A 40-something male presented to triage. He had suffered a couple bouts of typical chest pain in the last 24 hours. This ECG (ECG #3) was recorded immediately after the last episode of pain spontaneously resolved. The pain had lasted about one hour.
|There are classic Wellens’ waves in V2-V5.
This is “terminal” T-wave inversion: the latter part of the T-wave turns down (inverts).
There are preserved R-waves in the involved leads (necessary to be called Wellens’ waves)
There is no LVH in the involved leads. This is important, as LVH can cause PseudoWellens’ waves.
This Wellens’ pattern with terminal T-wave inversion (in contrast to deep symmetric T-wave inversion) was called “Pattern A” by Wellens hinself in the original papers.
Wellens’ original Papers:
(Some later authors ignored Wellens own classification of “Pattern A” and called this “Type” B!! — let’s go back to Wellens’ own classification)
Here is an example of the misclassification: https://www.resus.com.au/2017/03/24/wellens-syndrome/
This is Wellens’ syndrome: Since the patient had anginal chest pain that is now resolved, it meets the criteria for Wellens’ syndrome (criteria: resolved anginal chest pain, typical Wellens’ waves in LAD distribution with preserved R-waves, absence of LVH which can cause pseudoWellens’ waves).
See these posts for Wellens’ mimics:
Unlike many cases of Wellens’ syndrome, this patient actually presented with active pain
. So you are going to get to see what the ECG would have shown had you recorded one during pain!
This was the first ECG (ECG #1) recorded during pain:
|This shows ST elevation and hyperacute T-waves in the LAD distribution.
This is highly suspicious for acute LAD occlusion.
It even meets STEMI criteria:
2.5 mm STE in V3, 2 mm STE in V4 (at the J-point, relative to the PQ junction)
If you calculate the 3- and 4-variable formulas, you can use these numbers:
STE60V3 (ST Elevation at 60 ms after the J-point in lead V3) = 3.5
QTc (computerized) = 418
QRSV2 (total QRS amplitude in V2) = 5
RAV4 (R-wave amplitude in V4) = 24
See subtleSTEMI app for iPhone for the formulas:
3-variable = 21.024 (this is low because of the very high R-wave amplitude in V4)
4-variable = 18.266 (We now know that this is a more accurate formula, and a value above 18.2 is very specific for LAD occlusion.)
This is the actual 4-variable formula:
0.052*QTc-B – 0.151*QRSV2 – 0.268*RV4 + 1.062*STE60V3.
Just today, an external validation of 3- and 4-variable formulas to Differentiate subtle LAD occlusion from normal Variant ST Elevation was just published online in the Annals of Noninvasive Electrocardiology:
This is a validation of these 2 papers by Smith:
This validation confirms that the 4-variable formula is very accurate and is better than the 3-variable formula!
The patients pain resolved and another ECG (ECG #2) was recorded 18 minutes after the first:
|All STE is resolved.
Then this ECG (ECG #3, again) was recorded another 17 minutes later when the patient was completely pain free (this is the Wellens ECG you saw at the top of the post):
|This demonstrates how Wellens’ waves manifest the aftermath of a reperfused STEMI
The cath lab was activated and a 95% hazy LAD lesion with thrombus and TIMI 3 flow (good flow) was found and stented.
Here is the first post-cath ECG (ECG #4).
|Similar to the previous
This was recorded the next AM (ECG #5):
|Now the Wellens’ waves have evolved, as they always do (if it really is Wellens’).
They are now deeper and almost symmetric.
These are “Pattern B” T-waves.
What Wellens did not describe, but what I have found to be true, is that Wellens’ Pattern A are found soon after reperfusion, and that they always evolved into Pattern B waves.
Wellens did not have many serial ECGs to scrutinize. He wouldn’t have noticed this.
I have found it to be universally true.
Evidence for Wellens as a reperfusion syndrome
To my knowledge, there is no research paper demonstrating this. From my experience, I am confident that if it were formally studied, it would be born out.
I believe that I was the first to represent Wellens as a reperfusion syndrome, in my book, The ECG in Acute MI, pages 22-23 and 51, and in chapter 27 on Reperfusion and Reocclusion.
My recognition of this was based papers by Wehrens and Doevendans on terminal T-wave inversion as a sign of reperfusion after use of thrombolytics. Notice that both papers have Wellens as senior author, and it is very curious that he did not make the connection between his own syndrome and the identical ECG he described in these studies!
Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J. 2000 Mar;139(3):430-6. PubMed PMID: 10689257.
Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bär FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol. 1995 Jun 15;75(17):1206-10. PubMed PMID: 7778540.
Peak troponin I was 0.58 ng/mL
Echo the next day showed:
Regional wall motion abnormality-distal septum anterior and apex large.
Regional wall motion abnormality-anterior probable.
Ed Burns has a very nice complete summary of Wellens’ syndrome here:
Comment by KEN GRAUER, MD (6/28/2018):
———————————————————–Highly insightful post with superb explanation by Dr. Smith, illustrating by sequential evolution over 5 serial tracings what Wellens’ Syndrome is, and what it is not. I found comparison of the first ECG in this blog post (TOP nn Figure-1 — recorded immediately after the last episode of chest pain had spontaneously resolved) — with the initial ECG that was recorded duringchest pain (BOTTOM) to be especially interesting.
- Is there a difference in frontal plane axis between the 2 tracings?
- Is there a difference in QRS amplitude in the various leads between the 2 tracings?
- Is there voltage for LVH in either (or both) tracings?
- What might account for these differences? Why should we care?
|Figure-1: TOP ECG — recorded immediately after CP resolved. BOTTOM ECG — recorded during initial episode of CP (See text for details).
- The frontal plane axis has clearly shifted. In the TOP tracing — the axis is about -15 degrees (note the predominantly negative complex in aVF). In the BOTTOM tracing — the axis is about +40 degrees (clearly positive in aVF).
- Voltage criteria for LVH is satisfied in the TOP tracing in lead aVL (ie, an R in aVL ≥12mm). However, this criterion is no longer satisfied in the limb leads for the BOTTOM tracing, in which the frontal plane axis is no longer negative. NOTE: As per Dr. Smith — diagnosis of Wellens Syndrome is not impeded in the TOP ECG, because LVH criteria are clearly not present in the chest leads where the Wellens ST-T wave changes are noted!
- The zone of transition in the chest leads has also shifted. The R wave becomes predominantly positive only between leads V3-to-V4 in the TOP tracing — whereas transition occurs earlier (ie, already by lead V2) in the BOTTOM tracing. Along with this change in transition — QRS amplitude is markedly increased in the BOTTOM tracing. In fact, voltage criteria for LVH are satisfied in lead V6 (ie, R≥18mm in this lead).
Comment: The importance of attention to frontal plane axis, the area of transition, and relative QRS amplitude in various leads is often overlooked when comparing serial tracings. In this particular case — the astute conclusions highlighted by Dr. Smith (ie, Wellens Syndrome in the TOP tracing after CP resolved; Acute ST elevation in the BOTTOM tracing during CP) are not altered — but there are times when determining if there are or are not acute ST-T wave changes between serial tracings may be especially challenging IF differences in axis, transition zone and QRS amplitude are not noted.
- Ensuring consistent chest lead electrode placement is essential for serial comparison of findings in leads V1-thru-V6. Large body habitus, chest wall abnormalities, varied electrode place (over vs under the breast) in women, are among some of the reasons why differences may be seen in transition zone and chest lead QRS amplitudes over serial tracings if attention is not focused on consistent electrode lead placement. Also relevant in this case as a potential cause for change in transition zone and chest lead QRS amplitude, is intermittent LAD occlusion with spontaneous reperfusion.
- Often unappreciated is the fact that change in the incline of the patient’s bed may account for QRS axis shifts. How often are ECGs done on acute care patients who have difficulty lying in a completely flat bed? How you ever seen the angulation in degrees of the patient’s bed noted on the ECG when cardiograms are done on patients who are not completely flat? I have always suspected change in angulation of the bed over serial tracings to be one of the common causes of inferior lead Q waves that are sometimes seen one day and gone the next …