Tuesday, January 30, 2018

Bizarre (Hyperacute??) T-waves

Thanks to one our great HCMC nurses, Ryan Burch.  He figured this one out.

A dialysis patient presented with dyspnea.  He was a bit fluid overloaded and not hyperkalemic.

 This ECG was recorded:
This was sent to me in a text that woke me from sleep, but not simultaneous with patient care.
Truly bizarre T-waves in I, aVL, III, aVF, aVR
Lead II is unremarkable, and leads V3-V6 are also slightly bizarre.

What do you think?

My answer, as I looked with bleary eyes at my phone: "I have to say I've never seen this one before."

Later, I looked into the chart and found an ECG from a few days before:
I texted back:
"Those T-waves were gone 5 minutes later.  Artifact!"

Ryan Burch, RN, was the nurse caring for the patient, later sent me the same ECG, stating the following:

"This ECG had people stumped and concerned but I read an article in www.ecgmedicaltraining.com (see below) about an artifact a few weeks prior which I thought looked similar and the suggestion was that a lead had been placed over an artery.  I switched lead placement and this ECG was recorded 5 minutes later:"

He found that the left arm electrode had been placed near the patient's left arm dialysis fistula, which was pulsating with a palpable thrill.

This resulted in the following:
Wandering Artifact only


All leads are derived from 3 bipolar electrodes and one unipolar electrode.
Leads I, II, and III depend on bipolar leads voltage differences:
--Lead I uses the right and left arm
--Lead II uses the right arm and the leg
--Lead III uses the left arm and the leg.
--The Wilson (or Goldberger) Central Terminal is used to produce the augmented (a) leads:
aVR, aVL, aVF.
  • The voltages are calculated as follows (thanks to Ken Grauer for sending these):
  • I = L - R
  • II = F - R
  • III = F - L
  • aVR = R - (L + F/2)
  • aVL = L - (R + F/2)
  • aVF = F - (R + L/2)
As you can see, the only lead that does not use the left arm electrode is lead II.  Since lead II is the only normal lead in this ECG, the left arm electrode must be the affected electrode.  Indeed, the patients dialysis fistula was on the left arm and was pulsating with each heart beat, moving the electrode and causing artifact.

Arterial pulse tapping artifact


This online article references the article below by Emre Aslanger, a great guy who occasionally corresponds with me about ECGs.

Aslanger E, Yalin K. Electromechanical association: a subtle electrocardiogram artifact. Journal of Electrocardiology. 2012;45(1):15-17. doi:10.1016/j.jelectrocard.2010.12.162.

Incredibly, this case was just published in Circulation on January 22, 2018 (thanks to Brooks Walsh for finding this!) 
Asymptomatic ST-Segment–Elevation ECG in Patient With Kidney Failure.   https://doi.org/10.1161/CIRCULATIONAHA.117.032657.  Circulation. Originally published January 22, 2018

Here is a case from Circulation year 2000 that was misdiagnosed as due to pancreatitis.  But you can tell from the normal lead III that this was a right arm electrode problem:

It is full text!! 

Why is there also artifact in precordial leads?
Aslanger explains:
“[O]ne may expect that the leads not connected to the electrode affected by the source of disturbance would be free of distortion; but this is not the case. When one of the limb electrodes is affected by a source of disturbance, it distorts not only the corresponding derivation but also [the others] which are all calculated by mathematical equations…”
“…precordial leads [are also affected] because the Wilson central terminal, which constitutes the negative pole of the unipolar leads, is produced by connecting 3 limb electrodes via a simple, resistive network to give an average potential across the body.”

Sunday, January 28, 2018

Is this ECG diagnostic of coronary occlusion? Also: Inferior de Winter's T-waves on prehospital ECG??

This post was written by one of our fantastic Hennepin County Medical Center Emergency Medicine interns who is an ECG whiz, Daniel Lee.

A man is his late 50’s presents to the ED with 1 hour of post exertional chest pressure associated with diaphoresis and nausea.  He has a history of known CAD, diabetes, and dyslipidemia.

By pure clinical appearance, he looked like the textbook patient with acute MI.

This is his first ECG in the department, which I saw as it was being printed:
What do you think?

Here is his previous ECG:

This was my interpretation of the first ECG:
Sinus bradycardia with less than 1mm ST elevation in V4-V6, elevated compared to the previous ECG, suggestive of lateral MI.  Looking to the high lateral leads, instead of ST elevation that one might see in a lateral MI there is subtle ST depression in aVL less than 1mm along with new T-wave inversion.  
Leads II, III, aVF show about 0.5 mm ST elevation that is new compared to the previous ECG.  Furthermore there is a new positive T wave in lead III.  
Subtle changes, but with the history is very nearly diagnostic of acute inferior MI. 

Let's look at the 2 ED ECGs side by side:
Limb leads
Now you can see the differences more clearly

Precordial Leads

Acute ECG on the left, with slight STE in left precordial leads, 
compared to the previous ECG on the Right.

This patient had had two prehospital ECGs recorded, and these were viewed:
30 minutes after reported onset of pain:
Sinus rhythm with only a small amount of elevation in V5 and V6.  No ST elevation in the inferior leads, no T wave in III, no ST depression in the lateral leads.
T-waves are small in inferior leads.
This is a negative ECG.

10 minutes after first prehospital ECG, with continued pain:
Smith comment: This shows ST depression in multiple leads, most pronounced in V2-V4.  This is very suggestive of posterior MI.  
There is also some subtle ST depression in II, III, and aVF, and it is followed by T-waves of increased size over the previous.  

Notice how useful serial ECGs are!  

More Smith comment: it is true that ST depression (STD) due to subendocardial ischemia does not localize [it is usually diffuse ST depression, in multiple leads and not reciprocal to ST elevation in an opposite territory], this ST depression is different! The STD in V2-V4 is almost certainly reciprocal STD, reciprocal to STEMI in the posterior wall; this is evident because it is maximal in V2-V4, not in V4-V6.  

So what is the STD in II, III, and aVF?  While de Winter's T-waves have only been described in the LAD territory, there is no reason that they might not also exist in other territories.  Since this is upsloping ST depression followed by an enlarged T-wave, I believe these are Inferior de Winter's T-waves.

There is evidence that de Winter's T-waves really represent a tiny trickle of blood through the thrombotic stenosis.  There is enough limitation of flow to cause subendocardial ischemia with ST depression, and even enough limitation of flow to have hyperacute T-waves, but too little flow to have ST elevation!  I believe this based on much experience of seeing dynamic changes from STE to deWinter's and back again and correlating this with angiograms.

So this is an infero-posterior MI, with affected leads inferior (de Winter's and later STE), posterior (STD V2-V4), and lateral (STE V4-V6).

The interesting thing is that they manifest ischemia at different times:

--When there is clear ST depression of posterior MI in V2-V4, and inferior de Winter's T-waves, there is no ST elevation in V5 and V6.
--When there is STE in V4-V6, and in inferior leads, there is no ST depression in V2-V4.


The ED ECG in the context of the prehospital ECGs was indeed diagnostic of acute coronary occlusion.

Cath Results:

The cath lab was activated and co-culprit lesions were found: 99% circumflex and 95% right coronary artery (RCA).  Both were stented.

Peak troponin was (0.446 ng/mL) -- very low due to rapid reperfusion.

Subsequent echo showed no wall motion abnormality.

Learning Points

Lead aVL is incredibly useful.  New ST-depression (without LBBB or LVH) in aVL that cannot be blamed on an abnormal QRS is worrisome, and in the context of a patient with acute chest pain is almost certainly due to ischemia.  In patients with suspicion of acute MI who have any ST elevation, aVL is also a very useful lead to differentiate between pericarditis and MI.

This paper by Bischof and Smith compared inferior MI to pericarditis and found that of 154 patients with inferior STEMI, 17% of whom had less than 1 mm of STE in any inferior lead, all 154 had at least 0.25 mm ST depression in aVL.  Among 49 patients with pericarditis who had inferior ST elevation, zero of 49 had ST depression in aVL (though there are always rare exceptions such as this case).  Interestingly this study also looked at 54 “subtle” inferior MI’s, and of these 49 had some ST depression in aVL.  Thus it is not surprising that the current case of subtle inferior MI had ST depression in aVL. Moreover, T-wave inversion in aVL was also found to be 100% sensitive and 86% specific for inferior STEMI.

Here is a magnified in view of aVL side-by-side with the baseline ECG.
Presenting with STD and TWI
Old with no STD

In additions, this paper also found that all 33 patients with inferolateral MI, as manifested by STE in V5 and V6, still had ST depression in aVL.  V5 and V6 are caudal to aVL and so an inferior ST vector towards lead aVF is also slightly towards V5 and V6 but away from aVL!!  So V5 and V6 will have some ST elevation while aVL has ST depression.  Thus, even inferolateral MI has reciprocal ST depression in aVL.   

This patient functionally had an inferolateral MI given his two culprit lesions and in retrospect the elevation in leads V4-V6 were indicative that there was lateral wall involvement as well.  The lateral involvement may also explain the very subtle nature of the acute ECG findings given that much of the voltage in inferior and lateral occlusions are directly opposed to each other. 

This is the post cath ECG:
Resolution of ST depression and T wave inversion in aVL, as well as the new T wave that had been present in III.  There is some residual ST elevation in the inferolateral leads.

Summary of Learning Points:
1. New ST depression and T wave inversion in lead aVL is highly suggestive of inferior MI.
2. Even very subtle inferior MI will likely have ST-depression in aVL.  These ECGs must be scrutinized very closely!
3. Inferolateral MI will have ST depression in aVL in addition to ST elevation in V5 and V6.  
4. de Winter's T-waves may occur in any coronary distribution.

Friday, January 26, 2018

Our patients deserve better than the "STEMI criteria"

Written by Pendell Meyers, of the Stony Brook class of 2019, with edits by Steve Smith

Two Cases

Imagine that two patients present simultaneously to your Emergency Department with moderately concerning chest pain and the following ECGs (no priors available).

The first patient has this ECG:

The second patient has this ECG:

Do either of them, neither of them, or both, require emergent reperfusion therapy?

STEMI guidelines (and therefore most clinicians) provide you with a clear answer. Clear and yet perfectly wrong in these two cases.

Let's take them one at a time.

Case #1

A woman in her 50s presented with 2 weeks of fatigue and chest heaviness that started several hours prior to arrival. She stated that she had been diagnosed with influenza 2 weeks ago and had felt worse today with new chest heaviness, so she went to an urgent care facility where she was sent to the ED for an abnormal ECG.

Here is her initial ECG on arrival, complaining of active chest heaviness:
What do you think?

The ECG shows sinus bradycardia with deep wide Q waves and a large amount of ST elevation in the  inferior leads, with reciprocal depression and T-wave inversion in aVL and I. There are also Q waves in V4-V6 with ST elevation and relatively large T-waves. There is no ST depression in V2-V3, but there is a biphasic T-wave in V2.

I showed this ECG to Dr. Smith with no other information. He immediately replied: "normal variant or LVH." We knew this was not acute coronary occlusion, despite the features listed above. I thought the Q waves might be indicative of prior completed inferior MI, but I did not think the morphology looked consistent with even subacute MI. I felt that there was absolutely no evidence of acute coronary occlusion on this ECG.

Why we can say that it doesn't look like ACO despite these objective features is difficult to explain. 

The best answer is that you simply have to see thousands of ECGs and correlate which ones turn out to be ACO and which are false positives. When you do that, you will have seen this ECG many times. The first few times you will be fooled, and then you will learn why it's not ACO.

For those that want a less accurate but more concrete explanation, here are a few points to consider:

1) When there is ST elevation in inferior leads with reciprocal ST depression in aVL, inferior MI is all but diagnosed, unless this STE and STD is preceded by an abnormal QRS! (no LVH, no LBBB, no paced rhythm, no WPW, and no abnormal Q-waves)

Any abnormal depolarization causes abnormal repolarization. Here there is markedly abnormal depolarization with large and deep Q waves inferiorly. No matter what the cause of these Q waves, whether it be old MI, LVH, or a normal variant, they all cause abnormal repolarization. Usually this manifests as ST and T-wave deviation in the opposite direction of the largest/widest abnormality in the QRS ("appropriate discordance"). Such deep Q waves will frequently generate ST elevation and reciprocal changes in the opposite leads.

2) Another important feature that makes it NOT look like MI is the extreme concavity of the ST segments, such that the base of the T-wave is narrow, causing some peaking of the T-wave.

3) There is a small slurring of the end of the QRS complex in some leads, consistent with a J-wave. This is not a perfect rule, but it is very rarely found in true ACO.

The clinicians were alarmed by the ECG findings (as is recommended by all available guidelines), and activated the cath lab. Here are the cath images:

Normal left main, LAD, and LCX.

Normal RCA.

Her catheterization showed completely normal coronary arteries. She had three consecutive negative troponins. Echo was completely normal, no evidence of LVH or any wall motion abnormalities. Extended viral panel was negative.

This is always the most interesting part of the chart review for me, when the clinicians struggle to reconcile normal results with the intense mobilization of resources used and an ECG that they cannot bring themselves to consider a possible normal variant: The clinicians concluded that the patient has "viral myocarditis."

Smith comment: this is NOT myocarditis.  First, the ECG is a normal variant.  Second, myocarditis will always have a positive troponin.

I find it highly unlikely (but not impossible) that the patient has viral myocarditis causing her chest pain and ECG abnormalities without any troponin elevation, wall motion abnormalities, coronary artery abnormalities, or pericardial effusion. It is much more likely that this unfortunate woman simply has a very scary normal variant baseline ECG. Unless she presents to the same institution or carries a copy of her ECG for the rest of her life, this problem will recur. We have many similar cases on this blog.

Her post-cath ECG is unchanged:

This is more proof that is is a normal variant. Acutely abnormal ECGs, whether due to ischemia or myocarditis or takotsubo, will evolve. There is no evolution of the ST segments or T-waves in II, III, aVF, or aVL.

Case #2

A male in his 50s presented with episodic chest pain over the past few days, which recurred and became worse 1 hour prior to arrival. At the time of presentation his pain was 4/10 and decreasing.

Here is his initial ECG:
What is your interpretation?

I sent this ECG to Dr. Smith without any clinical information and he immediately replied "inferior MI."

Congratulations if you see the subtle but important abnormalities here. There is a very tiny amount of ST elevation in lead III which is proportionally significant given a small normal QRS complex. The T-waves are borderline large for their QRS complexes, and alone could not be called hyperacute. However, there is a tiny amount of ST depression and (more noticeably) T-wave inversion in lead aVL which is far out of proportion to the very small QRS complex. The findings in aVL are not appropriate for or explained by the normal QRS complex, and therefore confirm that the subtle findings in lead III are new and indicative of ACO.

There is also ST depression in V3-V6, maximal in V4. This should be assumed to indicate posterior wall involvement of ACO.

These findings were not appreciated. The patient received nitroglycerin and the pain resolved. He was planned to undergo coronary CT angiography for further risk stratification. First troponin was negative.

Repeat ECGs were appropriately obtained, while the patient was completely pain free:

These show (incomplete) resolution of prior abnormalities, confirming that they are dynamic findings and also confirming reperfusion. There is also a change in heart rate which could affect the ST segment and T-waves.  The vessel is open at the time of this ECG.

While waiting for CTCA, his second troponin T turned positive at 0.020 ng/mL. CTCA was cancelled. The third troponin returned at 0.030 ng/mL.

At this point the notes state that the patient had a recurrence of chest pain, was given one dose of sublingual nitroglycerin, followed by lightheadedness with sinus bradycardia in the 30s. Unfortunately there is no mention of an ECG being performed at this time, and no ECG on file. The patient was admitted to cardiology with plans for an urgent cath the next morning. No further troponins were measured.

The next morning, cardiac cath revealed the following:

 This was called a 99% proximal RCA thrombotic stenosis, however I don't see any distal flow. This appears to be 100% occlusion. Thrombectomy and stent was performed with the following angiographic result:

After stenting, the full course of the RCA is now visible.

Unfortunately no more troponins were ordered, so the peak troponin value is unavailable. Echo performed 8 hours after cath did not show any wall motion abnormalities but was suboptimal quality.

Both patients did well.

Great comments by Pendell Meyers:

These two selected cases demonstrate a critically important problem with the current paradigm of MI management. The patients who benefit from emergent cath are those with acute coronary occlusion or near occlusion with insufficient collateral circulation to a substantial portion of the myocardium - this is the anatomic substrate of the entity we are supposed to call "STEMI."

Unfortunately, the term "STEMI" itself and all the guidelines for the past 30 years have restricted our minds into thinking that acute coronary occlusion is diagnosed only by "STEMI criteria." As we have shown countless times on this blog, acute coronary occlusion (ACO) is a complex and dynamic process, and cannot be simplified to measuring millimeters of ST elevation. Numerous studies have documented the STEMI criteria missing at least 25% of ACO. Conversely, we all know there is an unacceptably high rate of false positives using the STEMI criteria, which distracts the clinician from a patient's actual dangerous pathology, causes premature closure, puts the patient at risk of unnecessary procedures and their complications, as well as unnecessary mobilization of scarce resources.

Expert ECG interpretation is almost certianly superior to STEMI criteria in every way. If we are to progress in the management of acute MI, we have no choice but to break the current paradigm. The term "STEMI" cognitively inspires you to think that only the ST segments matter, and that the ST segment deviation is the reliable marker of ACO. To combat this problem we have invented other terms such as "subtle STEMI," "STEMI-equivalent," or "semi-STEMI" in attempt to convey that there are other ECG findings that indicate the same pathology as classic true positive STEMI, but these have not produced widespread change in the knowledge or perception of optimal ACO management, except among the readership of this blog and other similar resources. We have tried too long to keep the term "STEMI" in the name to pay homage to the breakthroughs in the 1970s-1990s which pulled us into the reperfusion era. Eugene Braunwald and others have suggested a requiem for the term "unstable angina," yet we have shown repeatedly on this blog that unstable angina is alive and well. But perhaps the time has come for a requiem for the term "STEMI." While it is true that using STEMI criteria in the 1980s and 1990s was proven better than flipping a coin to decide who needs emergent reperfusion therapy, it is no longer our best option and is actually inhibiting us from discovering that we already have better options. Too long has it restricted our thinking and prevented further research from showing who actually benefits from emergent reperfusion. Experts routinely perform better, and hopefully one day neural networks or the like will make all this a moot point.

The next available step is to formally show that experts can recognize ACO with more accuracy than STEMI criteria and current practice. We are planning a retrospective study now, which will be designed as the first study in an arc of research aimed at evaluating whether expert ECG interpretation can cause better outcomes for patients by more accurately predicting who needs emergent reperfusion therapy. If retrospective studies can show that expert ECG interpretation may have led to faster reperfusion of ACO, then prospective studies may one day be justified in cases where there is otherwise clinical equipoise. If such an ECG were reviewed by an expert, prospectively at the moment of the decision to emergently reperfuse or not, I believe that we could show patient-important outcome improvements correlating with increased accuracy of ACO detection and emergent reperfusion.

Perhaps most importantly, please remember that ACO sometimes manifests with completely normal serial ECGs. The ECG is an accurate surrogate marker of ACO in the hands of experts, but can never be perfect. Some patients deserve immediate diagnostic cath even without ECG abnormalities.

See this lecture by Dr. Smith:
"The False STEMI-NonSTEMI Dichotomy"

Wednesday, January 24, 2018

A 40-something male with epigastric pain

A 40-something male presented with epigastric pain.

An ECG was recorded immediately (time zero):
This was texted to me asking for my opinion.
What do you think?

My answer: Normal variant

He had serial ECGs:

This was recorded at t = 40 minutes:

Subsequently, the patient was diagnosed with cholecystitis.

This was recorded at t = 110 minutes

Notice there is some change from ECG to ECG, but this is not uncommon in these normal variants.

That you cannot entirely rely on the temporal stability of the ECG to diagnose normal variants is, to use a favorite phrase, "Sad!".

All serial troponins were below the level of detection.

Learning points

How does one recognize one such ECG as ischemic and one as normal variant?  Why are these not Wellens' waves?

All I can say is that you need to read many many ECGs and get experience and follow up on the outcomes of your interpretations!  There are many cases on this blog that can help you to recognize the difference.

ECGs are like faces: you can easily tell different person's faces from one another, even though they mostly have the same features: 2 eyes with eyebrows, a nose, cheeks, mouth and lips, etc.  How do you describe the difference?  And yet you know it because of your experience with seeing tens of thousands (or more!) of faces over a lifetime.

Unfortunately, doctors who spend a lifetime learning to recognize such patterns eventually retire or die, and all that knowledge is lost.

We are working to produce a Deep Neural Network ECG algorithm that will learn forever.  It is sad for experts that such a network may one day replace human expertise, but very good for patients.

Here are other examples of normal variants with T-wave inversion that look scary:

Persistent Juvenile T-wave Pattern

8 year-old with report of "syncope and an abnormal ECG"

Here are cases of normal variant ST elevation that looks scary:

High ST Elevation in a Patient with Acute Chest Pain

A 50-something year old with typical chest pain

Several Cases of ST Elevation from Early Repolarization

Monday, January 22, 2018

Chest pain, sinus tachycardia, and ST Elevation

I was reading through ECGs on the system when I saw this one:
Sinus tachycardia, rate 120
Computerized QTc = 380 ms
What do you think? 

I was immediately worried about a proximal LAD occlusion.  Although sinus tachycardia generally argues against ACS, a large anterior MI may result in such poor stroke volume that there is compensatory tachycardia and possibly impending cardiogenic shock.

I looked to see if there was an ED cardiac ultrasound, and there was:

Parasternal Long Axis:

Poor image, but one can see that there is poor apical function

Parasternal short axis:

This shows poor contractility of the anterior wall.
Contrast the shortening and thickening of the posterior wall (opposite the transducer) to the anterior wall (closest to the transducer)

Apical 4 chamber:

Apical wall motion abnormality
The base is contracting well.

At this point I still knew nothing about the patient, but was worried about an acute anterolateral STEMI (Proximal LAD occlusion).

I went to talk with the treating clinicians.  They too were worried about LAD occlusion and had consulted cardiology.

Here is the history:

An elderly woman with history of diabetes and hypertension presented ambulatory with acute onset of crushing 10/10 chest pain that radiates to the back.  It started one hour prior to arrival.  She has never had anything like this before.

With that history, I had no doubt about the diagnosis.

Cardiology performed a formal echo.  Here is the result.  (She had previous normal echo with 65% ejection fraction):
--Normal left ventricular size, thickness and severely depressed systolic function.
--The estimated left ventricular ejection fraction is 27%.
--Very large area of regional wall motion abnormality, akinetic, involving apex, mid and apical segments of the anterior, lateral, inferior and septal walls along with hyperdynamic base.

Let's take one more look at the ECG:
There is STE in V2 and V3 of about 1 mm at the J-point (up to 1.5 mm "normal" for women)
However, there is 2 mm in V4-V6, so this is diagnostic of STEMI, by criteria.
There is also some STE in aVL and I, with reciprocal ST depression in III and aVF.

Just for interest's sake, how do the formulas perform?  (Really, since V4-V6 are diagnostic, as is the echo, we should not let a low number dissuade us from the diagnosis)

QTc = 380, STE60V3 = 2, RAV4 = 8; QRSV2 = 7
3-variable: 22.20 (low); 4-variable: 18.68 (high) 

(4-variable is more accurate, but not validated)

Interestingly, there is also a bit of ST elevation in lead II.  This suggests that there may be inferior ST elevation that does not fully manifest in III and aVF because the STE in aVL results in an opposing force to depress the ST segments in III and aVF.

So perhaps there is competing ST elevation in I and aVL on the one hand, and II, III, aVF on the other.  This would mean there is not only anterolateral MI, but also inferior MI, and implicates a "wraparound" (type III) LAD to the inferior wall.  This is also supported by the echo which shows diffuse wall motion abnormalities.

The patient was taken for emergent angiography:

The coronaries were clean.  The LAD was type II (NOT a wraparound).  Thus, even an autolysed thrombus in the LAD would not explain the ECG (a type II LAD occlusion would not produce this inferior findings on the ECG and on the echo).

Takotsubo stress cardiomyopathy became the most likely, or certain, diagnosis.

Troponin returned at 0.222. No other troponins were drawn.

Shortly afterwards, the patient spiked a fever and was diagnosed with pyelonephritis.

Here is the post cath ECG:
T-waves are not nearly as tall, and ST elevation is less

Here is the next day ECG:
Wellens' waves??  Looks like it, but can happen with takotsubo also.

And then the day after:
Very wide, rather bizarre inverted T-waves.
These are very typical of takotsubo.

Final Diagnosis:

Takotsubo stress cardiomyopathy, with an unusual onset of crushing chest pain, presumably due to sepsis from pyelonephritis.

Could this have been diagnosed by the ECG?

In retrospect, from the ECG alone, takotsubo may have been strongly suspected based on ST depression in aVR, absence of ST elevation in V1, and STE in lead II.  However, all these findings may be present with a wraparound LAD to the inferior wall.

Pathophysiology of Takotsubo
Diffuse small vessel ischemia, with resulting ischemic pain, wall motion abnormalities, and ECG findings.  It is only the distribution of these findings that is, or may be, different between STEMI and Takotsubo.

Can one reliably differentiate the ST Elevation of Takotsubo from the ST Elevation of LAD occlusion?

The quote below is from our paper just published online:

David F. Miranda, M.D, Angie Lobo, M.D, Brooks Walsh, M.D, Yader Sandoval, M.D,
Stephen W. Smith, M.D.  
New Insights into the Use of the 12-lead Electrocardiogram for Diagnosing Acute Myocardial Infarction in the Emergency Department.   
Canadian Journal of Cardiology 34(2):132; February 2018.  Issue: Advances and Controversies in Cardiac Emergency Care. 
(in Press, Accepted Manuscript)

Takotsubo Cardiomyopathy

Takotsubo may manifest T-wave inversion, but also STE that mimics STEMI.  Although earlier work had suggested that ECG criteria might distinguish this STE from anterior STEMI,57 recent literature does not support this result.58 59 Although the specificity of various combinations of ECG elements for Takotsubo may be > 95%, the positive predictive value may be as low as 67% due to the low prevalence of Takotsubo.  Many anterior STEMI, especially due to wraparound LAD to the inferior wall, have similar ECG findings and also apical ballooning.60   Therefore, coronary angiography is often essential to rule out acute coronary occlusion, even when the STE pattern and cardiac ultrasound both suggest Takotsubo.

57. Kosuge M, Ebina T, Hibi K, et al. Simple and accurate electrocardiographic criteria to  differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. Journal of the American College of Cardiology 2010;55:2514-6.

58. Frangieh AH, Obeid S, Ghadri JR, et al. ECG Criteria to Differentiate Between Takotsubo (Stress) Cardiomyopathy and Myocardial Infarction. Journal of the American Heart Association 2016;5.

59. Vervaat FE, Christensen TE, Smeijers L, et al. Is it possible to differentiate between Takotsubo cardiomyopathy and acute anterior STEMI? J Electrocardiol 2015;48:512-9.

60. Mugnai G, Pasqualin G, Benfari G, et al. Acute electrocardiographic differences between Takotsubo cardiomyopathy and anterior ST elevation myocardial infarction. J Electrocardiol 2015;48:79-85.

Annotated Bibliography (relevant quotes from abstracts)

57. Kosuge et al.:
"The absence of abnormal Q waves, absence of reciprocal changes, presence of ST-segment elevation in lead −aVR (i.e., ST-segment depression in lead aVR), and absence of ST-segment elevation in lead V1identified TC with sensitivities of 42%, 94%, 97%, and 94%, specificities of 74%, 49%, 75%, and 71%, and predictive accuracies of 71%, 53%, 77%, and 73%, respectively." 

58. Frangieh et al.:
"When comparing STEMI and STE-TTC, ST-elevation in –aVR (ST depression in aVR) was characteristic of STE-TTC with a sensitivity/ specificity of 43% and 95%, positive predictive value (PPV) 91%, and a negative predictive value (NPV) 62%. 0 .001= ST depression in aVR is accompanied by ST-elevation in inferior leads, sensitivity/specificity were 14% and 98% (PPV was 89% and NPV 52%) (P=0.001), and 12% and 100% when associated with ST-elevation in anteroseptal leads (PPV 100%, NPV 52%) (P less than 0 .001) On the other hand, STEMI was characterized by ST-elevation in aVR (sensitivity/specificity of 31% and 95% P less than 0 .001.

59. Vervaat et al. assessed these previous criteria:
"The existing ECG criterion was less accurate (76%) than in the original study (95%), with a large difference in sensitivity (26% vs. 91%). Only a frontal plane ST-vector of 60° could significantly distinguish TC from all acute anterior STEMI subgroups (p < 0.01) with an overall diagnostic accuracy of 81%. The mean amplitude in inferior leads II and aVF was significantly higher for patients with TC compared to all patients with acute anterior STEMI (p < 0.01 and p < 0.05 respectively) and the mean amplitude in the precordial leads V1 and V2 was significantly lower compared to proximal and mid LAD occlusion (p < 0.01)."

60. Mugnai et al.
"The absence of abnormal Q waves, the ST depression in aVR and the lack of ST elevation in V1 were significantly associated with TC (respectively: 52% vs 18%, p = 0.01; 47% vs 11%, p = 0.01; 80% vs 41%, p = 0.01). The combination of these ECG findings identified TC with a specificity of 95% and a positive predictive value of 85.7%."

More cases of Takotsubo Stress Cardiomyopathy

Bizarre T-wave Inversions in a Patient without Chest Pain

COPD exacerbation, what do the ECG and bedside echo show?

Is the Right Ventricle involved in Takotsubo Stress Cardiomyopathy?

RV SCM has been described, appears to accompany LV takotsubo cardiomyopathy up to 25% of the time and be associated with worse LV function.   See this article: and also this article:


There is no more vexing ECG mimic of acute STEMI than SCM because the underlying cellular pathophysiology is the same.  It is unusual to make the diagnosis without an angiogram. 

Saturday, January 20, 2018

A middle-aged man with severe syncope, diffuse weakness

A middle-aged male diabetic who is otherwise healthy was found unconscious by his wife, with incontinence.  He quickly awoke but was too weak to stand.  Initial vitals by EMS were BP 100/50 with pulse of 80 and normal glucose.  He remained weak and somnolent, and without focal neurologic abnormality.  He recovered full consciousness, but still felt weak and "not normal."  

There was a prehospital ECG:
What do you think?

He arrived in the ED and had this ECG recorded:
This one was sent to me for my opinion.  
I looked at it without any clinical information.
What do you think?

I wrote back that this is diagnostic of hypokalemia.  

It turned out the K was 2.6 mEq/L.

Why did I say this?

There is scooped ST depression in multiple leads, very typical of hypokalemia: I, II, aVL, V4-V6.

There are large U-waves.  Look particularly in V1 and V2.  This results in the appearance of down-up T-wave in V2; however, if it is a T-wave, resulting QT interval would be impossibly long.  Thus, it is a large U-wave, and the apparent QT interval is a QU interval.  Look directly above at V1 and you can see the U-wave clearly.

Such downsloping ST depression in V2 may frequently be misinterpreted as posterior STEMI (reciprocal to ST elevation of the posterior wall).

Case continued:

The patient had no chest pain or SOB.  His initial lactate returned at 5.0 mEq/L.  The patient and the vital signs completely recovered.  He seemed completely well.

After the K returned at 2.6, it was replaced.

The initial troponin I was 0.096 ng/mL, then rose to 0.191 at 2 hours after the first, and a second ECG was recorded 220 minutes after the first:
ST depression has resolved.
K has been replaced.

The third troponin I returned at 4 hours at 3.002 ng/mL, at which time the K was normal and another ECG was recorded that is not changed from the 220 minute one.

A 4th troponin returned at 6 hours at 7.905 ng/mL.

The clinicians decided to get a CT of the chest/abdomen/pelvis (I am not certain what they were looking for).  One image of the heart is shown here:
The arrows point to the inferior subendocardium.  It is dark because there is low contrast enhancement, which indicates absence of blood flow. 
This is a picture of inferior subendocardial ischemia.
Here is a closer up axial (transverse) view of the heart:
The arrows point to a subendocardial region with poor contrast enhancement due to ischemia.
This is posterior subendocardial ischemia.

This finding was seen in real time, and the patient was started on treatment for NSTEMI.

A repeat ECG was unchanged, and the potassium returned normalThus, in the presence of a normalized K, the ECG normalized in spite of ongoing myocardial ischemia.

A formal echo was done, which showed:
Normal EF
Regional wall motion abnormality (RWMA) of the apex, with dyskinesis (aneurysm)
RWMA of the distal inferior wall
Concentric LVH

A coronary angiogram was done a few hours later:
Culprit Lesion: 99% stenosis of the mid Circumflex with TIMI 1-2 flow (obstructed)
This was thrombus, acute (not a chronic lesion)
Diffuse severe disease of the mid and distal LAD
Chronic total occlusion of the mid right posterior descending artery (off the RCA) with left to right collateral

Three vessel coronary artery disease with probable mid circ culprit for NSTEMI.  Successful circumflex PCI with excellent angiographic result, 0% residual.

If the source of collateral filling from the "left" was the circumflex, then the PCI of the circ would have restored this flow and resulted in full reperfusion to the inferior wall in addition to the posterior wall.

Here is a post PCI ECG:
Normal ST elevation in V2, not ST depression
Normal U-waves
Also: Now there is a large T-wave in V2 (posterior reperfusion T-wave) and inverted T-waves in inferior leads II, III, aVF (inferior reperfusion).
This is good evidence for reperfusion of the inferior and posterior walls.

So what happened?

There were several clinicians who thought the the ST depression was due to posterior STEMI.  It is possible but I think unlikely.
1. We do not have any evidence that there ever was full STEMI of the posterior wall.  The CT scan only shows subendocardial ischemia, which would not present with ST depression in lead V2.
2. The ECG looks to me like hypokalemia, and the K was 2.6 mEq/L.
3. The artery was open with flow at angiogram, corresponding to the subendocardial ischemia (not to transmural ischemia, which would lead to STEMI on the ECG) --though it is possible that the artery was fully occluded at the time of the first 2 ECGs.
4. There never was any chest pain or SOB or other anginal equivalent (and this was not a very elderly or debilitated person who might only feel "weak" with his MI, though he is diabetic).
5. The ECG normalized with a normal potassium while the myocardial ischemia was ongoing.

Initially when I heard about the case, I knew only these 4 things:
1. I saw the ECG, thought it was diagnostic of hypokalemia and confirmed it by the K of 2.6
2. I knew the troponins were elevated
3. I had heard only this about the angiogram: that there was a 99% circumflex lesion.

With this information, I surmised that the syncope was due to ventricular tachycardia from hypokalemia and the elevated troponins were from demand ischemia (type II MI) due to hypotension (because of VT) and poor flow through an extremely narrow chronic circumflex stenosis.

However, this was erroneous, as it turned out that the circumflex lesion was definitely due to acute thrombus (ACS), not a chronic lesion (as existed in the RCA).

Thus, one can only say that there were 2 pathologies at once:

1. Acute coronary syndrome of the circumflex with acute myocardial ischemia, that manifested without any chest pain or SOB, and that probably was not manifesting on the ECG.  [Although the scooped ST depression could have been a manifestation of diffuse subendocardial ischemia, all of it resolved with replenishment of the K in spite of the fact that the myocardial ischemia was ongoing.]

2. Hypokalemia, that did manifest on the ECG.

Ventricular Tachycardia?

Hypokalemia in the presence of myocardial ischemia is a very strong risk factor for acute ventricular dysrhythmia, so it is very likely that the syncope was due to ventricular tachycardia (VT).

Here are down-up T-waves of posterior MI: 

Series of Prehospital ECGs Showing Reperfusion

Here is down-up "T-waves" of hypokalemia: 

Biphasic T-waves in a Middle-Aged Male with Vomiting

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