is this pattern specific for global ischemia due to the left main coronary artery disease? J Electrocardiol 2013, 46(3):240-8

14) Miranda DF, Lobo AS, Walsh B, et al. New insights into the use of the 12-lead electrocardiogram for diagnosing acute myocardial infarction in the emergency department. Can J of Cardiol 2018, 34: 132-145

15) Ferreira RM, de Souza E Silva NA, Salis LHA. Complications after elective percutaneous coronary interventions: A comparison between public and private hospitals. Indian Heart J. 2018;70(1):32-36. doi:10.1016/j.ihj.2017.06.012

16) McLaren, Jesse. “St Elevation in AVR, Stemi Equivalent?: ECG Cases.” Emergency Medicine Cases, 10 Mar. 2020

17) Shamim S, McCrary J, Wayne L, Gratton M, Bogart DB. Electrocardiograhic findings resulting in inappropriate cardiac catheterization laboratory activation for ST-segment elevation myocardial infarction. Cardiovasc Diagn Ther. 2014;4(3):215-223. doi:10.3978/j.issn.2223-3652.2014.05.01