Rhythm Nation – Wellens Syndrome

Author: Karen Jeoffroy

Peer Editors: Alec Feuerbach, Nicole Anthony

Faculty Editor: Mark Silverberg

Case

A 75-year-old male with a history of hypertension, diabetes, hyperlipidemia, and coronary artery disease (on aspirin and clopidogrel) presents to the Emergency Department (ED) four hours after an episode of left-sided, non-radiating chest pain with associated nausea, vomiting, and diaphoresis. His symptoms lasted roughly 45 minutes and resolved with rest. Upon arrival, the patient is completely asymptomatic. Vital signs are normal. The physical examination is unremarkable and the following ECG is obtained:

ECG interpretation

This ECG shows a heart rate near 60 per minute with a regular rhythm and normal axis. PR, QRS, and QT intervals appear normal and Sokolow-Lyon voltage criteria for left ventricular hypertrophy are not met. There are biphasic precordial T waves with initial positivity and terminal negativity, more prominent in V2 and V3. There is preserved R wave progression. These are classic ECG findings of Wellens Syndrome. 

Wellens syndrome is important to recognize because it represents an impending coronary occlusion involving the Left Anterior Descending artery (LAD). The syndrome typically involves chest pain that has resolved in a patient with the following ECG findings: [1,2]

      1. Preserved R wave progression and no pathologic Q waves

      2. Primary T wave inversion in the anterior leads that is not secondary to bundle branch block or ventricular hypertrophy and the following morphology:

                     Type A: a concave/straight ST segment followed by terminal T wave inversion (as shown in the ECG above)

                     Type B: a convex ST segment followed by deep and symmetric T wave inversion (most common – see below) 

Figure: Type B Wellens Syndrome (from Life in the Fast Lane)

The pathophysiology of these ECG findings is thought to involve the following mechanism. First, a sudden complete occlusion of the LAD results in transient anterior ST-elevations that may not be immediately captured on ECG. A small area of spontaneous recanalization of the LAD then allows for reperfusion of its territory. At this time, the patient’s chest pain resolves and T waves become biphasic or inverted. Because there is only transient total occlusion, patients may initially have normal or only mildly elevated cardiac biomarkers.[1]

Because of its similar mechanism, the ECG morphology of Wellens is similar to that seen during reperfusion after PCI. In the case of Wellens, however, perfusion is tenuous and unstable as the patient still has near-total occlusion of their LAD. It is important to note that if occlusion of the LAD occurs after the onset of Wellens Syndrome, an ECG would likely first demonstrate pseudonormalization of T waves as they become more prominent and upright from their previous biphasic/inverted position. Should the LAD remain occluded, the patient will then go on to develop anterior ST-elevations. 

The original study that described Wellens Syndrome revealed that 75% of patients with the characteristic findings of Wellen Syndrome developed extensive anterior wall myocardial infarction just a few weeks after admission and treatment with medical management alone.[3] Thus, percutaneous coronary intervention (PCI) is the definitive management of this condition.[4]

A patient with Wellens syndrome should be hospitalized for symptom monitoring, continuous telemetry, and serial ECG. Recurrent symptoms and dynamic ECG changes should be considered a “STEMI-equivalent” and prompt emergent PCI. Otherwise, PCI should be performed urgently given the poor outcomes of medical management alone. It is imperative to remember that stress testing these patients is contraindicated as this may precipitate MI and even death. 

References

1. Cadogan M, Butner R. Wellens Syndrome. Life in the Fast Lane. https://litfl.com/wellens-syndrome-ecg-library/. Published Sep 8 2021. Accessed on June 14, 2022

2. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002;20(7):638-643. doi:10.1053/ajem.2002.34800 

3. de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103(4 Pt 2):730-736. 

4. Al-Assaf O, Abdulghani M, Musa A, AlJallaf M. Wellen’s Syndrome: The Life-Threatening Diagnosis. Circulation. 2019;140(22):1851-1852. doi:10.1161/CIRCULATIONAHA.119.043780

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