Cardiac Arrest -- Is it STEMI?

A late middle aged male collapsed while walking and had immediate bystander CPR.  He achieved ROSC at the door of the ED, 30 minutes after arrest.

The CPR provided had been so effective that the patient began to follow commands upon arrival.  Why was it so effective?  Because they used the inspiratory threshold device, ITD (ResQPod) and ResQPump.

Go here for the latest in CPR, a fast evolving field: Lecture by Keith Lurie that includes the latest on head-up CPR.

This was his initial ED 12-lead, with pH 7.09, pCO2 69, and bicarb 19.  K was 2.8 (low K is common after resuscitation due to lots of exogenous epinephrine):

The computer diagnosed atrial fibrillation with left bundle branch block.  
I would have agreed with atrial fib except that the 3rd complex appears to be sinus (see double-peaked P-wave).  So perhaps it is an accelerated idioventricular rhythm?

Is it LBBB?

No.

LBBB should have a slow upstroke ("intrinsicoid deflection") to the R-wave in lateral leads of at least 60 ms.  This is a relatively rapid upstroke of about 40 ms (see red arrows below which show onset and peak of R-wave in lead V5).

Is this a wide QRS?  

Yes, but I believe not nearly as wide as it first appears.

In the annotated version of the ECG (below), I put a short black line in V4 where I believe the QRS ends.

This a QRS that looks very wide because its terminal portion is obliterated by ST elevation.

This is "shark fin" ST elevation. 

They have also been called "Giant R-waves":  JE Madias.
Full text, with image: https://drive.google.com/open?id=1fCpHey_vILU9jNld6a4oBtxQbML8Z88k. 

Here is an annotated version with lines and arrows:

The red arrows show the onset and peak of the R-wave in lead V5
The short black line in V4 shows what I believe to be the end of the QRS.
Thus, the QRS duration is about 140 ms. It would be easy to believe that it is 230 ms.

--I then draw a long black line from that same point and extended it down to lead II.
--I then draw that long black line from the corresponding points on other complexes of lead II, up to all other leads.
Now, assuming my estimate of the end of the QRS is correct:
1. You can see concordant ST elevation in I, aVL, V3, V5, and V6.
2. You can see concordant reciprocal ST depression (STD) in II, III, aVF
3. There is also STD in V1 and V2.

In any ventricular rhythm, including PVCs, concordant ST elevation implies subepicardial ischemia (STEMI)

for another example of that downsloping ST elevation, see this case:

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Management decisions

We are enrolling patients in a study called "ACCESS" (ClinicalTrials.gov Identifier: NCT03119571).  It is a randomized trial of early angiography/PCI for cardiac arrest victims who do not have "STEMI" or "STEMI equivalent."  (The research question is: do patients with shockable rhythms who do not have STEMI need emergent cath lab activation?)

So the ECG interpretation is critical to whether this patient gets:
1) immediate angiography as if he is a STEMI patient or 
2) randomized to early angiography vs. angiography later, as indicated by other data.

If you believe that:

A)  This is a simple post arrest ECG with very wide QRS and no ST elevation or depression
Then the patient is randomized and not automatically studied with immediate angiography.

B) The QRS really is much shorter and only appears to be wide due to ST elevation and depression which obliterates the end of the QRS
Then, you activate the cath lab and do not enroll the patient in this randomized trial.

I was convinced that it was ST Elevation and Depression.

We activated the cath lab based on this ECG, with the knowledge that this subepicardial ischemia may simply be a result of cardiac arrest alone.

ECGs Immediately after Resuscitation from  Cardiac Arrest

Any ECG recorded immediately after cardiac arrest can be wildly abnormal.  During the 30 minutes of cardiac arrest, even if there is no acute MI, or even without any coronary disease, there can be severe ischemia from the low-flow state of cardiac arrest , as well as alterations from acidosis.(Cardiac output and blood pressure during CPR chest compressions is a fraction of normal.)

If there are fixed coronary lesions, the flow beyond that stenosis may be exceedingly poor, and the ischemia may be focal.

Thus, one should always record another ECG after the patient stabilizes.  We recorded this one 25 minutes later:

Sinus rhythm.
Typical hypokalemia ECG.
There is some residual STE in aVL and reciprocal STD in inferior leads

What do you think?

Three Options:

1.  The QRS really was very prolonged, and there is and was no focal ischemia
2.  There was a thrombosis, probably of the LM or LAD, and it spontaneously reperfused (autolysis)
3.  There is a fixed stenosis in the LM or LAD.  During cardiac arrest, and shortly thereafter, there was profound ischemia in that territory, resulting in ST Elevation (a type 2 STEMI).

Further history came to light:

The patient had recently been experiencing exertional angina. He had a stress test a few days prior that was markedly positive, and was scheduled for an angiogram on the following day.

This suggests presence of a fixed stenosis.

What happened?

1. Maybe that stenotic plaque ruptured and thrombosed.
2. Maybe the stress of walking was enough to cause exertional ischemia and then ventricular fibrillation.

The patient went to the cath lab: 

A 95% stenosis of the proximal LAD was found.  The lesion did not appear to be acute (no ulcerated plaque and no thrombus).  The lesion was reduced to 0% with intervention and stenting.

Peak Troponin I = 19 ng/mL (STEMI is greater than 10 ng/mL in about 70% of cases)

Formal Echo
Normal left ventricular size and thickness.
Mildly decreased left ventricular systolic function with an estimated EF
of 45%.
There is hypokinesis of the mid anterior wall.


It looks as though Option 3 was the correct one.

Conclusion

This is a type II STEMI due to fixed stenosis in the LAD which, in the setting of very low flow state of CPR resulted in severe hypoperfusion to the anterior wall, a wide QRS, and ST elevation and depression consistent with STEMI.  The arrest was caused by exertional ischemia in the setting of a very tight fixed, non-thrombotic, LAD stenosis.

However, the discharge diagnosis was "NonSTEMI."

In retrospect, this patient could have been randomized in the ACCESS trial.  He did not need immediate intervention, though he did get it.

Learning Points:

1. It is critical to find the end of the QRS before concluding that there is not STE or STD.

2. In the presence of a fixed stenosis, exertion can lead to ischemia and ventricular fibrillation.  Stress tests are always done with resuscitative equipment available!

3. Low flow of cardiac arrest can lead to severe cardiac ischemia, especially in the presence of fixed coronary stenosis

4. The ECG immediately after cardiac arrest is often very abnormal. Wait 15 minutes after stabilization to record another one

5. We don't know if everyone who has cardiac arrest from a shockable rhythm needs emergent angiography.  My bias is to send them, but the ACCESS trial's goal is to find out.


More on Type 2 STEMI:

You Must Read the ECG in Clinical Context....

Inferior ST Elevation. BP 250/140.

Cardiac arrest, LBBB with STEMI on the ECG, but no Acute Coronary Syndrome!

Cardiac Arrest, acute ST elevation and depression superimposed on LVH, but NOT due to ACS

Atrial fibrillation with rapid ventricular response with ECG injury pattern

A 33 year old male with acute back pain radiating to the chest

Written by Pendell Meyers, with edits by Steve Smith

Case

I was called to the EMS control room to answer an RMA (Refusal of Medical Advice). After the call was over, just before I was about to go back to the grind in our acute emergency department, my fantastic EMS colleague paramedic Jess Boyle asked me for an opinion on these 2 ECGs from a single patient, one done immediately after the other, without any other clinical information:

What do you think?










Both of the ECGs show sinus rhythm with normal QRS complex morphology. There is ST segment depression in leads III and aVF with inappropriate large "volume" T-wave inversion. This is reciprocal to a small amount of ST elevation in lead aVL, with suspiciously large amount of area underneath the ST segment and T-wave, suspicious for hyperacute T-waves. In the context of the inappropriate (inappropriate for the QRS) STE in aVL with reciprocal inferior STD, these T-wave must be considered truly diagnostic for hyperacute T-waves. In the first ECG, take a close look at the PVC that occurs in leads aVR, aVL, and aVF just before the precordial leads start. What do you notice?


There is concordant ST elevation in that PVC in lead aVL. PVCs, like any other form of abnormal conduction (LBBB, ventricular paced rhythm, etc) generally follow the rule of appropriate discordance (which states that the ST segment and T wave will deviate away from the majority of the abnormally conducted QRS complex). So in the absence of superimposed ST elevation, the PVC in aVL should have an isoelectric or depressed ST segment following that large, abnormally conducted R wave. Instead, the J point is clearly above the baseline. This is concordant ST elevation, and we believe based on much experience with this exact question and many prior cases showing this, that this is also diagnostic of acute transmural ischemia just as it has been shown to be in LBBB (and soon, ventricular paced rhythm).

So this ECG is diagnostic for the fact that the high lateral wall has very recently lost its blood supply. The ECG reports the acute transmural thickness of the myocardium at the cellular level, and the cells do not know or care why they have acutely lost blood supply - any etiology of acute coronary occlusion, or even small vessel ischemia such as is seen in takotsubo stress cardiomyopathy, or in "No Reflow" phenomenon after opening of an occluded coronary artery, will produce the same ECG changes. On a population level, by far the most common etiology for acute coronary occlusion is type 1 ACS (plaque rupture causing acute thrombotic occlusion). But remember, the ECG just shows the fact that there is an occlusion, not the etiology of the occlusion.


Back to the case:

The EKG had been sent to medical control approximately 15 minutes prior to my review, and my paramedic friend had been worried by it so he took it immediately to an ED physician for review. Although he mentioned that he was worried about aVL and the inferior reciprocal changes, the reviewing attending disagreed and did not think that it warranted prehospital cath lab activation.

I was immediately worried about what might happen to the patient. I asked him which hospital the patient had been transported to (our medical control services oversees many different hospitals). Luckily, he responded that the patient had just arrived in our ED! So I went to find him and make sure that the receiving team had gotten copies of these prehospital ECGs.

As it turns out, the receiving team had not gotten a copy of these prehospital ECGs. I gave them the ECGs, told them my concerns, and asked for some info about the patient:

He was a 33 year old male with history of asthma and smoking who called EMS for sudden onset chest pressure beginning 1 hour prior to arrival. He stated he had just finished urinating when he was reaching to flush the toilet when he suddenly felt a cramping pain in his mid back. When he went immediately to lay down, the pain radiated into the center of his chest. He took tylenol with no improvement, then called EMS. EMS administered ASA, NTG, and 5mg morphine with improvement in pain. He adamantly denied any ingestions, drugs, cocaine, etc.


Here was his first ECG in the ED, during this time he supposedly had 2/10 pain which was improved since onset:

The findings are much more subtle compared to the prehospital ECGs, but still present. There is also a tiny new Q wave compared to the priors. Because the findings have decreased, but the T-wave is still upright, it is hard to say whether the artery is still fully occluded or whether we might be witnessing the beginning of the changes of reperfusion. 

If the artery is reperfusing, we should soon see complete resolution and/or the classic reperfusion sequence of terminal T-wave inversion followed by full T-wave inversion over time. 

Usually, improvement in pain is very helpful in this decision, however morphine may confound your assessment in the setting of ACS. Unlike aspirin, NTG, or other ACS medications, which improve pain by treating the underlying cause, morphine does not treat the occlusion, and unfortunately may be effective in masking the pain of acute coronary occlusion, inspiring less frequent serial ECGs and serial examinations of a sick patient. "Masking" of ischemia may be the reason that morphine is associated with worse outcomes in ACS (http://prdupl02.ynet.co.il/ForumFiles_2/14835373.pdf)

Overall, the treating team interpreted the clinical picture as improving, and did not immediately activate the cath lab but instead continued aggressive bedside evaluation and serial ECGs.

There was no appreciable wall motion abnormality upon bedside echo without contrast.

The iStat point of care troponin I returned at 0.38 ng/mL (elevated, normal less than 0.08 ng/mL). In general, iStat troponins can be unreliable, although the higher the result the more likely it is true. The initial troponin T returned at 0.04 ng/dL (also slightly elevated from normal which is less than 0.01 for this assay).

At this point, only ~20 minutes after arrival, they activated the cath lab.

The patient was taken immediately for cathetization, which showed "mid to distal 1st diagonal branch revealed 90% stenosis and mid-distal segment attenuated and appears in spasm, unresponsive to intracoronary NTG and intracoronary nicardipine." The RCA and LCX were normal. See the cath images below.

Normal RCA.

In this view you see the LAD (largest vessel coming down the center of the screen), with the large 1st diagonal  branching off and appearing robust until approximately halfway down its length, when it suddenly is extremely narrowed and then followed by downstream low attenuation. See next picture for annotation.

The arrow points out the beginning of the spasm of the D1.

The cath report states that he had improvement in symptoms and ECG findings despite the fact that the angiographic appearance was not improved after the intracoronary administration of NTG and nicardipine. Given this improvement and the suspected spasm as the etiology, they did not place a stent, but instead planned to treat the patient with medical therapy including amlodipine and NTG as needed.

His serial troponin T rose from initial 0.04 to 0.43 to 0.66, then started to trend back downward.

Here is his first post-cath ECG:

There appears to be no resolution of active injury on the ECG. Rather, it appears as though there is ongoing injury and progression along the classical pattern of OMI. This is concerning for persistent downstream ischemia despite an open artery angiographically.

Two more hours later. Now you can see the development of larger Q waves in lead aVL. There is persistent STE in aVL with reciprocal STD in III and aVF.

No longer any R wave in aVL, replaced entirely by Q wave. This does not necessarily mean that the full thickness of the high lateral wall has infarcted, because stunned but viable myocardium may also produce a Q wave and later recover.

The cardiologists plan on repeat catheterization in several weeks after medical therapy to reassess whether any other intervention will be necessary.


Learning Points:

Make sure you have a system in place so that your EMS ECGs get delivered to the receiving ED team every time, even when they are originally interpreted as normal.

The ECG cannot tell you the etiology of OMI. By the numbers, the etiology must be assumed to be one treated by immediate reperfusion therapy (in the absence of a specific known alternate cause). This is not a "false positive" OMI, rather this is one of the few patients who has something other than thrombus causing the OMI. The only appropriate way to differentiate occlusive spasm from occlusive thrombus is by performing an emergent angiogram. See our other cases of spasm here.

This patient never met the "STEMI criteria", like many other very significant acute coronary occlusions and near occlusions.

Young people can have acute MI.

Don't forget to look for the signs of OMI within PVCs.

I believe that even transient OMI/STEMI should ideally be taken to the cath lab if feasible, because it is unlikely that the patient will get serial ECGs and close monitoring enough to recognize reocclusion before more myocardium is lost, or worse, even in the best of hands.

The blood sample is hemolyzed. Twice. Is there hyperkalemia on the ECG?

This patient presented from dialysis because his shunt was malfunctioning.  He had no definite indication for dialysis unless his K was high.

But every time we drew the K level, it was "hemolyzed."

So we looked closely at his ECG for evidence of hyperkalemia.

Is there evidence of hyperkalemia?

Here is his previous ECG when K is normal and all his medications were the same at that time.

Are they different?

The objective evidence of hyperkalemia on that top ECG is the prolonged PR interval.  It is over 300 ms!  (The PR in the previous is 218 ms) This prolonged AV conduction puts the patient at risk if his K were to rise further. 

Further, one might be tempted to blame a prolonged PR interval on vagal tone, especially at a slow heart rate of 60 beats per minute.  But since the sinus rate in the old ECG is the same as the new ECG, there is no difference in vagal tone.

So we ordered an admission bed and he underwent dialysis.  A bit later, we obtained non-hemolyzed blood and the K was 5.5 mEq/L, which is elevated but not extremely so.  Nevertheless, the patient is on carvedilol (as he was at the time of the ECG with a PR of 218 ms), and the combination could lead to significant AV conduction delay.

I am a believer that if the ECG truly shows no evidence of hyperkalemia, that there will be no short term adverse events from that hyperkalemia.

The caveat is that one must be able to see all those possible abnormalities.  Some are exceedingly subtle, but real.

Case 3 on this post illustrates this problem very well:

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

There was an article on this published a year ago in Western J Emerg Med:

Severe Hyperkalemia: can the ECG risk stratify for short-term adverse events?


Pendell Meyers wrote a fine FOAM article on this topic on EmCrit:
https://emcrit.org/racc/critical-hyperkalemia/

OMI Can be Diagnosed by "Pseudonormalization of ST Segments"

This post was written by Tarissa Lai, one of our outstanding EM residents at Hennepin County Medical 
Center, with comments by Steve Smith and Dan Lee.

Case

A 30 something y.o. female with HTN, HLD, diabetes, ESRD on dialysis is brought in by EMS with 
sudden onset, left -sided chest pain for the past four hours.

This is her pre-hospital ECG:

 This is her first ECG in the ED:

What do you think?

I interpreted this as normal sinus rhythm with LVH, but no significantly peaked T waves concerning 
for hyperkalemia. I did not appreciate any significant ST elevation.

However, the prehospital ECG is more worrisome: the T-wave inversion in V5 and V6 is preceded
by ST Elevation. In LVH, T-wave inversion in leads V5 and V6 should be preceded by ST depression, or
at least by an isoelectric ST segment. These look like ischemic ST segments and T-waves.

More Clinical history:

I first met her on an overnight shift while she was sleeping in a hallway bed. She was a difficult 
historian as she kept answering in one word replies before falling back asleep. The patient had gone 
to dialysis that day without any significant change in her regimen. While she was in her bed at home, 
she had sudden onset of left sided chest pain that radiated to her shoulder.  The pain
was pleuritic, without nausea or diaphoresis. The nitro she took in the ambulance did not help. 
Her physical exam was remarkable for a young woman sleeping comfortably in bed, whose chest pain
was easily reproducible with palpation.

Although her comfortable appearance with pleuritic and reproducible chest pain were reassuring, some 
components of her story were concerning, including the sudden left sided chest pain and radiation to 
her shoulder. Given her risk factors (HTN, HLD, ESRD from diabetes) I decided to obtain a broad 
cardiac workup for the patient: serial ECGs, labs, serial troponins, CXR and bedside cardiac ultrasound. 
She also received an additional nitro in the ED after receiving aspirin and nitro via EMS.

This is the patient's old ECG from ~2 months prior:

There is ST elevation that is most notable in V1, V2 and aVR with ST depression that is most obvious 
in the inferior leads and V6. I interpreted these as findings consistent with "secondary" ST-T abnormalities due to
her known LVH.
When comparing the old and new ECGs, there is:
New relative ST depression in V1-V3 and
New relative ST Elevation in: II, III, aVF and in V5 and V6.
When I say "relative," I mean relative to the previous ECG, which is the baseline, chronic, non-ischemic ECG.

Here is the Point of Care Cardiac Ultrasound (POCUS), short axis:

This shows the anterior wall (top) and septum contracting perfectly, but the postero-lateral walls not contracting.

Parasternal Long Axis View

There is a posterolateral wall motion abnormality. This appears to be new, as her last formal 
echocardiogram 2 years ago was relatively normal.

All of this is consistent with an acute postero-lateral MI. [New relative ST elevation in V5 and V6 (lateral
wall), new relative ST depression in V1-V3 (posterior wall) and new relative ST Elevation in II, III, aVF
(inferior wall).

At this time, her initial troponin came back at 103.2 ng/mL (103,000 ng/L, extremely high!!),
and her K was 4.6 mEq/L.

While the patient was known to have mild troponin elevations in the past, this was clearly diagnostic of acute MI.

Given the WMA on her echo, a repeat ECG was obtained with posterior lead placement:

There is now STE in V7, V8 and V9, which is consistent with a posterior MI.
The decreased voltage noted in the first couple ECGs is even more obvious now.
There is now also ST depression in V2 and V3 (previously only relative)

On closer evaluation of her old ECG compared to the ones from today, you can see what might
be called "ST Segment Pseudonormalization." Her previous ST elevation in V1-V3 is now gone,
and the voltage from her LVH is decreasing with each successive ECG. This would make sense in
the setting of an acute posterior MI, which can present with precordial ST depression.

V1-V3 side by side:

NEW OLD  

The patient was emergently taken to the cath lab and found to have severe multi-vessel disease with 
high thrombus burden, and the culprit lesion was a 100% thrombotic occlusion in the proximal
left circumflex.

Diagnostic angiogram:

Post PCI of the circumflex artery. She had an uncrossable lesion in the LAD with an estimated 99% 
occlusion. Arrowheads represent some of the remaining thrombotic lesions.

Troponin peaked around 325 ng/mL (massive). Pertinent results of the formal Transthoracic Echo:

-Moderately severe concentric left ventricular hypertrophy.
-Severely decreased left ventricular systolic function with an estimated EF of 22%.
-Akinesis of the apical septal, apical inferior, and apical segments
-Hypokinesis of the basal to mid anterolateral and basal to mid inferolateral segments. (Basal
Inferolateral = Posterior)

Learning Points:
1. Pseudonormalization of STE and/or STD, as in this patient with LVH, but also in LBBB and other
etiologies of chronic ST shift, should raise concern for OMI (Occlusion Myocardial Infarction).
2. Likewise, ST shift from a previous ECG (relative ST elevation or depression) is equivalent to STE or STD.
3. Ultrasounds can be very helpful in guiding your diagnostic pathway: location of WMA on US led 
to obtaining posterior leads.
4. Clinical presentation is important, but so is history. Have a higher suspicion for true pathology in 
anyone with significant comorbidities such as ESRD from diabetes, even if they are young and 
appear “not sick” on presentation.
5. Refractory Chest pain with a clearly positive troponin, without an alternative explanation, is an indication
for emergent cath lab activation regardless of ECG or bedside echo findings.

Comments by Dan

This case was particularly interesting for several reasons. First, the patient is such a young woman to have an occlusion MI (OMI), the likely difference being her significant risk factors. If she had no risk factors, it is doubtful that she would have developed such extensive coronary artery disease as we see on the angiogram. 

Because the troponins were so high, the clinicians did not need to rely on other diagnostics, including posterior leads and ultrasound, to confirm OMI and salvage what myocardium could be saved after hours of constant chest pain before the patient presented.  However, this additional information was supportive.

Note that by current guidelines, this patient had a NSTEMI, but it would hard to argue that her condition would not have worsened if she was left to 'next day cath'.  I took part in her ICU care and she was extubated and stable to transfer to a stepdown unit after a few days. Her repeat ECHO showed an improving EF of 37%. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI. 

Her first EKG in isolation has no hard findings that are diagnostic for an acute coronary occlusion. The importance of having a baseline EKG for comparison cannot be understated. The old EKG shows LVH by Sokolow-Lyon and Cornell criteria but much of that voltage is resolved in the new EKG, which is commonly seen in acute occlusion superimposed onto LVH. For some reason (with debatable physiology), coronary occlusion often causes decrease in the high voltage of LVH on the EKG. Thus it is difficult to study occlusions, particularly subtle occlusions, in the context of LVH. Armstrong et al attempted to study it but may have included too many 'obvious' cases - the criteria from that paper would certainly have missed this case.

There is an interesting finding in this EKG which is the positive notching of the latter portion of the QRS complex, upright in I, II, aVL and downward notching in III, aVF.  

I believe these represent the equivalent of Q-waves, or infarcted myocardium, of the posterior (inferobasal, lateral) wall. They appear in the latter part of the QRS complex because the posterior/basal wall is the last part of the ventricle to depolarize. The notching is not seen in the precordial leads because as it is traditionally taught, a tall R wave in V1 represents the 'upside down' Q wave in posterior infarction.  Thus, if you have LVH in which baseline precordial voltages are already predominantly negative, a posterior infarction should 'cancel out' some of that voltage and possibly diminish the voltage evidence of LVH on the EKG. Note that this is completely different from 'terminal QRS distortion'. 

This paper by Nui et al describes this finding (the "Delayed Activation Wave") in left circumflex occlusions but (I believe mistakenly) compares it to terminal QRS distortion. This finding is not new, and is analogous to Cabrera's and Chapman's sign.  As a Q-wave equivalent, this notching would be expected to persist in subsequent EKGs, as seen in the patient's follow up EKG 6 days later:

T-wave inversions and dynamic ST elevation

Written by Pendell Meyers, with edits by Steve Smith

I received a text message with no clinical information other than the following ECG, with the question "Is this Wellens? No prior ECG available."

What do you think?


















I responded that this ECG represented benign T-wave inversion (BTWI), not Wellens. I asked for more history.

It turns out this was a 25 year old male with no past medical history presenting after he was found "passed out" or laying down on the floor of the nursing home facility where he works. He was reported to be intermittently answering questions and seeming "not himself." Family reported that he had 2 similar episodes in the past 3 months, which the patient describes as similar to "bad trips," including increased fatigue, confusion, and vague hallucinations. He had been evaluated last month at an outside hospital by a psychiatrist. He denied any substance use on the day of presentation. There was no history of exertional syncope or sudden death in the family.

Apparently a single troponin was ordered on the basis of the perceived ECG findings, which was negative. Three serial ECGs were performed which were all identical (though BTWI is not necessarily always perfectly constant).

He was discharged.

Two days later he presented again with a similar story. Here is his ECG on arrival from the second visit:

This ECG shows sinus rhythm around 65 bpm. The QRS complex has moderately high voltage but otherwise normal morphology. There is STE in V1-V3 of 1.0, 1.5, and 1.5 millimeters, which is completely normal. There are prominent J-waves in leads V4-V6, as well as leads II, III, and aVF. Lead V3 shows the first and third complexes with terminal T-wave inversions, but the second complex does not appear to have this terminal T-wave inversion - whether this is due to a brief episode of baseline wandering / lead manipulation, or beat to beat variation is unknown, but I believe it is more likely brief baseline movement. The terminal T-wave inversion is no longer present in V4 as it was in the first presentation. Overall the second ECG is better characterized as "benign early repolarization" or simply "benign ST elevation" than by BTWI.

Another single troponin was normal. He was discharged with outpatient psychiatry and primary care.


How do I recognize this as BTWI? 

Most importantly because it matches the examples of BTWI I have seen on this blog, and does not match Wellens syndrome. The T-wave inversion in lead V3 of the initial ECG just does not look like reperfusion. Lead V4 of the initial ECG has the complete morphologic package of BTWI, including high voltage (large R wave), smaller S-wave, prominent J-wave followed by minimal STE and then characteristic terminal T-wave inversion. The history obviously helps as well, as this was a young African-American patient with symptoms of near-zero pretest probability of ACS. Some cases will not be so easy clinically.

Also important, "Wellens' syndrome" requires clinical factors in addition to ECG findings, including chest pain which resolved prior to recording of the ECG. Wellens' syndrome is not diagnosed during ongoing pain, as this would not be consistent with reperfusion (which should produce resolution of pain). On the ECG Wellens' syndrome also requires that there are preserved R-waves in the precordial leads.

Below I have reproduced a list of findings of BTWI from a series of other blog posts on this topic on this site, and we will go through each one with respect to the first presentation ECG:



1. There is a relatively short QT interval (QTc less than 425)
YES. Computerized QTc in this case was 424 msec.

2. The leads with T-wave inversion often have very distinct J-waves
YES. J-waves are present in V4-6, as well as II, III, aVF.

3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
Here the TWI is in leads V3-4 only. So this doesn't really distinguish. Also, Wellens' syndrome is simply one particular example of reperfusion (in this case, of the anterior wall). Reperfusion can obviously happen in any coronary distribution, and the same pattern of findings will happen in any affected wall.

4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves)
There is certainly no evolution consistent with continued reperfusion from OMI (occlusion MI), as there would be in the case of Wellens' syndrome. The changes from presentation 1 to 2 are clear, but these are potentially explainable by lead placement or simply the normal variation of ECG findings in normal healthy patients from day to day or hour to hour (we don't really know the answer to this, except to say that we have a large amount of personal experience showing many cases of benign ECG patterns which show changes with repeat ECGs). We have shown many times on this blog that essentially no normal ECG is 100% guaranteed to be completely stable over time. See this case. And this case. And this case. And this very recent case with supporting references:

Huge Precordial ST Elevation in an ED Patient

The opposite, however, is fairly reliable: if the patient has OMI or reperfusion from OMI, the ECG abnormalities will evolve along the expected progression (depending upon continued occlusion and infarction or reperfusion). Therefore, lack of serial ECG changes in the appropriate time frame can be interpreted as evidence against ischemia, but presence of changes is not necessarily indicative of ischemia (it might be, but it might not because there is a significant amount of variation based on lead placement, day to day, etc). Those who have studied cases of OMI versus benign ECG patterns from this blog can usually tell the difference.


5. The leads with T-wave inversion (left precordial) usually have some ST elevation
In the first presentation ECG there is minimal STE. In the second presentation there is slightly more.

6. Right precordial leads often have ST elevation typical of classic early repolarization
In the first presentation, no. In the second presentation, yes.

7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
YES, seen in V4 of the first presentation ECG.

8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
YES, again seen in V4 of the first presentation ECG.

9. II, III, and aVF also frequently have T-wave inversion
YES, the first presentation ECG does have flat/minimally inverted T-waves in the inferior leads.


Learning Points:

Benign T-wave Inversion is recognizable and (with experience) reliably differentiated from anterior reperfusion (Wellens).

Almost all the patterns of normal variant ECGs may show some changes upon serial ECGs. This may be due to lead placement and/or actual primary morphologic change of unknown etiology and significance. These changes can be distinguished from ischemic progression changes.

If you record serial ECGs and there is no evolution over an appropriate time frame, then the lack of evolution is a fairly strong piece of evidence against ischemic ECG changes. The presence of dynamic changes on repeat ECGs, however, may be either progression of ischemia or meaningless, normal variation in a patient's baseline - with the experience provided by this blog these are usually not difficult to differentiate.

References

1. Kambara et al. Early repol is not stable over time.  https://www.sciencedirect.com/science/article/pii/0002914976901429

2. Mahaveer C. Mehta, MD.  Abnash C. Jain, MD.  Early Repolarization on Scalar Electrocardiogram. The American Journal of the Medical Sciences. June 1995; 309(6):305–311.

ABSTRACT

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1—5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

3. Here is a good review of early repolarization by Mehta:

https://drive.google.com/file/d/1HJXiD6j6BV7paLpmegq-jhlO-_jVmnwS/view