Not all new T-wave inversion signifies ischemia. Also, what is this irregular rhythm?

 This ECG was texted to me with the question "Wellens'?"

The computer read was: 

Atrial Fibrillation, marked ST Elevation. ***Acute MI***

The QT interval is short (377 ms, QTc = 399 ms)

This is NOT atrial fibrillation: 

There is sinus arrhythmia with an accelerated junctional rhythm that competes with the sinus node and results in some AV dissociation (no AV block!).  

This is completely benign.

I responded: This STE with T-wave inversion looks like a normal variant for an African American.  I would check the troponin, but I do not think it is pathologic.

Here is the history: The patient was being arrested for possession of methamphetamine, was sleepy, and when awoken endorsed some active chest pain.  

Then he wrote: "These are new changes compared to 4 months ago."

I went into the chart to find that previous ECG:

QT = 365 ms, QTc = 409 ms

First: if there are no symptoms of ACS, it cannot be Wellens' syndrome.  It is hard to say if this patient had symptoms.  Wellens is a syndrome, not an ECG finding, and it requires Anginal pain that is resolved at the time of the ECG, Typical T-wave inversion, and preserved R-waves.  False positives are very common when there is high QRS voltage (as here).  

This previous ECG shows typical benign ST elevation in leads V2-V4 (mimicking anterior STEMI) and large QRS voltage.  However, the STE is typical for this degree of voltage.  If you were to use the 4-variable formula for this, you would get a value of 14.74 which is extremely low and extremely unlikely to be due to LAD occlusion.

This short QT interval is an important clue that this is not Wellens', which almost always has a QT over 400 ms.

It is not uncommon for ECGs like this to have new, but benign, T-wave inversion.  One must check troponins, but if they are negative, this is not an ECG that is high risk and that should prompt further workup in spite of negative troponins.  This is especially true when there are no symptoms that are typical for ACS.

My response was: I see you have already measured 3 troponins and they are all truly negative. 

[This was high sensitivity troponin I, Abbott, and all values were 5 ng/L (very low, without any delta)].  That all but proves that this is not an ischemic ECG.  It is just a fact of life that new T-wave inversions can be normal.

Finally, the fact that this patient seemed to have active chest pain is very strong evidence against Wellens'.  However, this can be very confusing because unstable angina may have active T-wave inversion during pain that resolves when the pain resolves.  (The big difference is that the T-wave normalizes as pain goes away.  With Wellens', if pain recurs and the T-wave normalizes, then the artery is re-occluding!)

See several examples of T-wave inversion due to unstable angina here: 

Dynamic, Reversible, Ischemic T-wave inversion mimics Wellens'. All trops negative.

He had recorded a 2nd ECG:

This shows and even more profound sinus arrhythmia and again an accelerated junctional rhythm, which results in AV dissociation (again, no AV block!)

I guess he was not convinced, so he admitted the patient.

A formal echo was done and was normal.

All hs troponin I were = 5 ng/L.

Learning point

It is a fact of life that new T-wave inversions can be normal and the etiology is not always clear.  It takes a lot of experience in pattern recognition to know what is benign and what is not.  It is especially true that when there is a lot of QRS voltage, there is commonly T-wave inversion that mimics Wellens'

Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)

2 Cases of Resolved Chest Pain with Dynamic Terminal T-wave Inversion

Dynamic, Reversible, Ischemic T-wave inversion mimics Wellens'. All trops negative.

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MY Comment by KEN GRAUER, MD (10/9/2020):

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Dr. Smith reviews a number of important points about the series of 3 ECGs presented in today’s case. I’ll limit my comments to some additional points of interest, with focus on the initial ECG. For clarity — I’ve reproduced this initial ECG that was texted to Dr. Smith in Figure-1.

TAKE another LOOK at this initial ECG ( = ECG #1 in Figure-1):

• Is there LVH in ECG #1? WHY is this an important question to address when considering the diagnosis of Wellens’ Syndrome?
• WHAT is the cause of AV dissociation in ECG #1?
• Do we know for certain that this patient does not have any AV block? IF not — HOW could we confirm that there is no AV block?
• WHAT is unusual about the escape junctional pacemaker in ECG #1? What useful clinical information does this unusual feature suggest?

Figure-1: The initial ECG in today’s case (See text).

POINT #1: As per Dr. Smith — the diagnosis of Wellens’ Syndrome requires a prior history of anginal chest pain, that has usually resolved at the time the ECG is recorded. The characteristic ST-T wave abnormalities of Wellens’ Syndrome are the result of transient occlusion of a major coronary artery, with spontaneous reperfusion before significant infarction has occurred.

• The “goal” of recognizing Wellens’ Syndrome — is to intervene in a patient with a critical proximal LAD narrowing before infarction occurs. If anterior Q waves (or QS complexes) are already present — then the infarct has already occurred, which means it is too late for such an ECG to represent “Wellens’ Syndrome”. KEY Point — ST-T waves that look the same as those in true Wellens’ Syndrome may be seen as a result of reperfusion after an MI. Such reperfusion T waves are not Wellens’ Syndrome — because the infarct has already occurred.
• For insight into how the ECG pattern of Wellens’ Syndrome evolves — Please see our June 28, 2018 post.

POINT #2 in Today’s Case: ST-T wave changes that look similar to those seen in true Wellens’ Syndrome may also be seen with LVH. It’s therefore important to recognize ECG criteria for LVH.

• I’ve reviewed in detail a user-friendly approach to the ECG Diagnosis of LVH in My Comment at the bottom of the page in the June 20, 2020 post of Dr. Smith’s ECG Blog. For clarity — I’ve reproduced the Figure with Voltage Criteria for LVH that I favor (taken from this 6/20/2020 post) below in an ADDENDUM to today’s post ( = Figure-4 below).
• To facilitate seeing just how increased QRS amplitude is in ECG #1 — I’ve colored in the overly large R waves and S waves that are overlapping in leads V3-thru-V6 (Figure-2). It should be obvious that several criteria for LVH from Figure-4 are satisfied: i) Deepest S in V1,V2 (17 in V2) + tallest R in V5,V6 (21 in V5) ≥ 35 mm; ii) R wave in lead V6 ≥18-20 mm ( = 20 in V6); and, iii) Peguero Criteria = Deepest S in any chest lead + S in V4 ≥28 mm (24 in V3 + 24 in V4 = 48 mm!). 
• NOTE: Peguero criteria use ≥23 mm for women; ≥28 mm for men. And, if the deepest S is in V4, then double this value — so the value of 48 mm in today's patient far exceeds the required 28 mm criterion that satisfies LVH in males.
• While it clearly is possible for patients who have LVH to also have Wellens’ Syndrome — it turns out that most patients with marked LVH who manifest anterior T wave inversion will have their T wave inversion either as a result of their LVH and/or as a type of repolarization variant (as was true in today’s case).
• CAVEAT: Younger adults (ie, less than 30-35 years old) often have increased QRS voltage not necessarily due to LVH. Since we were not told the age of the patient whose ECG is shown in Figure-2 — it’s impossible to know if this age caveat applies to today’s case.

POINT #3: The cardiac rhythm in ECG #1 is interesting and complex — but I’ll emphasize that it should take no more than minimal time to recognize that this is most likely a benign rhythm. The 2 most helpful TIPS for me in evaluating challenging rhythm disorders such as this are to: i) Use Calipers (it is virtually impossible to assess this rhythm without calipers!); and, ii) Find and label the P waves (colored arrows in Figure 2). Using calipers speeds up your analysis (and instantly improves accuracy) — and labeling P waves almost "magically" facilitates recognition of which beats are likely to be conducted.

• NOTE: I presented a case with a similar type of rhythm in great detail in the January 31, 2019 post of Dr. Smith’s ECG Blog. I recommend review of that post to anyone desirous of more practice in assessing arrhythmias like the one in today's case.

On To Rhythm Analysis of ECG #1:

• By the Ps, Qs & 3R Approach — P waves are present but irregular — the QRS complex of all beats in this tracing is narrow — the atrial/ventricular rate varies from ~55-85/minute — and, some P waves conduct, but others don’t.
• Moving on to What We KNOW: Beats #1,2; and 7,8 and 9 appear to be sinus conducted — because each of these beats is preceded by a P wave with a constant and normal PR interval (RED arrows in the lead II rhythm strip in Figure-2).
• The P wave preceding beat #6 (BLUE arrow) has too short of a PR interval to be conducted normally. Since the QRS complex of beat #6 is narrow and looks similar to sinus-conducted beats — beat #6 must therefore be a junctional beat.
• An unmistakable notching is seen to occur immediately after the QRS complex of beats #3,4,5; and 10, 11 (PURPLE arrows). Given the slightly changing location of these notches (with respect to the QRS that precedes them) — and given the lack of anything resembling this notched shape in sinus-conducted beats — these notches (PURPLE arrows) must be P waves occurring within (and just after) the QRS of these beats.
• Since none of the P waves represented by the PURPLE arrows could possibly be conducting (since they all occur after the QRS begins) — this means that beats #3,4,5; and 10,11 are all junctional beats (ie, None of these beats are preceded by P waves).
• By definition — since none of the P waves highlighted by the PURPLE and BLUE arrows are conducting (ie, none of these P waves are related to their neighboring QRS complexes) — this means there is AV Dissociation during a portion of this rhythm strip.
• BUT — Since none of these non-conducting P waves ever have a “chance” to conduct (ie, because they either occur at the beginning of the QRS, during or immediately after the QRS) — this means that there is NO evidence of AV block seen in ECG #1.
• KEY POINT: The fact that we see no evidence in ECG #1 of AV block does not prove that this patient does not have any AV block! In order to prove this — We would have to see P waves occurring at all points in the cardiac cycle (which means we would need a much longer period of monitoring). All we can say from the long lead II rhythm strip that we see in Figure-2 — is that there is an underlying sinus rhythm with transient AV Dissociation, but no evidence of AV block seen on this tracing.

Figure-2: I’ve colored in large-amplitude overlapping complexes — and I’ve labeled P waves in ECG #1 (See text).

WHY is there AV Dissociation in ECG #1?

• I reviewed in detail in the January 31, 2019 post the 3 Causes of AV Dissociation. The cause of AV dissociation in ECG #1 is not the result of AV block. Whether the cause is “usurpation” (by an accelerated junctional rhythm) or “default” (by slowing of the underlying sinus rhythm) or some combination of these two possibilities, depends on the rate of the sinus and junctional rhythms.
• There is marked sinus arrhythmia in ECG #1 (ie, the rate of the colored arrows varies from ~55-to-85/minute).
• The R-R interval preceding the 6 junctional beats in ECG #1 is also not regular — with this corresponding to a junctional rate varying from ~64-73/minute. This suggests that the cause of AV dissociation in ECG #1 is a combination of “default” (Note sinus slowing after beat #2) — and — “usurpation” (The rate of all junctional beats is faster than the usual junctional escape rate of 40-60/minute).
• KEY POINT: Most of the time — the junctional escape rate will be regular. The fact that the junctional rate varies to the degree seen here, in association with this marked degree of sinus arrhythmia — suggests a significant increase in vagal tone. While we saw no evidence of vagotonic AV block in any of the 3 tracings shown in today’s case — it is important to be aware of this unusual cause of various forms of AV block that may sometimes be seen in otherwise healthy patients who manifest evidence of increased vagal tone. This means that even IF additional rhythm monitoring of today’s patient did reveal some evidence of AV block — the chances are excellent that this would still be a benign rhythm! (CLICK HERE — for more on the entity of Vagotonic Block).

For clarity — I conclude with a laddergram for the rhythm in ECG #1 (Figure-3).

Figure-3: Laddergram for the rhythm in ECG #1 (See text).

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Figure-4 = ADDENDUM: Criteria for LVH voltage that I favor. For more on my user-friendly approach to ECG Diagnosis of LVH — Please check out My Comment at the bottom of the page in the June 20, 2020 post on Dr. Smith’s ECG Blog.