Biphasic T-Wave Pattern: Is it Wellens Syndrome? -

Author: Esteban Davila

Editor: Alec Feuerbach

The Case

An 18-year-old male without past medical history presented to the ED with one day of fever, headache, and left-sided chest pain starting 4 hours prior to arrival. The patient described the chest pain as achy, non-radiating, and worse with deep inspiration and lying flat. He reported a mild sore throat but denied shortness of breath, cough, diaphoresis, or trauma. Initial vital signs were notable for a temperature of 102 F and a heart rate of 110/min. The exam revealed no murmur or friction rub, clear lung sounds, a soft non-tender abdomen, and no lower extremity edema. An ECG was performed:

Initial ECG

ECG interpretation: Rate ~70/min, notched P wave in lead II and upright in lead V1 with possible ectopic atrial rhythm, normal axis, normal intervals. There are large QRS amplitudes throughout, small/narrow Q waves in V5-V6 and biphasic T waves in leads V2-V5 with T-wave inversions in the inferior leads. There was no prior ECG available.

The Differential for Biphasic T-Wave Pattern

The differential diagnosis of biphasic T-waves and deep T wave inversions (TWI) includes Wellens Syndrome, myocardial ischemia, left and right ventricular hypertrophy, pulmonary embolism causing right heart strain, hypertrophic cardiomyopathy, increased intracranial pressure (cerebral T-waves), myopericarditis, takotsubo cardiomyopathy, and both left and right bundle branch block.

Sources: T wave, Lupus myopericarditis as a preceding stressor for takotsubo cardiomyopathy, Takotsubo Stress Cardiomyopathy, with Echocardiography

The treating ED physicians were concerned about Wellens syndrome given the ECG or myopericarditis given the presenting symptoms. They gave the patient 800 mg of ibuprofen and consulted Cardiology. A point-of-care ultrasound revealed normal ejection fraction and no regional wall motion abnormalities or pericardial effusion. Cardiology recommended aspirin 324 mg, atorvastatin 80 mg, and transfer to a PCI-capable center. Initial blood work returned with a white blood count of 3.8, troponin < 0.01, BNP 33, ESR 12, and CRP 3.4. A chest x-ray revealed no underlying cardiopulmonary abnormalities. No repeat ECG or troponin testing was done. The patient was transferred to a PCI-capable center for further evaluation of “ACS”.

At the receiving hospital, the blood testing showed high-sensitivity troponin of 11 (lower limit of detection is 21.9), normal lipid panel, and D-dimer < 177 ng/mL (reference range of < 230 ng/mL). Transthoracic echo showed EF 65% without other abnormalities. A repeat ECG did not show any dynamic changes.

Repeat ECG

Repeat ESR and CRP remained normal, and the physicians ruled out acute MI with normal serial troponins. The patient’s chest pain resolved hours after arrival at the outside hospital, and the patient was discharged with outpatient follow-up for cardiac MR to evaluate for possible infiltrative disease.

Reevaluating this case, two relatively common ECG patterns could have been considered in the initial differential diagnosis. These are a Persistent Juvenile J-wave Pattern and a Benign TWI Pattern.[1] It is important to be aware of these benign ECG patterns as they are known to lead to over-activation of cardiac catheterization laboratories and extensive workups, potentially exposing patients to the unnecessary risks of PCI including bleeding, coronary artery dissection or occlusion, and renal injury.[2,3]

Given the presentation consistent with a febrile etiology, mild tachycardia, and no prior ECG to compare, the ED physicians evaluated this patient for myopericarditis and Wellens Syndrome with cardiac markers, POCUS, and inflammatory markers that all were normal. Despite the decreased post-test probability of clinically important myopericarditis and history inconsistent with Wellens Syndrome (more on Wellens Syndrome can be found here), the patient was eventually transferred to a PCI-capable hospital. Coronary angiography was not performed. There is room to learn here.

The Data

A recent review by Walsh et al examined six ECG patterns seen more commonly in healthy Black adults that appear malignant but can be benign.[1] Before discussing these findings, it is imperative to recognize that the term “Black adults” frequently used in literature describes a genetically diverse group. Studies have shown a different prevalence of ECG findings within groups of Black adults from different geographical origins.[4,5] In other words, race is not a biological or genetic category. Still, an understanding of these potentially benign patterns is important given many have been commonly described in Afro-Caribbean populations similar to that served at Kings County Hospital and Downstate Medical Center.

The patterns described by Walsh et al included 1) LVH criteria with associated repolarization producing ST elevations (STE), 2) benign anterior STE, 3) early repolarization and benign inferolateral STE, 4) persistent juvenile TWI, 5) anterior TWI with J point elevation, and 6) TWI in lateral precordial leads. A quick glance through the article will show two morphologies that look very similar to our patient: anterior TWI with J point elevation and TWI in lateral precordial leads.

Source: Distinctive ECG patterns in healthy Black adults[1]

Anterior TWI with J point elevation is usually biphasic, often with “convex-up” STE. In one study of healthy, non-athlete Black males (mostly of African/Afro-Caribbean origin) the prevalence of anterior TWI was 4.2% compared to 1.9% in white male adults.[6] Additionally, this same pattern was found in 14% of Black European female athletes compared to 2% of white female athletes in another study. [7] J point elevation > 0.1 mV and TWI limited to V1-V4 will differentiate anterior TWI from the other two etiologies that have similar morphologies: arrhythmogenic right ventricular cardiomyopathy and hypertrophic cardiomyopathy (HCM). In our case, our patient had TWI in anterior leads with morphology consistent with anterior TWI with J point elevation pattern; however, the TWI extends to V6, so we cannot definitively say this is an example of this pattern. Lateral TWI pattern usually shows end-QRS notching and/or slurs of the early repolarization, usually with J point elevation.[8] This pattern also commonly has TWI in inferior leads, which is consistent with our patient. The prevalence of this pattern in Black, non-athlete males is 3.3% to 4.2%, depending on the patient population studied.[6,9] It is important to recognize that a lateral TWI morphology can be seen in 70% of Black patients with HCM. Confidence in this prevalence is limited because HCM is understudied in the Black population; only 5% of patients in the U.S. HCM registry are black.[10] Still, patients with Lateral TWI morphology and high clinical suspicion of HCM by good history, family history of sudden cardiac death, and a physical exam should receive an outpatient Cardiology referral for risk assessment and echocardiography.[11] Returning to our patient, however, the point-of-care echo and TTE performed did not show any signs of HCM. He had TWI in the lateral leads consistent with the benign Lateral TWI pattern, but again cannot be definitely assigned this pattern based on ECG alone given the large inversion in V2.

Back to the Case

Our patient presented with a febrile illness, vague chest pain, and a concerning ECG. The ED physicians evaluated the patient for myocarditis and had a normal repeat ECG and echo. The lack of progression of the ECG and a history of chest pain during the ECG made Wellens syndrome exceedingly unlikely. The marked improvement in the patient’s symptoms with the extensive negative workup including an echocardiogram without signs of HCM supports the ECG being a benign pattern that is common in our patient population. When the history and exam do not fit the ECG, an ED physician should consider these benign ECG patterns on the differential. In this situation, the decision to proceed with further inpatient testing and transfer to a higher level of care can be shared between clinician and patient.

Summary

1) Healthy adults can have “malignant”-looking ECG patterns that are benign.

2) These benign ECG patterns should be considered if the ECG does not fit the clinical presentation or workup.

3) The malignant-appearing ECG patterns are more frequent in Black patients; however, the term “Black patients” describes a genetically diverse group with different prevalence of ECG findings depending on the specific population.

4) Diagnosing a benign ECG pattern depends on a thorough review of the individual patient’s history, a detailed examination of serial ECG, and an appropriate diagnostic workup.