ECG Case 132

• Normal sinus rhythm, rate 72 bpm
• Deeply T-wave inversion in V2-4, without significant ST segment changes
• R wave progression is preserved (R wave in V3 > 3mm)

We recall from ECG Case 123 that our differentials for right precordial T-wave inversion in patients with symptoms of acute coronary syndrome (ACS) include:

• Ischaemia (including Wellens Syndrome)
• Posterior myocardial infarction
• Right ventricular strain (including pulmonary embolism)
• Hypertrophic cardiomyopathy (especially apical type) — with high mid-anterior QRS voltages

Whilst working through your above differentials, our patient has a further episode of chest pain. ECGs are captured at the time of pain and also following self-resolution:

t + 8 minutes (recurrence of pain)

What is your interpretation?

t + 17 minutes (pain resolved)

What is your interpretation?

Such dynamic T-wave changes in V2-4 suggests this is indeed Wellens syndrome. “Pseudonormalisation” in our second ECG represents evolving infarction (as opposed to ischaemia) – given recurrent episodes of chest pain in the department, this patient requires emergent intervention.

Urgent angiogram revealed severe diffuse left main coronary artery stenosis and severe mid LAD stenosis for which he underwent successful PCI. Initial troponin taken in the emergency department later returned a negative result.

Wellens Syndrome is a clinical syndrome characterised by a pattern of biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain that is not resolved. It is highly specific for critical stenosis of the left anterior descending artery (LAD). These patients usually require invasive therapy, do poorly with medical management, and may suffer MI or cardiac arrest if inappropriately stress tested.

“Pseudonormalisation” may mask all ischaemic changes

Although our second ECG above is concerning in itself due to anterior STE and HATW, such evolving infarction may not always be so evident. Pseudonormalisation of previously inverted T waves may manifest as a “normal” ECG. With self-resolution of chest pain, serial troponins in these patients are often negative. If only one ECG is taken on arrival with the occurrence of pain, the diagnosis of Wellens syndrome may be missed. It sounds simple, but Wellens syndrome underpins the importance of all patients presenting pre-hospital and to emergency departments undergoing serial ECGs, especially with changes in pain.

Understanding T wave changes

Patients with Wellens Syndrome present with one of two ECG patterns:

• 75% will have a pattern of deeply inverted T waves in leads V2-3 (type B)
• 25% will demonstrate a biphasic T wave with negative terminal portion (type A). These type A changes can be subtle and are more often overlooked.

In patients with Wellens, a sudden complete occlusion of the LAD causes a transient anterior MI, manifesting as either “pseudonormalised” anterior T waves or an anterior STEMI. Reperfusion of the LAD (e.g. due to spontaneous clot lysis) causes resolution of ST segment changes, and T waves become biphasic or inverted. The T wave morphology is identical to patients who reperfuse after a successful PCI.

Note that this sequence of events is not limited to anterior leads – similar changes may be seen in inferior or lateral leads, e.g. with RCA or circumflex occlusion.

Differentials for right precordial T wave inversion

In patients presenting with chest pain and ECG features in V2-3 suggestive of Wellens Syndrome, we must always consider and examine for changes suggestive of pulmonary embolism. As seen in ECG Case 123, associated T-wave inversion in leads V1 and III is highly specific for the diagnosis of PE. In addition, ECG changes will usually not be dynamic with recurrence of pain.