ECG Marksmanship: Posterior Wellen’s Syndrome

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One of the most rewarding elements of emergency medicine is spotting a potentially catastrophic situation at an early stage, and proceeding to ‘nip it in the bud’ before things start getting hairy.

To coin a military analogy: a battalion might be perfectly capable of neutralising the enemy in close-quarters combat, but in an ideal world, a shrewdly placed sniper will take care of business ahead of time. No need for bayonets if you’ve got a man on the roof.

The emergency physician acts as the sniper when Wellen’s Syndrome is spotted on the 12-lead ECG. A pain-free, haemodynamically stable patient might be moments away from a ‘widow-maker’ infarct, but if the subtle precordial biphasic T-waves are picked up, the enemy lesion can be taken out from range via percutaneous coronary intervention (PCI), sparing the patient’s anterior myocardium. No drama.

What is Wellen’s Syndrome again?

It was first discovered in 1982 by Hein J. J. Wellen, and describes characteristic T-wave changes in the right precordial leads (V1-V3) that represent critical stenosis of the left anterior descending (LAD) artery.

Most cases (approximately 75%) of Wellen’s Syndrome have a ‘Type B’ pattern – deep and symmetrically inverted T-waves. This is an easy spot, and should ring alarm bells even at novice level.

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Wellen’s Type B (Image from ‘Life in the Fast Lane’)

A minority of cases (approximately 25%) will have ‘Type A’ pattern – biphasic T-waves. These are often more subtle, and easily overlooked, particularly if the patient is clinically well.

Wellen's Type A (Image from 'Life in the Fast Lane')
Wellen’s Type A (Image from ‘Life in the Fast Lane’)

The physiological basis for Wellen’s is spontaneous reperfusion of a previously occluded artery. Often patients will present to the ED following a bout of severe chest pain which has resolved. Classically, the ambulance ECG will demonstrate an impressive STEMI, which has disappeared once the patient has arrived in resus, pain-free. Despite being symptomatically better, these patients will have an active thrombus and are high risk for re-occlusion and STEMI. They need aggressive medical management, with a view to urgent angiogram/PCI.

Wellen’s waves are not exclusive to the anterior leads. They have been shown to correlate with spontaneous reperfusion in the left circumflex (LCx) and right coronary artery (RCA) when ECG changes are seen in the inferior and lateral lead distribution.

Interesting recent EMJ article – Driver et al, August 2016

Until recently, the literature has not described the ECG appearance of posterior MI (PMI) reperfusion.

An article published online first in the EMJ last month takes on this very challenge. Tellingly, one of the authors is Stephen Smith, author of ‘Dr. Smith’s ECG blog’ – one of the most prominent ECG #FOAMed resources available.

The classical acute PMI ECG demonstrates new ST depression in the right precordial leads – a mirror image of ST elevation in the hypothetical posterior leads (V7-V9). The posterior myocardium is supplied by either the LCx or RCA, depending on the patient’s anatomy.

The authors of this paper hypothesised that spontaneous reperfusion of the offending artery in acute PMI patients would result in Wellen’s waves (deep T-wave inversion) in the posterior leads, which would correlate with an increase in positive T-wave amplitude in the right precordial leads – again, the mirror image concept.

It was a retrospective observational analysis of 72 patients with LCx or RCA occlusions who underwent PCI – mimicking spontaneous reperfusion. Forty eight patients met criteria for PMI – ‘presence of right precordial ST depression, maximal in leads V2 and/or V3, not explained by QRS abnormalities’. Twenty four patients did not meet criteria – i.e. they had occluded their LCx/RCA, but the posterior myocardium was not infarcted.

Post reperfusion:

  • PMI patients had a greater increase in V2 and V3 T-wave amplitude when compared to non-PMI patients (p=0.0005 and 0.03 respectively).
  • PMI patients had greater maximal T-wave amplitude in lead V2 (p=0.04) when compared to non-PMI patients.

The authors believe they have described an ECG finding for PMI reperfusion that is ‘analogous’ to typical Wellen’s waves. ‘Posterior Wellen’s Syndrome’ is born.

Of course there are the inherent limitations of a single-centre study with a small patient population, but nonetheless the paper is compelling reading. It’ll make you a more accomplished ECG marksman, taking better aim from the roof of your department.

For me, the take-home point is to always carefully consider treating and admitting a patient with resolved ischaemic-sounding chest pain and unusually big right precordial T-waves (however subtle) – particularly if they have risk factors for coronary artery disease. At the very least previous ECGs should be hunted down and interrogated.

As always, would love to hear others thoughts on the paper.

Robert
@PonderingEM

The Paper

Driver BE, Shroff GR, Smith S. Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall. Emerg Med J. 2016 Jul 29.

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