Sunday, September 24, 2017

Chest pain and precordial ST depression which resolve, followed by a wide complex rhythm

Here is another case written by Pendell Meyers, a G2 at Stony Brook.  As I mentioned before, Pendell will be helping to edit and write the blog.  It is edited by Smith.

This case might be quite obvious for long-time readers of this blog, but there is an interesting twist.

A male in his 50’s with no medical history presented at time = 0 complaining of chest pain for the past few hours. He was hemodynamically stable, with a normal physical exam. He had been given aspirin 325 mg via EMS. 

Here is his presentation ECG (at time = 4 minutes):

What is your interpretation?

Sinus Rhythm. There is approximately 1mm STE in aVL with reciprocal STD in II, III, and aVF. There is STD in V3-V6, with hyperacute T waves (de Winter's morphology) in V3-V6 and also hyperacute T waves in leads V5, V6, and I. This is unequivocally diagnostic of acute transmural injury to the anterior and lateral walls, with the most likely etiology being acute occlusion (or near occlusion) of a coronary artery supplying these walls, such as the LAD, large diagonal, ramus intermedius, or sometimes the LCX or its branches.

STE in the lateral leads with STD in precordial leads might lead you to diagnose posterolateral STEMI, believing that the ST depression in V3 is reciprocal to ST elevation in the opposite wall. One might also believe that posterior STEMI is diagnosed in the presence of right precordial STD with an upright T-wave, as we have in this case.

This would be incorrect for two reasons:

First, posterior STEMI does not always have an upright T-wave (see the explanation at the bottom of this post: Right precordial ST depression in a patient with chest pain). Acute posterior STEMI with persistent occlusion may present with an upright T-wave, but it may also have an inverted one. Only reperfused or subacute posterior STEMI consistently has an upright T-wave.

Second, and more important, the upright T-wave is very large. Again, posterior STEMI which is reperfused (pain gone) may have a large, hyperacute appearing T-wave ("posterior reperfusion T-waves": see 2 Examples of Posterior Reperfusion T-waves), but acute posterior STEMI with active pain does not.  

This morphology is distinctly de Winter's T-waves (article: "Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion"; here is full text).   The de Winter pattern is characterized by ST depression and hyperacute (large) T-waves in the distribution of the ischemia. This is in contrast to upright T-waves from posterior MI, and also in contrast to the inferior ST depression in this case, which is reciprocal to the STE in aVL. In de Winter's T-waves, if the ischemia worsens before reperfusion, the ST depression may evolve into ST elevation with or without hyperacute T-waves.

The physicians who read the ECG documented that they saw ST-depression in III and aVF, but that they did not appreciate any definite ST-elevation on the ECG.

A repeat ECG was ordered (time = 40 minutes):

Not much change, but perhaps slight improvement in some ST segments.

An initial troponin I returned at 0.10 ng/mL (slightly elevated) at time = 49 minutes. 

The patient reported a decrease in his chest pain. Another ECG was ordered (time = 2 hours, 7 minutes):

Definite improvement in ST segments and morphology. There remains subtle STE in aVL, now with an inverted T wave consistent with reperfusion, along with slight STD in II, III, and aVF. The decrease in chest pain and improvement in the ECG implies at least partial spontaneous reperfusion (thrombus autolysis) or reperfusion through collaterals.

Immediately following the ECG, the patient was noted to have had a change in the cardiac monitor despite no change in clinical status, and another ECG was acquired (time = 2 hours, 9 minutes):

What is happening here?

There is now a wide complex regular rhythm with a ventricular rate of approximately 75 bpm. So let's review the differential of a wide QRS:

Rate of 75 bpm is by definition not VT. The morphology does not match LBBB or RBBB, and there are no pacer spikes. No particular features of hyperkalemia or Na channel blockade, but lack of these features should not be a reason to stop thinking about hyperkalemia in particular.

Thus we are left with NSICD, cardiomyopathy, hyperkalemia, and AIVR (a benign and transient rhythm associated with successful reperfusion). For the sake of education, let us suppose for a moment that the clinical scenario was not obviously in support of AIVR (because sometimes it won't be!), and take a closer look at the ECG.

The black arrows point out some sort of atrial activity which is likely present throughout the tracing but may be hidden within QRS complexes where it is not marked by the arrows. The atrial waves do not have a fixed relationship with the wide QRS complexes, and are therefore dissociated, indicating they are competing with the wide complex rather than causing it (with an exception at the end of the ECG which we will discuss).

When there is a wide complex rhythm, you must check all the leads and the full rhythm strip to make sure that there are no QRS complexes with alternative morphology. If you do find a QRS with a different morphology (especially when it is narrower than the predominant rhythm), you should analyze it carefully for clues.

The long black line shows the duration of the predominant wide complex rhythm. If you weren't looking carefully at all 12 leads, you might not have noticed that it is interrupted at the very end, in leads V4-V6 and the associated rhythm strip below. As sometimes happens, the change in QRS morphology and width is not easily seen in the rhythm strip, and is only revealed in leads V4-V6. There are two QRS complexes which have differing morphology from the prior predominant wide complex rhythm, marked with red and then green arrows. These QRS complexes are narrower than the prior wide complex rhythm; in fact, the QRS marked with green arrows is very narrow.

The finding of a truly narrow beat is important for the differential. Hyperkalemia present on a cellular level cannot vary on a second-to second basis. If hyperkalemia is so severe to cause acute widening of the QRS complex, you cannot possibly conduct a single truly narrow QRS complex beat in the middle of your hyperkalemia-widened rhythm. The same is true for Na channel blockade, severe acidosis, and cardiomyopathy. Bundle branch blocks, on the other hand, can sometimes vary on this time frame, as they are an "all-or-nothing" event that depends whether that single cell in the bundle branch was refractory or not at the precise instant the action potential arrived and asked permission to proceed down the bundle branch.

Also, when you find a narrow beat like this among a wide complex rhythm, you should compare to a prior ECG if available. If you compare the green QRS complexes V4-V6 with the same leads from the prior ECG before the wide complex arrhythmia, you'll see they are identical in width and morphology:

The QRS complex marked by green arrows has identical morphology to the patient's prior normal sinus rhythm.

It appears as though the atrial activity which had been competing (and "losing") against the wide complex rhythm, begins to take back over at the end of the ECG (and/or the AIVR is subsiding). As it starts to do so, it creates a fusion beat (QRS marked by red arrows) which results when a supraventricular action potential merges in the ventricles with a ventricular action potential. In the very next beat, the atrial activity comes early enough to usurp the AIVR beat and thus to produce a fully supraventricular QRS complex [narrow and with identical morphology to prior (green arrows)]. 

As previously alluded to, this is an accelerated idioventricular rhythm (AIVR), which is a classic but relatively unusual sign of reperfusion. It often has a stereotyped morphology with very large/tall monomorphic positive complexes in the inferior leads, with the obligatory reciprocal ST-segment and T-wave changes that come with any abnormal QRS complex.

Back to the case:

The second troponin returned elevated at 4.98 ng/mL at time = 2 hours, 28 minutes. No further troponin measurements are available.

The patient was noted to be pain free at this time. Cardiology was called due to the elevated troponin and came to see the patient.

Another ECG was obtained at time = 2 hours, 37 minutes:

Continuing reperfusion with decreasing ST deviations and normalizing T waves, but persistent inverted (reperfusion) T wave in aVL.

Continuing reperfusion with decreasing ST deviations and normalizing T waves, but persistent inverted (reperfusion) T wave in aVL.

He was then taken to the cath lab at time = 3 hours, 24 minutes. They found “an acute, 75% occlusion of D1 (this means the first diagonal artery off of the LAD, which can often be quite large) with thrombus, with no other significant disease.” 

This finding is consistent with the suspicion that he had total or near-total occlusion at the time of pain and at the time of the first ECG. 

Despite all the ECG findings, the final ED note says: “...Mr. _____’s acute chest pain was the result of an NSTEMI.  He had anterior T wave abnormality and ST-depression without ST elevation on his EKG.  He had elevation of troponins and CK-MB.  This rise in troponins without ST elevation is diagnostic of NSTEMI.”

Take Home Messages:

  • Recognizable acute coronary occlusion is missed frequently due to poor ECG interpretation, and in this case resulted in at least a 3-hour delay in necessary reperfusion therapy.
  • In the presence of active symptoms (e.g., chest pain), ST depression followed by a large T-wave in the precordial leads is a sign of occlusion of the LAD or one of its large branches, and these are referred to as "de Winter's T-waves." 
  • Fortunately, sometimes when these ECGs are missed, the thrombus "autolyses" and the artery reperfuses without therapy (or as a result of aspirin). Luckily, this patient reperfused during the delay.
  • Acute coronary occlusion frequently does not manifest the ST elevation millimeter criteria for diagnosis of STEMI.
  • ST-depression in a coronary distribution should activate a "hard stop" in your mind to look for signs of acute coronary occlusion (ST elevation, even if minimal) in the opposite (reciprocal) distribution.
  • AIVR is a rare clue that also points toward the diagnosis of reperfused acute coronary occlusion.
  • Understanding of the differential for a wide QRS complex and recognition of common QRS patterns is key to ECG interpretation.
  • Breaks in the rhythm and interjecting narrow complex beats contain vital clues to the evaluation of a wide QRS complex rhythm.

Here are 10 more cases of de Winter's T-waves.

These cases are particularly interesting:

A Hybrid of de Winter's T-waves and Diffuse Subendocardial Ischemia: Left Main Ischemia


  1. Thanks - excellent case and ECGs.

    I suspect the final ED note was a subconscious effort to reduce cognitive dissonance. No senior clinician wants to have missed a "STEMI", therefore, calling it an "NSTEMI" easily avoids the anxiety involved with the former.

    I see it often.

    1. I agree! However, it is not "by definition" a STEMI. It is certainly pathophysiologically equivalent to a STEMI.

  2. Very nice case, with special credit to Pendell Meyers for his detailed evaluation. I’ll add a few thoughts. i) It is important to recognize DeWinter T waves — because once you see them in a patient with acute symptoms (as in this case) — your diagnosis should become obvious. This case is an extreme example — because overly large and much-fatter-than-usual T wave peaks are seen in no less than 4 chest leads, all of which show J-point ST depression. Often with DeWinter T waves, one will not see such an obvious picture, and the “too-fat-too-tall T waves may only be present in one or two chest leads — and you may not always see the obvious J-point depression that we see here. So, just like the Brugada ECG pattern — the image of DeWinter T waves (that was missed by more than one physician in this case) should be “engrained” in the brain of all emergency providers. ii) One confirms the presumed diagnosis of DeWinter T waves with acute (or impending or intermittently-fluctuating) LAD occlusion by findings in the limb leads — including looking for ST elevation in lead aVL (which is really an anterior, not a lateral lead) — and reciprocal ST depression in the inferior leads. These findings are marked in this tracing (also with a hyperacute ST-T wave in lead I). iii) NOTE — ALL tracings in this case show large QS complexes in leads V1-thru-V4! While true that one sometimes cannot distinguish between anteroseptal injury that is recent vs old — in the context of this patient with recent-onset chest pain and the dramatic ongoing ST-T wave changes — this LOSS of anterior wall R waves is highly relevant. iv) In my experience, AIVR and/or end-diastolic (ie, end-cycle or late-in-the-R-R interval) PVCs are not rare, but surprisingly common when looked for during the process of acute coronary occlusion following by reperfusion. These clues are often missed, because they tend to be transient and short-lived. Pendell’s chart very nicely displays the differential diagnosis of regular wide rhythms — but important to emphasize that in the context of new chest pain + DeWinter T waves, that this slower form of ventricular tachycardia (ie, AIVR) virtually confirms that there has been reperfusion. v) GREAT points by Pendell regarding AV dissociation — and his skillful use of simultaneously-recorded leads V4,V5,V6 to confirm fusion. In fact — the degree of fusion varies for the last few beats on this tracing. This is logical because the PR interval preceding the 2nd-to-last beat is a bit shorter than the PR interval preceding the last beat (on the colored-arrow diagram) — which is why the last beat most resembles sinus-conducted complexes. vi) The importance of AV dissociation and/or fusion beats during a regular wide tachycardia — is that seeing this finding confirms ventricular etiology. Unfortunately, most fast VT (which are the cases for which we tend to need the most diagnostic help) usually does not show these findings. Instead, slower forms of VT (such as AIVR) in which there is more time for sinus P waves to “peak through”, is when we most often are able to appreciate AV dissociation. viii) Note how deceptively narrow the QRS is throughout the long lead V1 in the colored-arrow diagram. This point that Pendell made deserves to be repeated — because it emphasizes how even in VT one can be fooled into thinking a rhythm is supraventricular if only a single monitoring lead is used. “12 Leads are Better than One” — so essential in hemodynamically stable patients whenever there is doubt about the etiology of a tachyarrhythmia to get a 12-lead recording. Again — GREAT case by Dr. Smith, with superb teaching by Pendell Meyers!

  3. Does the first ekg in lead v1 and v2 have a brugada type appearance? How does thos fit with the rest of the ekg. I appreciated all your finding immediately. But the brugads appearance seemed unusual.

    1. I see what you're describing. Notice that V1 in this case is almost identical to this prior post of a (very atypical) Brugada pattern ECG:

      V2 looks more like a small amount of "saddleback" ST elevation, and it does not have a wide enough beta angle for type 2 brugada, see this post for further details:

      Overall there is a morphology that slightly reminds you of type 2 brugada, but the details that make it true brugada pattern are missing, and the clinical scenario makes these findings almost irrelevant. Some people simply have V1 and V2 that look like that at baseline.

  4. an extraordinary case, and detailed review and analysis by three fellows i highly respect, steve, pendell, and dr ken.
    you guys are amazing.

    very cool case. unfortunate, but cool. thank you.


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