ECG Blog #455 — VT Until Proven Otherwise?

I was asked to interpret the ECG in Figure-1 — told only that this 30-ish year old man had a history of having undergone a number of operations for CHD (Congenital Heart Disease) as a child. 

QUESTIONS:

• In Figure-1 — Is the rhythm VT — or — SVT with aberrant conduction — or — potentially neither of these possibilities?
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• IF told that this patient was hypotensive in association with the rhythm in Figure-1 — Does It Matter what the specific etiology of this rhythm is? If it does matter — Why does it matter?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~225/minute, without clear sign of atrial activity.

• QRS morphology — is obviously very abnormal because: i) There is an unusual (indeterminate) frontal plane axis (with predominant negativity in standard leads I,II,III); — ii) There is a monophasic R wave in lead V1 (consistent with RBBB conduction — but lacking the usual triphasic rsR' configuration of RBBB in lead V1); — and, iii) The QRS is essentially all negative in lead V6.
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• NOTE: In most instances — the finding of a regular WCT rhythm with very abnormal QRS morphology, and without clear sign of atrial activity in an adult has to be assumed VT (Ventricular Tachycardia) until proven otherwise. Statistical odds that such a regular WCT rhythm will turn out to be VT are ≥80%.

The above said — I was not convinced today's rhythm was VT.

• PEARL #1: The KEY feature in today's history is that this patient was diagnosed with CHD as a child, and underwent a number of operations for this. As a result — ALL bets are off as to what his "baseline" ECG might look like! Regardless of how atypical QRS morphology might be in Figure-1 — given this history of multiple surgeries for CHD, there is no predictive value forthcoming regarding QRS morphology in Figure-1 (See ECG Blog #422 for another regular WCT case with abnormal QRS morphology in an adult with CHD).
• PEARL #2: Today's case provides an excellent example for which finding a baseline ECG in this adult with CHD would clearly provide insight. It would probably tell us whether the abnormal QRS morphology that we see in Figure-1 is the result of VT vs SVT (ie, with the abnormal QRS morphology being the result of the patients underlying Congenital Heart Disease). 
• PEARL #3: The survival of children with CHD is much higher than most clinicians realize. At the present time, up to 97% of children with CHD live to reach adulthood — and over 75% of children with CHD who reach 18 years of age, go on to live past middle age (Dellborg et al — Circulation 147(12):930-938, 2023). As a result, it should not be surprising that many children who may have been diagnosed with even severe CHD — are living to later present to the ED with complications (such as tachyarrhythmias) as adults.
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• PEARL #4: Looking closer at today's initial ECG — there is a feature in favor of this rhythm being an SVT (SupraVentricular Tachycardia) instead of VT. Note that the initial deflection of the QRS in several leads is narrow (within the dotted RED ovals in leads I, aVL, V5 in Figure-2). Typically with VT — because the impulse arises from the ventricles (away from the conduction system) — the initial deflection of the QRS tends to be slower (wider) than what we see within the dotted RED ovals in Figure-2.

Figure-2: I've labeled KEY findings in today's WCT rhythm.

• PEARL #5: Figure-2 serves as a reminder of the Every-other-Beat (or in this case, Every-Third-Beat) Method for rapid estimation of heart rate. RED numbers show that in order to record 3 beats — it takes 4 large boxes (BLUE numbers). Thus, 1/3 the heart rate = 300 ÷ 4 = 75/minute X 3 = 225/minute (See ECG Blog #210 for more on the Every-other-Beat Method).
• Fast, accurate estimation of heart rate often provides an important clue to the etiology of certain arrhythmias — though in today's case, a rate of ~225/minute has no value for distinguishing VT from SVT rhythms.
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• PEARL #6: We are told that today's patient was hypotensive in association with the rhythm shown in Figure-1. As a result — it does not matter whether this rhythm is VT or an SVT, because initial treatment is the same! Synchronized cardioversion was applied — and successfully converted the patient to the bottom tracing shown below in Figure-3.
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• PEARL #7: The differential diagnosis that is most commonly cited for the regular WCT rhythm in today's case is between VT vs SVT with aberrancy. More than simply a semantic point — it's important to appreciate that the other common reason for an SVT with QRS widening is a preexisting BBB (Bundle Branch Block). This is different than QRS widening that develops because the very rapid heart rate does not allow sufficient time for recovery of conduction properties in a part of the conduction system (ie, rate-related aberrant conduction — for which a narrow QRS will be seen on the baseline tracing and with return to sinus rhythm after conversion of the fast WCT).

QUESTION:

• Now that we see the post-conversion rhythm ( = ECG #2) — Has this changed your interpretation of the cause of the regular WCT in ECG #1?

Figure-3: Comparison of the initial ECG in today's case — with the repeat ECG done after Cardioversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWER:

The post-cardioversion rhythm in ECG #2 is sinus at a rate of ~110/minute — as we clearly see upright P waves in lead II with a constant PR interval of ~0.20 second.

• Doesn't QRS morphology in the post-cardioversion tracing look very much like QRS morphology during the WCT? Although there are slight differences in QRS morphology between the 2 tracings in Figure-3 — there are many more similarities, including: i) The frontal plane axis is markedly leftward — with very similar-looking predominant negativity in leads II,III,aVF; — ii) The appearance of the monophasic R wave in leads V1,V2,V3 is virtually identical in both tracings; — and, iii) There is predominant negativity for the QRS in leads V4,V5,V6 in both tracings — with a nearly identical almost-all-negative QRS in lead V6.
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• BOTTOM Line: I interpreted the marked similarity in QRS morphology during the WCT and after conversion to sinus rhythm — as indicative of today's tachycardia being the result of an SVT with preexisting RBBB/LAHB in this 30-ish year old man with known CHD, and a history of having undergone a series of operations as a child.
• This impression could be confirmed by obtaining a previous baseline ECG on today's patient. That said, regardless of the likely supraventricular etiology of today's WCT — EP study (with potential ablation treatment) is indicated given hypotension associated with the potential life-threatening arrhythmia that we saw in Figure-1.
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• P.S.: As a technical point — the PR interval of 0.20 second seen in the post-conversion tracing in Figure-3 is not "long enough" by the standard arrhythmia definition to qualify as 1st-degree AV block. That said, the PR interval generally shortens with tachycardia. As a result — the PR interval in ECG #2 looks longer-than-it-should-be. Considering this patient's history of severe CHD as a child and the presence of bifascicular block (RBBB/LAHB) after conversion to sinus rhythm — I'd interpret this as probable indication of a PR interval conduction disturbance (and another reason for EP consultation).

 

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Acknowledgment: My appreciation for the anonymous submission of this case.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
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• ECG Blog #422 and Blog #425 — Cases with Congenital Heart Disease in Adults.
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
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• ECG Blog #211 — WHY does Aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 — Another regular WCT rhythm ...
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• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

 

 

 

ECG Blog #454 — Look for the "Break" ...

I was sent this ECG recording — and asked for my interpretation of the rhythm in Figure-1. I had little clinical information.

QUESTIONS:

• How was I able to guess the probable correct answer in less than 5 seconds?
• How was I then able to prove that my guess was correct?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

How did I Know in Less than 5 Seconds?

With experience — it takes only seconds to systematically consider the 5 KEY Parameters for interpretation of any arrhythmia by the Ps, Qs, 3R Approach (See ECG Blog #185):

• While realizing that we only have a single lead to look at in Figure-1 (and that there are times when a single-lead rhythm strip may falsely suggest that the QRS is narrow — whereas in reality, other leads clearly show QRS widening) — the QRS complex in this lead V1 rhythm strip truly appears to be narrow. So — I instantly suspected that today’s rhythm was supraventricular!
• The overall rhythm in Figure-1 looks to be Regular (at a Rate of ~85/minute) — with the exception of a “break” in the rhythm between beats #8-to-#9.
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• PEARL #1: The BEST Clue to the etiology of a complex arrhythmia tends to be found somewhere within or around any pause that you may find in the rhythm. The RED arrow in Figure-2 shows that whereas P waves were not at all obvious elsewhere in Figure-1 — because of the slight "pause" in the rhythm that we seen between beats #8-to-9 — we are able to clearly identify a P wave in front of beat #9.
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• PEARL #2: The fact that we clearly see a P wave in front of beat #9 (ie, the RED arrow in Figure-2) — should immediately raise the question as to whether this P wave might be conducting (ie, Related to neighboring beat #9) — albeit this P wave would be conducting with a very long PR interval (ie, of 0.48 second).
• We can "test" this hypothesis — by looking for other "ECG evidence" of "hidden" P waves, keeping in mind that if other P waves were to be found, that they might also be conducting with a very long PR interval.
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• PEARL #3: Looking for "hidden" P waves is tremendously facilitated (and expedited) by using calipers. The reality is that clinicians (including cardiologists) who do not use calipers will typically not be able to interpret complex rhythms such as this one in today's case.
• PEARL #4: The BEST way to find "hidden" P waves — is to determine what a "normal" QRS and ST-T wave look like — and then to carefully look at all QRS complexes and ST-T waves on the tracing. In today's rhythm — I found it easiest to identify hidden P waves by comparing the shape of the "normal" ST-T wave of beat #9 — with the subtle-but-definite deformities present near the beginning of the ST-T waves of beat #10 and beat #11 (ie, the 5th and 6th PINK arrows in Figure-2).
• PEARL #5: Knowing that the 5th and 6th PINK arrows are almost certain to be consecutive "hidden P waves" — allows us to postulate what the P-P interval might be IF there was an underlying regular atrial rhythm (ie, the P-P interval would be the distance between these 5th and 6th PINK arrows).
• PEARL #6: It is common for 2nd-degree and 3rd-degree AV block rhythm to manifest slight irregularity (that is called ventriculophasic sinus arrhythmia) — so this needs to be kept in mind as you set your calipers to the above postulated P-P interval — and attempt to "walk through" P waves through the entire rhythm strip (See ECG Blog #344 for more on ventriculophasic sinus arrhythmia).
• Do YOU see the slight-but-real deformity in the initial part of the QRS for beats #5,6,7,8 (under the first 4 PINK arrows in Figure-2)? This subtle deformity of the initial part of the QRS is notably not present in the QRS of beat #9.
• Do YOU notice that the P-P interval between these first 4 PINK arrows is virtually the same as the P-P interval between the 4th PINK arrow and the RED arrow? 

Figure-2: I've labeled selected atrial activity (See text).

PEARL #7: At this point — I was now able to "walk out" where underlying P waves were "hiding" but present throughout the entire rhythm strip ( = RED arrows in Figure-3). 

• The fact that each of the RED arrows in Figure-3 either occurs over some slight deformity in the QRS or ST-T wave, or at a place in which atrial activity might be entirely hidden by the QRS — supports my suspicion that there is a surprisingly regular underlying sinus rhythm in today's tracing!
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• To Emphasize: I have described my approach to today's rhythm in "slow motion". In practice — it took me less than 5 seconds to work through these 7 PEARLS.

Figure-3: RED arrows highlight the surprisingly regular underlying sinus rhythm that was are able to "walk out" using calipers set at the P-P interval.

Clinically: What Does this All Mean? 

• PEARL #8: Common things are common. Since we have established that there is an underlying surprisingly regular sinus rhythm — we know that at the least — there is a very markedly prolonged 1st-degree AV Block (PR interval ~0.48 second before beat #9).
• It is very common for 2nd-degree AV Block of the Mobitz I Type (also called AV Wenckebach) — to be associated with a prolonged PR interval for those beats that are conducting.
• Although most cases of Mobitz I 2nd-degree AV Block manifest fairly short groupings of beats with a clearly evident increasing PR interval until a beat is dropped — sometimes there may be very long Wenckebach cycles until the P wave is dropped. Seeing the very long PR interval before beat #9 in today's case immediately prompted me to look for Mobitz I.

PEARL #9: Support for Mobitz I in today's rhythm was immediately forthcoming by quick search for Wenckebach Periodicity (affectionately labeled by Marriott as "The Footprints of Wenckebach). As reviewed in ECG Blog #251 — several of "the Footprints" are present in Figure-3:

• The QRS complex in today's rhythm appears to be narrow (whereas the QRS is much more likely to be wide when the form of 2nd-degree AV block is Mobitz II ).
• There is a regular underlying atrial rhythm (which rules out blocked PACs as the cause for "dropped" beats).
• There is 1st-degree AV block of conducted beats — which is commonly associated with Mobitz I (the prolonged PR interval before beat #9).
• The pause containing the dropped beat is less than twice the shortest R-R interval (as seen here since the R-R interval between beats #8-to-9 is less than twice the R-R interval between beats #7-8).

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Laddergram Confirmation:

As noted — the above discussion outlines my thought process for strongly suspecting a very long cycle of Mobitz I, 2nd-degree AV Block at the etiology of today's rhythm.

• The BEST way to confirm today's rhythm diagnosis — is to prove my suspicion by being able to draw a laddergram that illustrates progressive increase in the PR interval until a beat is dropped. 

Consider the laddergram I have drawn in Figure-4:

• PEARL #10: Because there are so many beats in a long Wenckebach cycle until an on-time P wave is finally non-conducted — there will be minimal increase in the PR interval from one beat-to-the-next. As a result — it may be difficult to appreciate that the PR interval is increasing over the course of the rhythm strip.
• The BEST way to confirm a long cycle of AV Wenckebach is to look at the PR interval just before the pause (which measures 720 msec. in Figure-4) — and to compare this to the PR interval that is seen near the end of the pause (which is 520 msec in Figure-4).
• It can be seen that the PR interval then increases for the next couple of beats (to 600 — and then 640 msec. before beats #10 and 11 in Figure-4). But after these first few beats — the "increment" (ie, increase) in PR interval from one-beat-to-the-next becomes much less in a long Wenckebach cycle.
• In Figure-4 — the on-time YELLOW arrow P wave is not conducted — and this leads to the pause, after which the PR interval "shortens" to 520 msec. as the next long Wenckebach cycle begins.

Figure-4: My proposed laddergram for today's rhythm.

BOTTOM Line: Today's arrhythmia is challenging! That said — my hope is that review of the above 9 PEARLS — and increasing your comfort with the regular use of calipers will increase your confidence in knowing that with a modest amount of practice, you'll be able to dissect complex arrhythmias in a fraction of the time it used to take for interpretation without calipers.

• In "real life" — I do not use calipers to interpret simple arrhythmias, because there is no need to do so.
• There is not time to pull out calipers when the patient in front of you is "crashing" — and you need to administer emergency measures that instant.
• BUT — Today's patient was not hemodynamically unstable with this rhythm — and no matter how much time I might have spent pondering this tracing, I simply could not have definitively solved this rhythm without calipers. Using calipers — it literally took me less than 5 seconds to know with high probability that today's rhythm was a long cycle of AV Wenckebach (which I then proved was the correct interpretation with the above laddergram).

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Acknowledgment: My appreciation to Kianseng Ng (from Malaysia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• r Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #164 and ECG Blog #251 —Review of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
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• ECG Blog #404 — Walks you through a step-by-step approach to this AV block case (with links to a VIDEO of this case, and to Blog #344 for more details).
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• ECG Blog #352 — emphasizes that 1st-degree AV block with a very long PR interval may have hemodynamic consequences.

ECG Blog #453 — Is this Wellens' Syndrome?

The ECG in Figure-1 was obtained from a middle-aged man who presented with a 2 week history of progressively increasing CP (Chest Pain) with exertion. He had his most severe episode of CP the day before he was seen with this ECG. His CP was much less compared to the day before — but it had not yet completely resolved.

• An initial Troponin drawn less than 1 hour after the ECG in Figure-1 was recorded was over 10,000.

 

QUESTIONS:

• Given this history — How would YOU interpret this ECG?
• Is this Wellens’ Syndrome?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today’s CASE:

The rhythm for the ECG in Figure-1 is sinus at ~85/minute. The PR and QRS intervals are normal; the QTc appears to be borderline prolonged (counting the terminal negative part of the T waves in V3,V4). There is no chamber enlargement. 

Regarding Q-R-S-T Wave Changes:

• Small q waves are seen in each of the inferior leads. The q wave in lead III is a bit wider than usual for a normal septal q wave — so I was uncertain if these inferior q waves might be of clinical significance.
• That said — there is a definite QS complex in lead V3 (See Figure-2). This QS complex takes on additional significance because there is loss of r wave from lead V2-to-V3. As a result of this QS in V3 — I interpreted the small Q wave in lead V4 as also significant.
• Small and narrow q waves of uncertain significance are seen in lateral chest leads V5 and V6.
• R Wave Progression is delayed because of the loss of anterior forces in leads V3 and V4.

Regarding ST-T Wave Changes:

• There is ST segment straightening with slight ST elevation in lead V2.
• The ST segment take-off in lead V3 is slightly elevated and coved in shape — with sharp descent into terminal T wave negativity (BLUE arrow in this lead in Figure-2).
• Similar ST segment straightening with terminal T wave negativity continues in lead V4, and to a lesser extent in lead V5 (Blue arrows in these leads).
• There is nonspecific ST-T wave flattening in lead V6 — and in the limb leads.

My Impression of ECG #1 given Today's History:

In this middle-aged man with a 2-week history of CP — with his most severe episode the day before ECG #1 was recorded — and with reduced (but not completely resolved) CP at the time this ECG was recorded — this tracing suggests there has been anterior infarction.

• My "eye" was immediately drawn to the 2 leads within the RED rectangles in Figure-2 — which highlight the QS complex in lead V3 and the Q in V4 that indicate infarction.
• NOTE: Preservation of the initial positive deflection (that is the r wave) in leads V1,V2 — suggest the septum is still intact.
• The initial Troponin of >10,000 confirms infarction has occurred — perhaps the day before ECG #1 was recorded, since CP was most severe at that time.
• The modest amount of residual ST elevation in anterior leads, in association with terminal T wave inversion in leads V3,V4,V5 and greatly reduced CP — suggest there has been some spontaneous reperfusion.

BOTTOM Line: Clinical correlation with today's ECG point to LAD (Left Anterior Descending) occlusion, now with reperfusion T waves (in association with the reduction of CP). 

• The above said, this is not Wellens' Syndrome — because a large infarction has already occurred! (See below for full explanation).
• P.S.: Cardiac cath was performed — and showed a distal LAD "culprit" lesion that was successfully stented. Echo revealed an ejection fraction of 35-40%.

Figure-2: I've labeled the initial ECG in today's case.

What is Wellens’ Syndrome?

When we talk about Wellens’ Syndrome — It is all about timing. As reviewed in ECG Blog #350 — the clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). 

The above said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. The following are the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
• There should be no more than minimal (if any) troponin elevation. 
• There are no new infarction Q (or QS) waves. R wave progression should be preserved (so there is not loss of anterior forces).
• There may be slight (but not marked) ST elevation in one or more of the chest leads.
• There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4).
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• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" appearance).

Why Today's ECG does Not represent Wellens' Syndrome:

Appreciation of the pathophysiology of Wellens' Syndrome facilitates understanding why today's case does not qualify. 

• The characteristic biphasic T wave with rapid T wave descent into terminal T wave negativity — is indication that there has been brief total occlusion of the LAD, which has now spontaneously reperfused. This ECG finding is a "reperfusion T wave". It may look identical to the ST-T wave appearance seen after a STEMI with marked troponin elevation, that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
• The Chest Pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. The reason the patient is pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
• The reason there is no more than minimal (if any) troponin elevation with Wellens' Syndrome — is because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. In contrast, if Troponin is significantly elevated — this implies significant myocardial damage has already occurred (which by definition means you are dealing with a completed infarction — and not with the "warning" of an impending large infarction).
• For this same reason — there should not be new infarction Q (or QS) waves, which would imply completed infarction.
• The reason there is no more than slight ST elevation — is because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
• The clinical risk posed by Wellens' Syndrome — is that it is proof there has already been acute thrombotic occlusion of the LAD (albeit brief in duration and followed by spontaneous reopening of the vessel). BUT — What has spontaneously occluded and then spontaneously reopened — is at high-risk of another spontaneous reocclusion (with no guarantee that there will again be spontaneous reopening this next time that the vessel occludes).

Regarding Today's CASE: 

Reread the history in today's case (in the opening paragraph above) — and Take another LOOK at the ECG in Figure-2.

• Loss of r wave from lead V2-to-V3, so as to form the large QS complex in lead V3 (with Q wave also in lead V4) — indicates that significant anterior infarction has already occurred in today's patient, whose CP has not yet completely resolved — and whose initial Troponin value is already markedly increased (at over 10,000). This indicates completed infarction — and does not fit the definition of Wellens' Syndrome.

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Acknowledgment: My appreciation to Josep Serra Tarragon (from Tarragona, Spain) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
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• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
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• ECG Blog #326 — Reviews a case of Wellens' Syndrome that was missed.
• ECG Blog #350 — another case of Wellens' Syndrome.
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• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
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• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).

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ADDENDUM (10/26/2024): I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog).

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The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published over 40 years ago! I thought it insightful to return 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-3 — 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.
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• 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 hospital 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-3:

• 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-3: 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-4 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose ECGs are shown in Figure-4 — 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.
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• 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-3 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
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• Not shown in Figure-4 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-4). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
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• 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-4: 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).

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Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described over 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-3, 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 remained normal, or were 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).
• BUT: What spontaneously occludes, and then spontaneously reopens — may continue with this cycle of occlusion — reopening — reocclusion — reopening — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
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• Clinically: 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 — resolution of chest pain in association with reduction of ST elevation suggests that the "culprit" vessel has spontaneously reopened. And, if this is followed by return of chest pain in association with renewed ST elevation — the "culprit" artery has probably reclosed.
• 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 CP (Chest Pain) at the time one of the ECG patterns in Figure-3 are seen. Active CP suggests that the "culprit" artery is still occluded.
• 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 2 ECG Patterns in Figure-3. As suggested from data in the original 1982 manuscript, 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-3 — Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. Deep, symmetric T wave inversion per se is seen in a number of other conditions, and is much less specific for Wellens' Syndrome.

In Conclusion: The 145 patients studied by de Zwaan, Bär & Wellens in 1982 continue to this day to provide clinical insight into the nature of Wellens' Syndrome.