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13. ECG Surprise Attack!: Chest Pain and the “Forgotten Lead”
Keywords
ST elevationaVRSTEMI equivalentChest painLeft main coronary artery diseaseCase 2
Pertinent History
An 84-year-old Caucasian male presents to the emergency department at 2100 by ambulance. He reports that roughly 45 minutes ago he developed an episode of central chest pressure while walking up the basement stairs after moving some boxes. This was associated with some shortness of breath. His wife then witnessed him have a syncopal episode at the top of the stairs. He regained consciousness quickly without confusion or drowsiness. The patient reports that since that time he has had persistent pressure-like chest pain. He reports he has had occasional chest pain while doing gardening and ascending stairs for several years but has never lost consciousness or experienced persistent pain.
PMH
Diabetes, Type II
Hypertension
Hypercholesterolemia/hyperlipidemia
Meds: Aspirin, atorvastatin, metoprolol, lisinopril, insulin glargine, insulin Aspart
SH
Former smoker, 40 pack years (quit 20 years ago)
Denies drug or alcohol use
FH
Father – myocardial infarction, age 66
Mother + father: diabetes, type II
Pertinent Physical Exam
BP 97/62, Pulse 105, Temp 98.6 °F (37.0 °C), RR20, SpO2 96% on RA.
Except as noted below, the findings of the complete physical exam are within normal limits.
Cardiovascular:
Tachycardia with regular rhythm, normal heart sounds without murmur. JVD to the angle of the jaw. No costochondral tenderness. Pulses 2+ to all extremities. No pitting edema.
Respiratory:
Tachypnea. Speaking 4 words or less at a time. No wheeze. Mild crackles to the bases bilaterally.
Pertinent Test Results
CBC, CMP, PT/INR, PTT – All unremarkable.
Troponin I: 5.31 ng/mL (Reference range < =0.06 ng/mL).
Portable CXR: Mild blunting of the costophrenic angles. Increased pulmonary vasculature. Fluid in the horizontal fissure. Diffuse fluffy opacities present.
12 Lead ECG: (See attached image) Sinus rhythm, rate 98, left axis deviation, STD in leads II, III, aVF, V3-V6, STE in lead aVR of 2 mm, T-wave inversions I, aVL, V3-V6.
ST Elevations in aVR
Sinus rhythm, rate 98, left axis deviation, STD in leads II, III, aVF, V3-V6, STE in lead aVR of 2 mm, T-wave inversions I, aVL, V3-V6
Image used with permission courtesy of Amal Mattu
ED Management
2100 The patient is roomed immediately, seen by the provider, and all investigations are ordered. He is administered 324 mg of chewable aspirin. As the patient is dyspneic, he is immediately placed on non-rebreather mask at 10 LPM with an increase in SpO2 to 100% and mild improvement in respiratory distress. However, his chest pain and hypotension remain.
Updates on ED Course
(2120) Upon examining the patient’s ECG and CXR, we elected to immediately call the interventionalist. They agree that the patient should be expeditiously transferred to the cardiac catheterization laboratory (cath lab) for emergent coronary angiography. The cath lab is activated, and the patient is administered a heparin bolus followed by infusion. Though listed in the hospital’s pre-cath lab bundle, clopidogrel is withheld.
Learning Points
Priming Questions
- 1.
What specific diagnosis or diagnoses does the ECG with ST-segment elevation (STE) in lead aVR suggest?
- 2.
Is STE in lead aVR indicative of a true STEMI?
- 3.
Should I always be concerned about STE in lead aVR?
- 4.
If sending a patient to cardiac catheterization for STE in aVR, why might you omit some of your hospital’s standard precatheterization medications?
Introduction/Background
- 1.
Lead aVR is an augmented unipolar limb lead placed on the right upper extremity providing fundamental information about:
The superior right region of the heart including the basal septum.
The right ventricular outflow tract.
The endocardial surface of the entire left ventricle and apex.
- 2.
- 3.
ST-segment-elevation (STE) in aVR has proven association to multivessel coronary disease (MVD), and occlusions of the left main coronary artery (LMCA) and proximal left anterior descending (LAD) coronary artery [2, 5–7].
- 4.
Though not recognized by many practitioners as an example of ST-Segment Elevation Myocardial Infarction (STEMI), the diagnostic utility of STE in aVR has been recognized by various guiding international organizations.
In 2009, the American Heart Association (AHA), American College of Cardiology (ACC), and the Heart Rhythm Society released a scientific statement advising programming computerized ECG interpretation to suggest MVD or Left Main Coronary Artery (LMCA) ischemia when STE in aVR and/or V1 is accompanied by ST-segment-depression (STD) ≥1 mm in ≥8 leads [8].
In 2010, an international consensus document recommended prioritizing Acute Coronary Syndrome (ACS) patients for urgent invasive angiography due to high probability of severe angiographic coronary artery disease (CAD) with similar criteria [9]:
STD in ≥6 leads (maximal in V4-V6) AND STE in aVR.
- 5.
The importance of recognizing STE in aVR lies in the major coronary artery distributions it displays, its ability to localize coronary lesions, as well as its independent prognostic and diagnostic value:
Culprit Lesion:
Widespread STD and symptoms of ischemia may be indicative of LMCA occlusion regardless of presence of STE in aVR. However, likelihood of LMCA occlusion is increased with concomitant STE in aVR [10].
If STE in V1 is also present, this may indicate either LMCA or proximal LAD occlusion; however, if the STE in aVR ≥ V1, this is indicative of a LMCA occlusion as opposed to isolated LAD occlusion [6].
Magnitude of STE in aVR is the strongest diagnostic indicator of LMCA and/or MVD [11, 12]:
STE ≥0.5 mm, OR 19.7, p < 0.001.
STE ≥1 mm, OR 29.1, p < 0.001.
This supersedes the value of a positive Troponin T (OR 1.27, p = 0.044 to OR 3.08, p = 0.048).
Kosuge et al. found that STE in aVR ≥1 mm predicts LMCA and/or MVD with 80% sensitivity and 93% specificity [11].
In non-ST-Elevation ACS (NSTE-ACS), STE in aVR is more predictive of LMCA disease or MVD than STD in other leads [11].
The prognostic value STE in aVR extends beyond active ACS to include provocative testing as precipitation of STE in aVR via treadmill stress testing denotes stenosis LMCA or proximal LAD [6].
Coronary Anatomy
By Coronary.pdf: Patrick J. Lynch, medical illustratorderivative work: Mikael Häggström (Coronary.pdf) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons
- 6.
Prompt recognition of STE in aVR and therefore its implicated lesions is crucial as investigation and treatments typically indicated in other cases of ACS may be precluded:
Stress testing: The culprit high-risk coronary lesions of aVR are contraindications to exercise stress tests as they may trigger fatal ischemia or arrhythmias. These patients should be directed to primary coronary angiography [3, 13].
Coronary artery bypass grafting (CABG): ACS Patients with LMCA and/or MVD are more likely to require CABG than other patterns of occlusion [12].
This is vital, as administration of dual antiplatelet therapy (aspirin + clopidogrel) comes with a class I recommendation from the ACC & AHA in NSTEMI patients planned for percutaneous coronary intervention (PCI) [14].
The 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery advises against administration of clopidogrel, ticagrelor, prasugrel, glycoprotein IIb/IIIa inhibitors, and abciximab for several hours to days preoperatively as they have been associated with increased risk of post-CABG bleeding, transfusion requirement, and major bleeding complications [15].
Parenteral anticoagulant therapy such as unfractionated heparin (UFH), enoxaparin, or bivalirudin prior to PCI is supported in both NSTEMI and STEMI patients [14, 16]. However, perioperative enoxaparin has been shown to increase postoperative bleeding and need for re-exploration over UFH [15, 17] and is therefore prudent to avoid.
Physiology/Pathophysiology
- 1.
There are two predominant pathophysiologic pathways that lead to STE in aVR:
Infarction of the basilar interventricular septum – STEMI via LMCA or proximal LAD occlusion. STE in aVR occurs as a direct change from the transmural infarction of the LVOT or basilar interventricular septum.
Diffuse endocardial ischemia – as a reciprocal of widespread STD as caused by severe MVD, or mismatch of oxygen supply and demand (e.g., post-ROSC following cardiac arrest, massive PE, or severe tachydysrhythmias). STE in aVR occurs as a reciprocal change to the subendocardial STD in the leads electrically opposite (I, II, aVL, and V4-V6).
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