Wednesday, August 17, 2022

Does this ST Depression Maximal in V3 Represent Posterior OMI?

 I saw this EKG when reading through the system:

What do you think?








This is what I wrote:


ATRIAL FIBRILLATION WITH RAPID VENTRICULAR RESPONSE

RIGHT AXIS DEVIATION  [QRS AXIS > 100]

RIGHT BUNDLE BRANCH BLOCK  

MARKED ST DEPRESSION, CONSIDER SUBENDOCARDIAL INJURY  

"Severe ischemia (STE in I and aVL with reciprocal STD in inferior leads; precordial STD precordial maximal in V3): subendocardial ischemia vs. acute coronary occlusion.  Atrial fib may cause Occlusion mimic."

***ACUTE MI***


(I allowed Acute MI to be in the report because I knew there would be an elevated troponin from ischemia, which is the definition of acute MI -- but in this case it would most likely be a Type 2 MI from tachycardia)


There is also LA-RA lead reversal.


STD Maximal in V1-V4

We have shown in the Journal of the American Medical Association that ST Depression Maximal in V1-V4 (vs. V5, 6) is 97% specific for OMI in a patient population at high risk of ACS.  However, this does NOT apply to patients who have atrial fibrillation, and may not even apply to patients with tachycardia.  


RBBB and STD

ECGs with RBBB have non-ischemic ST depression in V1-V3, discordant to a positive R'-wave; this STD is very moderate, and when "excessive," it represents ischemia, as it does here.  In this case, the ischemia is NOT OMI; it only mimics OMI because of the atrial fib.



I looked into the chart:


Patient was very elderly and had had a fall, was unable to get up and therefore was down on the floor for a long time.  She had some fractures.


It would be possible for acute OMI to initiate such a fall, so it must be on the differential diagnosis.


It is critical to understand that atrial fibrillation can result in ST Depression that mimics posterior OMI.


This was recorded one hour later:

Lead Reversal is no longer present

The ischemia is not as severe (less STD)


High sensitivity troponin I peaked at 82 ng/L (consistent with type 2 MI)

Formal Echo showed hyperdynamic LV function with EF of 78%, no wall motion abnormality.


Next day ECG:

There is sinus rhythm and the ischemia is gone

Learning point:

In the setting of atrial fibrillation with RVR, ST depression maximal in V1-V4 may be due to demand ischemia and not OMI.  This is in contrast to sinus rhythm with a heart rate below 100.



===================================

MY Comment, by KEN GRAUER, MD (8/17/2022):

===================================

I was shown today's ECG without the benefit of any history. Because of an abundance of interesting findings — I focus my comments on this tracing, which I've reproduced in Figure-1
  • The rhythm is rapid AFib.
  • The QRS complex is wide and all upright in lead V1, with a wide terminal S wave in lead V6 — so there is complete RBBB.
  • There is lots of ST depression beyond that expected for simple RBBB. This ST depression is maximal in leads V1-thru-V4 — which suggests acute posterior OMI.
  • There also appears to be ST elevation in high lateral leads I and aVL. This would seem to suggest postero-lateral OMI (presumably from acute LCx occlusion).

KEY Points (as per Dr. Smith): It turns out that neither posterior nor lateral OMI were present! These are the "Take-Home" Lessons from today's tracing:
  • As per Dr. Smith — Rapid AFib may sometimes simulate acute posterior OMI. While common to see diffuse ST depression with regular SVT rhythms — ST depression with rapid AFib has a tendency to be maximal in anterior leads (as in Figure-1), in such a way that falsely suggests posterior OMI. This anterior ST depression often resolves (or at least greatly decreases) when AFib is controlled and the heart rate slows.

  • The QRS complex in lead I looks "funny". This lead almost never normally manifests as deep of a Q wave as is seen in Figure-1. Whenever you see an overly large initial negative deflection in lead I — Think of LA-RA Lead Reversal!

Figure-1: The initial ECG in today's case.

QUESTION: 
  • HOW did I know there was LA-RA Lead Reversal?


ANSWER:
My Confession: Initially — I was not at all certain about lead reversal, since ST elevation in high-lateral leads I and aVL seemed to "fit" with a picture of acute LCx occlusion causing postero-lateral OMI — BUT —
  • Rapid AFib is prone to produce transient ST depression that is maximal in the anterior leads, not due to posterior OMI.
  • AND — with LA-RA Lead Reversal, the appearance of leads I and aVR is reversed. That is, the large initial negative deflection in left-sided lead I (ie, the deep Q wave) looks perfectly consistent with what the QRS should normally look in lead aVR — and — the positive R wave with wide terminal S wave in right-sided lead aVR looks perfectly consistent with what the QRS should look like in lead I when there is RBBB.

What Happens with LA-RA Lead Reversal?
My favorite on-line Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, LITFL Lead Reversal in the Search bar — and the link comes up instantly.
  • This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
  • By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right ArmelectrodesThis is the mix-up that occurred in todays case. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-2.

Figure-2: LA-RA Lead Reversal (adapted from LITFL).



What Should the Initial ECG Look Like?
For clarity — I've taken the initial ECG in today's case ( = ECG #1A) — and inverted lead I — switched leads II and III — and switched leads aVL and aVR ( = ECG #1Bwhich is the lower tracing in Figure-3).
  • Doesn't ECG #1B now look perfectly consistent with what we might expect for this initial ECG with rapid AFib and RBBB? Note that there is now: i) A positive R wave and wide terminal S wave in leads I and aVL; ii) A deep initial negative deflection in lead aVR; andiii) An rSR' complex in lead III (instead of lead II) — as is commonly seen when there is RBBB.

  • KEY Point: Note that there is no longer any suggestion of high-lateral OMI — because with the leads correctly placed (as in ECG #1B) — there would be no ST elevation in leads I and aVL!

Figure-3: Applying the manipulations specified in Figure-2 for LA-RA Lead Reversal — reveals in ECG #1B what the initial tracing should have looked like if the LA and RA electrodes had been properly placed.


There was No Posterior OMI
Finally — I've placed the "corrected" initial tracing ( = ECG #1B) together with the repeat ECG recorded 1 hour later (Figure-4).
  • Note how this comparison confirms that there was LA-RA Lead Reversal in the initial ECG from Figure-1 — as QRS morphology in ECG #1B and ECG #2 is virtually identical!
  • As per Dr. Smith — the repeat ECG showed significantly less ST depression. The modest HS troponin elevation with lack of wall motion abnormality and excellent ejection fraction on Echo were consistent with Type-2 MI — confirming that the initial ECG did indeed give the false impression of acute coronary occlusion.

Figure-4: Comparison of the "corrected" initial tracing — with the repeat ECG done 1 hour later. The virtually identical QRS morphology between the 2 tracings confirms that there was LA-RA Lead Reversal in Figure-1. Note the amount of ST depression has decreased considerably in ECG #2 (See text).



ADDENDUM on Lead Reversal:
What has helped me over the years to rapidly recognize most cases of lead misplacement is attention to the following parameters:
  • Lead I — usually manifests a predominantly positive QRS complex, because this left-sided lead normally sees the heart’s electrical activity as traveling toward lead I. It is of course possible to have right axis deviation — but you will virtually never see an all-negative (ie, QS) complex in lead I unless there is: i) lead reversal; or ii) dextrocardia.
  • It is also extremely uncommon for there to be a very deep and wide Q wave in lead I in the presence of a QR complex in this lead. Of course, there are exceptions (ie, a large lateral MI) — but I always consider the possibility of lead misplacement whenever there is a predominant initial negative deflection (ie, a large and wide Q wave in the presence of a QR complex) in lead I.
  • IF there is global negativity” (ie, negative P wave, QRS complex and T wave) in lead I — then the diagnosis of either lead reversal or dextrocardia is virtually assured! (ie, IF lead I looks like you expect aVR to look — and aVR looks like you expect lead I to look — then suspect LA-RA lead reversal!)
  • Lead aVR — usually manifests a predominantly negative QRS complex, because this right-sided lead normally views the heart’s electrical activity as traveling away from the remote (looking down from the right shoulder) viewpoint of lead aVR. Clearly, there are instances in which the QRS manifests positive activity in lead aVR — but the finding of an all negative QRS in lead I with an all positive QRS in lead aVR is virtually diagnostic of either lead reversal or dextrocardia!
  • The P wave should always be upright in lead II when there is sinus rhythm. The only 2 exceptions (ie, when there may be sinus rhythm without the P in lead II being upright) — is when there is either lead reversal or dextrocardia.
  • Finally — the way to distinguish between lead reversal vs dextrocardia on ECG is to look at R wave progression. When there is dextrocardia — there will be reverse R wave progression (ie, a modest R wave in lead V1 will quickly become smaller and disappear as you move across left-sided chest leads). Repeating the ECG with right-sided leads when the patient has dextrocardia will normalize R wave progression.

OTHER Examples of Lead Reversal on Dr. Smith's Blog:
Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — we'll continue to periodically publish clinical examples of lead misplacement. For review — GO TO:


Monday, August 15, 2022

A woman in her 30s with several days of chest pain and an episode of altered mental status.

Written by Pendell Meyers, reviewed by Smith, Grauer, McLaren


A woman in her early 30s with history of diabetes had 2-3 days of gradual onset nonradiating chest pain with associated nausea, malaise, and shortness of breath. Then she had an "abrupt change in her mental status and became more somnolent and less responsive" at home in front of her family. Her family called EMS, who found the patient awake and alert complaining of worsening chest pain compared to the prior few days.

En route to the ED, they recorded this ECG and transmitted it, asking whether the cath lab should be activated:

What do you think?










There is sinus rhythm at just under 100 bpm. The QRS has high leftward voltage consistent with LVH more than simple healthy young voltage. There is large STE in V1-V3, as well as aVL. There is STD in V5-6, II, III, and aVF. The T waves are questionably hyperacute in V1-V4, but the QRS is also very tall and dramatic. We have very few cases of LVH with large voltage present simultaneously with anterior hyperacute T waves, but the concern is that this could be one of them. A baseline ECG would help greatly (available below).

The subtle LAD OMI vs. normal variant STE formula is not applicable due to the presence of inferior reciprocal STD and lateral STD, and because it was not trained on LVH patients. 

If you had erroneously applied the formula, it would be falsely reassuring due to the large QRS voltage present in this case:




A prior baseline was available (though I doubt it was at hand when EMS asked for a prehospital decision on the ECG above):

Baseline (assuming baseline, no clinical info available) from last year.



With the baseline (just LVH with some normal variant STE), it is obviously easy to see that the initial ECG above is LAD OMI.




Here is her ECG immediately on arrival to the ED:

Obvious STEMI(+) OMI.





An ED echo reportedly showed an anterior wall motion abnormality and grossly depressed EF.


"Given patient's change in mental status, CTA of the chest was ordered to rule out dissection." 

Meyers note: I think CT angio for dissection is unnecessary in this case, as it is in almost all OMI cases. As Jesse McLaren pointed out to me, STEMI or OMI secondary to dissection is very rare (https://pubmed.ncbi.nlm.nih.gov/28511806/), so looking for it in the absence of compelling reasons (eg focal neuro or pulse deficit) will just delay reperfusion (https://pubmed.ncbi.nlm.nih.gov/22534052/).


"While at CT scanner, the patient lost pulses and appeared to have polymorphic VT cardiac arrest, then she achieved immediate ROSC with one defibrillation."

The initial high sensitivity troponin I returned at 34 ng/L.

The CT showed no dissection.

She proceeded to cath where they found total thrombotic proximal LAD occlusion (see images below).








ECG hours after PCI:





Next day ECG:



Troponin peaked at 23,591 ng/L.

Cardiac MRI done 5 days later:

EF 35%. Severe hypokinesis of the entire septum, anterior wall, and distal/apical segments. No LV thrombus. 



Learning Points:

LVH can make OMI interpretation more difficult. It is rare to see high LVH voltage in the same leads as OMI. But this one is an excellent example.

The first troponin is minimal when the benefit of reperfusion is maximal.

Comparison to baseline, and serial ECGs, can make a difficult interpretation easy. 

Sudden syncope or "seizure" in sick patients should be assumed to be cardiac arrest until proven otherwise.

Young people and women have OMI, and like other populations they may have delayed recognition.

OMI always evolves on ECG, if you have the ECGs to see it.

Young Women do suffer from thrombotic coronary occlusion!!





===================================
MY Comment by KEN GRAUER, MD (8/15/2022):
===================================
I saw the initial tracing in today’s case ( = ECG #1) — knowing only that the patient was a woman in her 30s on her way to the ED. I presumed she must have been having chest pain — but didn’t know how worrisome the history was (or was not) for a new cardiac event. I focus my comment on this initial tracing — which for clarity I’ve reproduced below in Figure-1. My thoughts on this initial ECG were the following:
  • The rhythm is sinus at ~90-95/minute. Intervals (QR, QRS, QTc) and the frontal plane axis are normal (about +20 degrees).
  • QRS amplitudes are greatly increased — especially in the chest leads, where there is significant "lead overlap" of complexes.


Regarding Q-R-S-T Changes:
  • There are small and narrow Q waves in lateral leads (I,aVL,V5,V6) — which are almost certain to be normal septal q waves.
  • R wave progression is normal (with transition appropriately occurring between leads V2-to-V3).


The KEY Question is whether ST-T wave appearance in ECG #1 is (or is not) suggestive of an acute cardiac event.


Figure-1: The initial ECG in today’s case.


Should the Cath Lab Be Activated?
As emphasized by Dr. Meyers — assessment of the initial ECG in today’s case was complicated by the presence of LVH. It is simply not common to see the picture of markedly increased QRS amplitude, in association with hyperacute T waves in the anterior leads.
  • Dr. Meyers also emphasized that on occasion — finding a baseline tracing on the patient for comparison can be diagnostic. This was the case with today’s patient — as a quick comparison with the previous ECG left NO doubt that the chest lead ST-T wave peaking in ECG #1 was a new (and therefore acute) finding. Unfortunately, baseline ECGs are not always available at the time they are needed for initial triage decision-making of whether or not to activate the cath lab. So HOW to proceed?

I’d point out the following.
  • There are many ECG criteria for the diagnosis of LVH. I list those that I favor in Figure-2 — and discuss in detail my approach to the ECG diagnosis of LVH at THIS LINK.
  • Note addition of the patient’s age to the criteria I suggest in Figure-2. The reason for including age — is that younger adults often manifest increased QRS amplitudes on ECG without true chamber LVH. While there is no universally-agreed-upon discrete “maximal age dividing point” — I’ve found ~35 years of age to work well clinically in my experience over decades.

  • This number “35” facilitates recall — because, of the 50+ criteria for LVH in the literature — by far the most sensitive and specific criterion in my experience also involves the number “35” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥35 mm satisfies voltage criteria for LVH in adults ≥35 years of age).

  • Assessment of LVH in the pediatric population is problematic — because of the difficulty determining reliable diagnostic voltage criteria for each age group (complicated further by technical issues of ensuring precise chest lead electrode placement in these smaller body frame patients). As a result — I routinely refer to tables for assessing maximal expected amplitudes for each specific age group.

  • To “simplify life” when assessing for LVH in younger adults (ie, patients in their late teens, 20s and early 30s) — I’ve found over the years that reversing the number 35 provides a quick “ballpark” assessment criterion as to whether there is sufficient voltage on the ECG of a younger adult (ie, who is under 35yo) to qualify for “LVH” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 53 mm).

Figure-2: Criteria I favor for the ECG diagnosis of LVH. (NOTE: I’ve excerpted this Figure from My Comment at the bottom of the page in the June 20, 2020 post in Dr. Smith’s ECG Blog).


Is there Voltage for LVH in Figure-1?
The patient in today’s case was a woman in her 30s — therefore more likely to manifest increased QRS amplitude not necessarily the result of LVH. Given the challenge of confusing “amplitude overlap” in the chest leads of Figure-1 — I clarify the limits of QRS deflections by coloring the complexes in Figure-3.
  • Note that even accounting for the fact that today’s patient is a younger adult — the 53 mm criterion threshold is attained, suggesting true voltage for LVH in this younger age group patient.

  • Remember: The ECG is an imperfect tool to assess LVH. If true chamber size is needed — then an Echo (which also provides information on cardiac function) is far superior to ECG for assessment of chamber enlargement. That said — “pre-ECG interpretation likelihood” for LVH is clearly increased in today’s patient because of longstanding diabetes.

Figure-3: I’ve colored the QRS complex in 5 of the chest leads — to illustrate the actual size of the QRS complex in each of these leads. The deepest S wave is in lead V2 ( = 27 mm, as shown in RED) + the tallest R wave in lead V5 ( = 27 mm, as shown in GREENexceeds 53 mm. Note that the S wave in lead V1 is also unusually deep ( = 26 mm) — and the R wave in lead V4 is of unknown amplitude, since it is cut off by the top of the ECG paper (See text).


Final Look at the ECG in Figure-1:
I fully acknowledge that I was not at all certain from seeing the initial ECG in Figure-1 whether this patient was (or was not) having an acute event. Against an acute event was the following:
  • The patient has LVH on ECG — and as we have mentioned, it is uncommon to see hyperacute anterior T waves in association with marked LVH. Among the types of benign repolarization variants is T wave peaking that is often surprisingly tall in anterior leads in which there are deep S waves.
  • There is excellent R wave progression — with an extremely tall R wave in lead V3 (R wave amplitude is typically reduced when there is anterior OMI).
  • The QTc is at most no more than minimally prolonged (whereas acute infarction often produces significant QTc prolongation).


On the other hand — In Favor of an acute event until proven otherwise are the following:
  • Although the patient in today's case is a young adult — this woman in her 30s has diabetes mellitus (presumably for some period of time) — therefore she clearly is at greater risk of myocardial infarction at an earlier age.
  • Even accounting for LVH — the T wave in anterior chest leads is taller than is usually expected. This is especially true in lead V3 — where the 15 mm tall T wave is nearly as tall as the R wave in this lead. The "shape" of LV "strain" when seen in anterior leads tends to be the mirror-image opposite of the slow downslope-faster upslope ST depression typically seen in leads V5,V6 with LVH. It would be unusual to see such a tall, pointed T wave with narrow base from LVH as we see in lead V3.
  • Neighboring leads V2 and V4 also appear taller and pointier than is usually seen with either LVH or depolarization variants.
  • Finally, while the ST-T wave may normally be negative in lead III when the QRS is predominantly negative — there usually is not the J-point depression seen in Figure-3 (RED arrow in lead III).

BOTTOM Line: This young woman in her 30s has diabetes mellitus — and presented with a history of "worsening chest pain". While I was uncertain from her initial ECG if an acute process was ongoing — the worrisome history and questionable ECG features described above combine to clearly merit diagnostic cath to clarify the anatomy.
  • To Emphasize: Once the prior ECG became available for comparison — there no longer was any doubt that the ECG findings highlighted above were acute!

Friday, August 12, 2022

Inferior ST Elevation and Hyperacute T-waves, but Patient is Pain Free. What is going on?

A 60-something female presented with episodes of chest pain for the previous 2 days that lasted 20 to 30 minutes each.  On the day of presentation, her episode lasted much longer and she came to the emergency department.  In the ambulance, she was given nitro and her pain was relieved.  On arrival to the emergency department she was pain free.

What do you think?


Here is an ECG from 3 years prior














This is classic Wellens' pattern B morphology, and fits with the entire presentation.  

So it is Wellens' syndrome The ECG is so classic that when I saw the ECG on the system, I knew it was the full syndrome and wrote that "this patient would be pain free at this moment."  Then I confirmed that when I went to the chart.

See important description of Wellens' syndrome below.



The providers who saw the patient were concerned about inferior OMI due to the subtle STE in inferior leads, and STD in aVL.

How do we KNOW it is not active inferior OMI?  
1. The patient is completely pain free and 2. Such inferior STE, and even apparent hyperacute T-waves, are commonly reciprocal to anterior and high lateral reperfusion.

Here is a similar case: 

How do you explain these inferior hyperacute T-waves?


1 hour later:

Further evolution (deepening) of symmetric T-wave inversion in precordial leads



Angiogram:

Acute MI Non ST Elevation Myocardial Infarction .

Culprit is 90% stenosis in the proximal LAD .


After PCI:



2 days later



Wellens' syndrome 

Wellens' syndrome is a syndrome of Transient OMI (including transient STEMI) of the LAD, in which the ECG was not recorded at the time of the anginal pain, but only after sponaneous resolution of the pain, at which time the ECG shows reperfusion T-waves in the LAD distribution.  Pattern A = terminal T-wave inversion (biphasic); Pattern B shows deep symmetric T-wave inversion.  Wellens' syndrome also requires preservation of R-waves. 
Thus, in Wellens' syndrome, the patient is: 
1) Pain free after an episode of angina,
2) Has a typical T-wave inversion morphology (not all T-wave inversion is Wellens!!), 
3) Will have preserved R-waves
4) Will have evolution of the T-wave inversion, 
5) Will always have some rise and fall of troponin, 
6) Will have an OPEN artery OR good collateral circulation (the myocardium is perfused)
7) At high risk of re-occlusion (with pseudonormalization of T-waves if it occurs)

Such T-wave inversion also occurs in all the other coronary distributions.

See these posts for a variety of Wellens and mimics:





===================================

MY Comment, by KEN GRAUER, MD (8/12/2022):

===================================

An appreciation of Wellens' Syndrome is a must in emergency care. The "beauty" of this clinical entity is 3-Fold: i) Awareness of what to look for in the History and in the ECG allows diagnosis within seconds (as per Dr. Smith's instant analysis in today's case)ii) Recognition of Wellens' Syndrome tells you the anatomy (ie, accurate prediction of a high-grade proximal LAD stenosis)andiii) Recognition of Wellens' Syndrome prompts the need for timely cath and life-saving treatment
  • In addition to today's case — we've posted numerous examples of Wellens' Syndrome on Dr. Smith's ECG Blog (See the June 28, 2018 post — and the December 14, 2018 post — to name just 2 instances).
  •  
  • Unfortunately, despite the above expert commentary by Dr. Smith in today's case — Wellens' Syndrome remains a misunderstood diagnosis by all too many healthy care providers.

The History of Wellens' Syndrome:
It's hard to believe that the original manuscript describing Wellens' Syndrome was published 40 years ago! As I contemplated today's case — I thought it would be insightful to go back to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):
  • The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
  • I've reproduced (and adapted) in Figure-1 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
  • Most patients also showed characteristic changes in lead V4.
  • Most patients showed some (but less) ST-T wave change in lead V1.
  • In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.

  • Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after admission.

  • Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:
The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-1:
  • Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
  • Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep. 

Figure-1: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).


ST-T Wave Evolution of Wellens' Syndrome:
I've reproduced (and adapted) in Figure-2 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.
  • The patient whose ECGs are shown in Figure-2 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
  •  
  • Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-1 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).

  • Not shown in Figure-2 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-2). During this time — this patient remained asymptomatic and was gradually increasing his activity level.

  • Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-2: Representative sequential ECGs from one of the patients in the original 1982 article. Panel A: The initial ECG on admission to the hospital; Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing)Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).


Relevant Findings from the 1982 Article:
The ECG pattern known as Wellens' Syndrome was described 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.
  • One of the 2 ECG Patterns shown in Figure-1, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
  • Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remain normal, or are no more than minimally elevated.
  • Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.



LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.
  • We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.

  • The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).

  • What spontaneously occludes — and then spontaneously reopens — may continue to reocclude, and then reopen — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).

  • As per the above discussion by Dr. Smith — We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example, in today's case — the finding of deep, symmetric T wave inversion in virtually all chest leads in association with resolution of the chest pain immediately told Dr. Smith that the LAD had spontaneously reopened.

  • The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
  • Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
  • It is not "Wellens' Syndrome" — IF the patient is having chest pain at the time the ECG patterns in Figure-1 are seen. Active chest pain suggests that the "culprit" artery has reoccluded.
  • Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.

  • Finally — a word about the ECG Patterns of Wellens' Syndrome shown in Figure-1 is in order. Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
  • Unlike the example in Figure-1Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. This is the pattern seen in today's case — which given the history, was immediately diagnosed as Wellens' Syndrome by Dr. Smith.

In Conclusion — the 145 pts studied by de Zwaan, Bär & Wellens in 1982 continue to provide clinical insight into the nature of Wellens' Syndrome some 40 years after this manuscript was written.
  • P.S.: And sometimes — there may be a similar evolution of ECG findings indicative of acute occlusion and spontaneous reperfusion (corresponding to changes in chest pain severity) in not only anterior leads — but also in the inferior leads. As per Dr. Smith in today's case — this is not active acute inferior OMI — but rather a "reciprocal part" of the Wellens' Syndrome evolution.


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