(P08) Wellens' Syndrome Case Report

Chief Complaint : Chest Pain

History of Present Illness : A 66 year old male with a past medical history of hypertension presented to the emergency department with a chief complaint of chest pain. The patient reported that the chest pain was intermittent, began 3 days ago and was substernal. He denied any worsening or improving factors, any radiation of the pain or any other associated symptoms. The patient reported that he had the chest pain this morning, which prompted him to come to the ED, but it had since resolved and he was currently pain free.

Pertinent Physical Exam: The patient was not in distress, had normal work of breathing and was not diaphoretic or in any apparent discomfort
No murmurs, gallops or rubs. No reproducible chest pain.
Bilateral vesicular breath sounds present bilaterally, no wheezes or crackles appreciated.

Pertinent Laboratory Data: Initial ECG showed somewhat biphasic and deeply inverted T waves in leads V2 and V3
Initial serum troponin was mildly elevated at 0.169
Bedside ultrasound was performed which showed signs of septal wall motion abnormality

Case Discussion: The case describes a presentation of Wellens’ syndrome in which the patient was pain free on arrival to the ED with reports of waxing and waning chest pain during the days prior. The ECG showed biphasic and inverted T waves in V2 and V3 concerning for Wellens’ syndrome, however the patient remained very well appearing. The addition of a bedside ultrasound showed clear signs of anterior/septal wall motion abnormality which assisted greatly in making the diagnosis and expediting the patient’s transfer to the cath lab.

As mentioned above, the ECG changes in Wellens’ syndrome indicate critical LAD stenosis. It is considered a pre-infarction state as there is typically a ruptured atherosclerotic plaque with subsequent disruption of the occlusion before complete myocardial infarction can take place. This continued ischemia and reperfusion is thought to lead to the characteristic T wave changes seen in Wellens’ syndrome. There can even be “pseudonormalization” of the T waves during periods of re-occlusion7.

In the absence of chest pain and with normal cardiac biomarkers, as is often the case with Wellens’, this can be a difficult diagnosis. Furthermore, even within Wellens’ syndrome, there are varying presentations which can make the diagnosis even more complicated. As demonstrated in our case, bedside ultrasound can be an invaluable tool in clinching the diagnosis when it comes to ACS, especially with a presentation as varied as Wellens’ syndrome. Our patient was very well appearing and had no complaints initially in the ED. Although his ECG was concerning, the addition of a septal wall motion abnormality seen on bedside ultrasound was key for making the diagnosis.

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