A man in his 50s with anterior ST elevation and a "tall T wave in V1"

Written by Pendell Meyers

Take a look at this ECG from a 57 yo M without any context first:

What do you think? Imagine he presented with chest pain.

There is normal sinus rhythm. QRS shows high voltage, likely representing LVH. There is STE in V1-V4 measuring up to 3-3.5 mm, and STD in V5-6. V2 has saddleback morphology, and V3 has a straight ST segment. V4 has slightly convex ST segment.

Findings that would potentially favor OMI: large absolute amount of STE, large proportion of STE to QRS in V1-2, STD in areas like V5-6 that would be considered reciprocal to V1-2 area, straight ST segment in V3 and slightly convex in V4.

Findings that would potentially not favor OMI: high voltage, LVH, saddleback morphology in V2, LVH with appropriate discordant ST/T segments explaining STE in right precordial leads and STD in left precordial leads. Saddleback morphology in V2, when in the same location as the STE that you are potentially worried about, is a quite strong feature suggesting a pseudoSTEMI pattern rather than true OMI.

In the proper clinical context, it would not be wrong to call this concerning for STEMI(+) OMI. But with more and more experience, some of these false positive features can be distinguished from true positives. Regardless, the first things to check would be the clinical context and any prior ECGs if available.

This ECG was sent to me without any context, and I responded, "I see why you are concerned, but I think this is likely a false positive from LVH. I would not activate the cath lab for this ECG at this point, but tell me more about the clinical picture and any prior ECG if available."

I sent it to Dr. Smith with no context, and he immediately responded: "very interesting pseudoSTEMI pattern"

In this case, the patient had only syncope which was explained by alcohol intoxication, poor PO intake otherwise, and standing in a line for a prolonged period of time. He did not have any active ACS symptoms. 

Additionally, he was fortunate enough to go to an ED where they had his prior ECGs on file: 

One of the clinicians who saw this patient told me they were worried because of "new tall T wave in V1." They stated that the prior T waves in V1 were flat or had terminal inversion. The present ECG above has a fully upright and larger T wave. That is true, but there is something about the morphology of it that does not match the many prior hyperacute T waves I have seen in lead V1. It comes with experience, and with seeing the other pseudoSTEMI features in this case.

 

His troponin was less than 6 ng/L, and other basic labs within normal limits.

He had a prior echo on file showing symmetric LVH which was attributed to longstanding hypertension. 

He had no family history of sudden death or obvious known HOCM, Brugada. 

He was observed for sobriety and no further episodes of syncope or cardiac dysrhythmias were noted.

He was discharged.

See these examples of saddleback morphology in V2:

Saddleback ST Elevation. Is it STEMI? Is it type II Brugada?

Is this Saddleback a STEMI??

Epigastric pain, Syncope, and Saddleback ST Elevation

A 65 Year Old Man with Chest pain and Precordial ST Elevation

Non-Vagal Syncope and Saddleback Morphology in V2

Is this STEMI? Pattern Recognition is Key

RSR' with ST elevation: is this Right Bundle Branch Block with STEMI? Type 2 Brugada?

Why is there ST Elevation in lead V2? Think Lead Placement.

Here are the only two examples we've been able to find with V2 saddleback that represented LAD Occlusion:

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

A Very Subtle LAD Occlusion....T-wave in V1??

See these other great and related posts about LVH:

Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?

Profound ST Elevation in V1-V3. What do you think?

A 31 year old with Diabetes and HTN complains of bilateral arm tingling and headache

LVH with anterior ST Elevation. When is it anterior STEMI?

Huge Anterior Voltage, with ST Elevation

ST Elevation and Positive Troponin. Is it STEMI? No. And it is not even ACS.

Hyperacute T-waves? Anterior STEMI? No, LVH with PseudoSTEMI pattern!

Learning Points:

LVH causes some of the most common and most difficult ECG patterns to differentiate from STEMI and OMI.

When LVH causes pseudostemi patterns, the STE that catches everyones eyes is usually in the right precordial leads V1-V3, where it is discordant to the QRS of LVH.

Saddleback morphology, often in or around lead V2, is very uncommon in OMI of that same location, to the point that we have only been able to report 2 such cases (see links above), despite 1,326 (!) published as of today.

ST segment convexity and straightening are features that somewhat favor OMI, but this is most applicable in a normal QRS complex context.

Comparison to prior ECGs and the clinical context are obviously and always paramount, and can frequently help you out of false positive STEMI criteria scenarios like this.

Narrow Complex Tachycardia at a Rate of 220

40-something yo who is on flecainide and diltiazem had sudden onset chest pain, palpitations, shortness of breath and diaphoresis:

Rate is 220.  What do you think?

It is fast, narrow, and regular, without P-waves.  So it is not atrial fib and not VT.   It is a regular narrow complex tachycardia.   There is a lot of ST depression -- this is ischemia caused by the very fast rate and is an indication for emergent electrical cardioversion.

What is the DDx?  

----PSVT (which includes AVNRT and orthodromic AV reciprocating tachycardia) [AVRT uses an accessory pathway, a "bypass tract" and thus is seen in WPW; about 30% of PSVT is orthodromic AVRT] 

----Atrial Flutter with 1:1 conduction.

Which is it?

The fact that the patient is on Flecainide and Diltiazem is good evidence that this is atrial flutter with 1:1 conduction.  These medications are primarily given to patients with atrial fib or flutter (the flecainide keeps the patient in sinus rhythm, and the diltiazem prevents 1:1 AV conduction when the patient is in flutter).

If you look closely at lead II across the bottom, it appears there are flutter waves.

This is atrial flutter with 1:1 conduction.  The patient is not on anticoagulants, but the very fact that he is on flecainide is evidence that he probably spends most time in sinus rhythm.

The providers thought this was AVNRT.

He was given adenosine 6mg, then 12mg, with no change.  If AVNRT, then one would expect conversion.  If flutter, one would expect AV blockade and uncovering of obvious flutter waves.  But the dose of adenosine clearly was not high enough to sufficiently block the AV node.  One could escalate to 18 mg.  This was not done.

Instead, they appropriately decided on electrical cardioversion.  The decided to sedate with etomidate. After giving the etomidate, but before cardioversion, they noticed that the patient had "converted":

Here is the 12-lead:

What happened?  Rate is now 120.

Ischemia is gone.

The providers thought that the patient had spontaneously converted.  

However, look closely (this explanation is fascinating -- pay attention!!): there are still flutter waves.  The flutter rate is 240 and there is 2:1 conduction with a ventricular rate of 120.  Go back to the first ECG, and the ventricular rate was 220, which means that the atrial flutter rate has INCREASED from 220 to 240!!

The reason that the ventricular rate has slowed is that the flutter rate has increased!!

The AV node cannot conduct as a rate of 240, but it can conduct at a rate of 220.  When the atrial flutter rate increased, the AV node could not keep up and the patient got much better because of a decreased ventricular rate.

Why did the flutter rate increase?  Not certain, but just a change in sympathetic tone would do it.

A short time Later the patient actually converted to sinus:

What would have a happened with a higher dose of adenosine?  The AV node would have blocked the conduction for a brief time and the flutter waves would have become obvious. Then the adenosine would be quickly metabolized, and the AV node would resume 1:1 conduction.  So adenosine does not treat this, but sometimes makes the diagnosis obvious.

Learning Points:

1. Patients who get atrial flutter and are kept in sinus rhythm with a type I antidysrhythmic, usually flecainide, must be on an AV nodal blocker to prevent 1:1 conduction.  In this case, it is uncertain if he had not taken his diltiazem, or if he needed a higher dose.

2. Regular Narrow complex tachycardia, if not sinus tach, is AVNRT, AVRT, or atrial flutter with 1:1 or 2:1 conduction.

3.  Never try to convert atrial flutter with a drug such as procainamide without first giving an AV nodal blocker.  You will cause a slowing of the atrial flutter rate with potential to INCREASE the ventricular rate.

Syncope in a young man

 Written by Pendell Meyers

Let's say a young person presented with exertional syncope. They are now at baseline, asymptomatic, normal vital signs, and they have this ECG at triage:

What do you think?

Below are two other variations of this patient's resting ECG from different time periods:

Answer: Arrhythmogenic Right Ventricular Cardiomyopathy

See the end of the post for review and details on ARVC and it's ECG findings, but suffice to say that this patient has sinus rhythm, small epsilon wave in some of his ECGs, and R waves in V1-V3 with TWI.

Here is a close up of V1-V3:

Notice the very subtle micro-voltages at the J point.  These are epsilon waves.

As a teenager, this patient was playing basketball when he suddenly collapsed and became unresponsive. EMS found him in ventricular fibrillation. He returned neurologically intact. During his hospitalization he received an ICD. Genetic testing confirmed arrhythmogenic right ventricular cardiomyopathy/dysplasia with a mutation in his desmoglein-2 gene. During hospitalization he was started in mexiletine for frequent uniform PVCs which seemed to significantly decrease ectopy burden. He was restricted from activity and later also metoprolol was added.

Over the years he has had several ICD shocks, several medication adjustments, but is otherwise doing well. 

ARVD Review below, reproduced from this post: 

Young man with syncope while riding a bike [Arrhythmogenic Right Ventricular Dysplasia (ARVD)]

ARVD, also known as arrhythmogenic RV cardiomyopathy, is estimated to have a prevalence of 1 in 5000 adults and is responsible for approximately 11% of sudden death in young adults and 22% in a study of athletes in northern Italy.  The diagnosis is not easy (see below).

Gemayel C, Pelliccia A, Thompson PD.  Arrhythmogenic right ventricular cardiomyopathy.  J Am Coll Cardiol. 2001;38(7):1773.  Full text: http://content.onlinejacc.org/cgi/reprint/38/7/1773.pdf

There is a 2010 publication by the Task Force in Diagnosis of ARVD: Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. 

Free full text: http://circ.ahajournals.org/content/121/13/1533.full.   

There are 6 categories of criteria: 

1) Imaging

2) Pathologic

3) ECG Repolarization

4) ECG Depolarization

5) Arrhythmias

6) Family History.  

ECG and historical Highlights of this publication are (Suspect ARVD with):

1) High risk syncope with no other etiology; Family History

2) Depolarization abnormalities (Major criteria):

        a) Epsilon Waves

        b) Localized prolongation (greater than 110 ms) of the QRS complex in right precordial leads (V1-V3)

3) Repolarization abnormalities in patients of age at least 14 years (because younger patients often have juvenile T-waves)

        a) Minor: Inverted T-waves in right precordial leads V1-V2 

        b) Major: Inverted T-waves in right precordial leads V1-V3 or beyond (major criteria) 

4) Arrhythmias

        a) Major criterion:

                i) VT of LBBB morphology with superior axis (negative or indeterminate QRS in leads II, III, aVF and positive in lead aVL) (major criteria)

        b) Minor criteria:

                i) VT of LBBB morphology with inferior axis (positive QRS in leads II, III, aVF and negative in lead aVL) (minor criteria)

                ii) More than 500 PVCs per hour

5) Finally, it is a progressive disease and patients without ECG abnormalities may develop them over time.

Here is an example of an epsilon wave (image C).  And another example.  Here are some great examples from the post on RV dysplasia (translated by Google translate!) on Pierre Taboulet's great French site:  #1, #2, #3

Here's a great example on Wave Maven.

Here is an explanation od the importance of leads V1 and V2.

Here is another nice example.  I've taken the liberty of blowing up part of the ECG at this link for better viewing.  Look closely at V1-V2:

There are Epsilon waves (small waves at the end of the QRS) and also a slight prolongation of the QRS at the very end. 

Some excellent references on ARVD:

This is a case report with lots of good info, from 2019, but you can only read it if you have a subscription to American J Cardiol:

Holshouser JW and Littmann L.  Usefulness of the Electrocardiogram in Establishing the Diagnosis and Prognosis of Arrhythmogenic Right Ventricular Cardiomyopathy

Other References, from the above article:

1

FI MarcusEpsilon waves aid in the prognosis and risk stratification of patients with ARVC/D

J Cardiovasc Electrophysiol, 26 (2015), pp. 1211-1212

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2

FI Marcus, W ZarebaThe electrocardiogram in right ventricular cardiomyopathy/dysplasia. How can the electrocardiogram assist in understanding the pathologic and functional changes of the heart in this disease?

J Electrocardiol, 42 (2009), pp. 136.e1-136.e5

Article

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RNW Hauer, MGPJ Cox, JA GroenewegImpact of new electrocardiographic criteria in arrhythmogenic cardiomyopathy

Front Physiol, 3 (2012), p. 352

eCollection 2012

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FI Marcus, WJ McKenna, D Sherrill, C Basso, B Bauce, DA Bluemke, H Calkins, D Corrado, MG Cox, JP Daubert, G Fontaine, K Gear, R Hauer, A Nava, MH Picard, N Protonotarios, JE Saffitz, DM Sanborn, JS Steinberg, H Tandri, G Thiene, JA Towbin, A Tsatsopoulou, T Wichter, W ZarebaDiagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria

Circulation, 121 (2010), pp. 1533-1541

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5

WC Roberts, N Kondapalli, SA HallUsefulness of total 12-lead QRS voltage for the diagnosis of arrhythmogenic right ventricular cardiomyopathy in patients with heart failure severe enough to warrant orthotopic heart transplantation and morphologic illustration of its cardiac diversity

Am J Cardiol, 122 (2018), pp. 1051-1061

Article

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6

JE Madias, R Bazaz, H Agarwal, M Win, L MedepalliAnasarca-mediated attenuation of the amplitude of electrocardiogram complexes: a description of a heretofore unrecognized phenomenon

J Am Coll Cardiol, 38 (2011), pp. 756-764

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A man in his late 40s with chest pain

 Written by Pendell Meyers with edits by Smith

A man in his late 40s with no known medical problems was at work when he suddenly experienced midsternal chest pain radiating down both arms. Approximately 1 hour after onset of symptoms he was triaged at the ED, with ongoing chest pain, normal vitals, and this triage ECG:

What do you think?

Twice, months apart, I sent this ECG to Dr. Smith without any context or other information (I do this many times per day, with many normal or false positive cases mixed in). The first time he responded "acute ischemia but not active occlusion". The second time he responded "LVH and subendocardial ischemia." It is the same response each time: active subendocardial ischemia.

The computer interpretation states "Left ventricular hypertrophy with repolarization abnormality." So it states there is an abnormality, but attributes it to LVH.

There is sinus rhythm with normal QRS (except for borderline high voltage and LAD, some would call it LAFB - LVH can mimic LAFB). There is a tiny but definite hint of STD in V4-V6, maximal in V5 and V6. There is a tiny amount of STD in I and II and aVL. There is a tiny amount of reciprocal STE in aVR. There is a tiny amount of STE in V1. With such a normal QRS complex, none of these ST segment changes are explained by the QRS complex, and all of them must be considered new and significant until proven otherwise. 

In this pattern, with STD maximal in V5-6 with reciprocal STE in aVR, the ECG is diagnostic for supply/demand mismatch ischemia, also known as subendocardial ischemia (as opposed to OMI, or focal subepicardial ischemia). The ECG pattern of supply/demand ischemia is largely identical regardless of the cause, whether or not it is due to decreased oxygen supply (e.g. left main ACS but with collaterals or without total occlusion, triple vessel disease with non-occlusive ACS, decreased blood pressure, hypoxemia, etc.), increased demand (infinite number of non-ACS causes), or both.

Thus, the interpretation of the supply/demand mismatch pattern on ECG depends completely on the clinical context. 

This patient's clinical context is clearly most likely ACS. Therefore the interpretation is acute, active, non-occlusive ischemia until proven otherwise. This could be compatible with left main ACS (but not total occlusion without collateral circulation) or basically any other acute non-occlusive ACS event causing a significant area of supply/demand mismatch. 

So the patient has definite ACS symptoms, with an ECG showing active ongoing ischemia. He should be assumed to have an acute culprit lesion which could fully occlude at any moment, or could cause significant ischemia and complications at any moment even without fully occluding.

Below you can see close-ups of leads V5, V6, and aVR, with and without red lines showing the baseline, highlighting the small but definite and very important STD and STE.

Case Continued:

The ECG was read as sinus rhythm with no signs of STEMI (that's of course true). Due to overcrowding, and thinking that he had normal vital signs and a "normal" ECG, he had initial labs drawn and was sent to the waiting room until a regular room became available. No medicines were given at that point.

Approximately 30 minutes later, he called out for help in the waiting room. He vomited and collapsed, and was found to be in cardiac arrest. CPR was started and he was brought to the resuscitation area where his rhythm was described as "fine VFib." Multiple defibrillation attempts were made, as well as continuous high quality CPR, but there was no change in rhythm, never any brief ROSC. Thrombolytics were considered but not given due to concern that the etiology was not clear, and they stated they were considering aortic dissection as a possible cause. The arrest was called after about 40 minutes.

The troponin drawn at triage resulted at 121 ng/L (upper reference limit 20 ng/L for men). It is unclear whether the team had this information during resuscitation.

An autopsy was later performed, showing no PE or dissection, but an 80% stenosis of the proximal left circumflex artery. The report does not comment on whether there were signs of fresh thrombus at this location, or whether they could tell if there were definitively acute plaque rupture. There was also 50% luminal stenosis of the mid RCA. 

The autopsy report states:

"Myocardial infarcts less than four hours old show no histologic changes so it is difficult to prove an acute myocardial infarct in less than that time period. Correlating the patient's substernal chest pain and coronary artery disease with cardiac arrest and inability to return to sinus rhythm, a myocardial infarct is the presumed cause of death. Pertinent negatives include that there was no evidence of aortic rupture or dissection. There was no pulmonary embolus. There were minimal pathologic changes throughout the body."

We did not need an autopsy to conclude that ACS was the most likely cause of death, but this autopsy obviously supports that theory. It seems overwhelmingly likely to me that the LCX lesion was the acute culprit. It could have caused VF arrest without fully occluding, or it could have fully occluded in the waiting room and then caused VF arrest (without any ECG performed after triage). One third of patients with confirmed STEMI on the ECG do not have 100% occlusion (TIMI 0 flow) at the time of their emergent cath, so it is very likely that a full LCX occlusion could be only 80% at the time of autopsy. But again, one need not have occlusion for ischemia to result in VF arrest.  

Learning Points:

1. Any ischemia can result in ventricular fibrillation, even non-occlusive ischemia.

2. Moreover, non-occlusive thrombi can become occlusive: thrombi are dynamic; they propagate and lyse continuously.   

3. Patients with symptoms that have even just a moderate likelihood of being due to ACS or due to any ongoing ischemia should not be sent to the waiting room.  They need to be on a monitor in case of dysrhythmia, and take priority over most other patients in the ED.

4. Even if you are not certain that ST depression represents ischemia, it is prudent to at least have the patient in a monitored bed while you are undertaking more investigation. These patients should be a "stat placement" to monitored bed.

Commentary

There is confusion created by the educational campaign of "ST elevation in aVR."  Often, the first thought that providers have when they see STE in aVR is that the patient has "left main occlusion," even in a clinical context that is not consistent with ACS.  And yet when this patient with clear clinical ACS presents with1 mm of reciprocal STE in aVR, it was not seen or understood. We have a significant number of unnecessary cath lab activations due to STE in aVR because providers do not understand that it is one of the most common ECG findings in patients who have any significant illness causing supply/demand mismatch. This is why I title my aVR lecture: "Lead aVR: Once "forgotten," now remembered, always misunderstood." It's gotten to the point that cardiology perceives that we are crying wolf. This is one of the most common findings other than obvious STEMI that cardiologists get consulted for, but the majority of the time it is simply supply/demand mismatch due to a variety of etiologies, including AF with RVR, hypovolemia, GI bleed, respiratory failure, sepsis with hypotension, aortic stenosis, and others. 

STD maximal in V5-6 and lead II, with reciprocal STE in aVR, indicates global supply/demand mismatch subendocardial ischemia, which can be due to ACS or non ACS causes.  

It is important to realize that ischemic ST depression due to subendocardial ischemia does not localize to the leads which show ST depression.  There is usually an ST depression vector towards the apex of the heart (leads II and V5, V6), with reciprocal STE in aVR, and if it is very profound, it is often due to left main or LAD ischemia, or due to non-occlusive ACS of any vessel along with disease of all 3 vessels.  However, non-occlusive ischemia of any artery can result in such ischemic ST depression even in the absence of 3 vessel disease.

STD maximal in V1-V4, in contrast to V5-V6, is reciprocal to subepicardial ischemia due to OMI (reciprocal to what would manifest as ST elevation of overlying leads if they were there).   The exceptions are when there is an abnormal QRS to account for secondary STD, such as RBBB or to a non-ischemic etiology of STD such as hypokalemia.  

Stay tuned for our upcoming publication in JAHA on STD maximal in V1-V4 vs. V5-V6.

Aspirin should be given at triage for a clinical history and ECG like this, unless there is some strong suspicion of dissection (not present in this case). Dissection is far less common than ACS.

After a VF arrest, there should be no doubt that this was ACS and that coronory thrombosis was the etiology.  When the patient could not be resuscitated, this patient would have been a prime candidate for ECMO. If he had arrested in cities such as Minneapolis, with refractory VF ECMO programs (before the program was suspended due to Covid), he would likely have been an ideal candidate for ECMO, in a population that seems to be receiving a nearly 50% chance of neurologically intact survival. If ECMO is not an option, and going to the cath lab during arrest is not an option, I would try thrombolytics before ending the resuscitation on a young healthy witnessed ACS arrest.

Transesophageal echo (TEE) can help decide between asystole and fine VF.

A man in his 70s with chest pain, shortness of breath, and acute huge anterior ST elevation

Written by Pendell Meyers

A man in his 70s presented to the ED complaining of various symptoms including chest pain and shortness of breath. He had a very hard time explaining his symptoms, and it was very hard to obtain an accurate history. It was unclear to us how long the patient had been experiencing symptoms, but I feel confident that he was actively having symptoms at the time of my evaluation. He did seem to admit to using cocaine, possibly yesterday evening, but unclear. His vitals were within normal limits except mild tachycardia.

Here was his triage ECG:

What do you think?

I texted it to Dr. Smith with no information and he said "Very weird. I have seen a patient with Brugada who also had acute LAD occlusion. That is what this looks like!"



Needless to say, it is alarming. There is sinus tachycardia with a narrow QRS complex that has poor R wave progression and some minimal right axis deviation. There is striking, huge STE in the anterior and lateral leads. But is also has a prominent J wave and saddleback morphology, also with elements of brugada pattern. I do not see any signs of hyperkalemia, which also frequently creates acute STE and brugada pattern in V1-3.

Saddleback STE is very rarely present in the same leads as acute OMI. 

Just to make sure, I checked all the leads and got another immediate repeat ECG:

I compared this to his prior ECG on file:

All STE and T waves are reasonable for this narrow large voltage QRS complex, which has poor R wave progression and possible LVH. If it did not have tiny R waves in V2-V4, I would say it is close to LV aneurysm morphology. Regardless, the anterior findings in his presentation ECG are clearly new.

With a limited history endorsing chest pain and shortness of breath, and this striking STE, I activated the cath lab. But I had some doubts about what was going on. While waiting for the cardiology team, I did a bedside echo (no contrast) that was slightly limited by poor windows, but I feel confident that I could see some areas of the anterior and lateral walls, and I saw only good function, good thickening and movement.

The cardiology provider arrived and we discussed how unsure we both were of this being acute coronary occlusion. But ultimately we agreed that it would be best to proceed with emergent angiogram and find out. The initial troponin had not returned yet when we made this decision.

He went to cath and was found to have no acute culprit lesion. He had several chronic lesions including mid LAD 50%, D1 50%, D3 50%, none of which were felt to be acute or culprits. The summary of the report reads "Surprisingly, no significant coronary stenoses were found, possible cocaine induced LAD spasm."

However, there was no spasm directly shown on the angiogram, and no intracoronary treatments for spasm. The EF was estimated at 55%, without any wall motion abnormalities.

Initial troponin returned within normal limits at 8 ng/L (upper reference limit up to 20 ng/L for men).

His only repeat ECG after cath was 5 hours later, shown here:

All anterolateral findings resolved, back to baseline. Not currently any evidence of reperfusion in that area, such as terminal T wave inversion. The inferior leads have some artifact and baseline movement, but there is possibly some STE in II, III, and aVF which is normal and seen on some of his prior ECGs below.

Two more serial troponins were the unchanged, all 8 ng/L.

A formal echo showed EF 64% with no wall motion abnormalities.

Urine drug screen was positive for cocaine. Potassium was 4.6, CBC and basic metabolic panel all normal.

He was discharged the next day with a diagnosis of cocaine chest pain and vasospasm.

Out of curiosity, I decided to dig into his prior visits (multiple for various vague complaints, sometimes cocaine, sometimes chest pain and shortness of breath) and see if any ECGs before have shown similar findings:

None of these visits included any evidence of AMI. Not a single positive troponin, no other angiograms ever done, never any abnormal cardiac echo.

These ECGs are just variations of his normal variant baseline. You can see that some days his ECG is slightly different that others, some days his normal variant STE is greater in some locations that others. Sometimes tachycardia, hypertension, etc. can exaggerate these findings. These types of variations between ECGs are seen commonly and I have a hard time explaining to learners why they are not "dynamic," or why they are meaningless even if they can be described as "dynamic." The bottom line is that I have seen many of these fluctuating baseline ECGs, and seen many OMIs with subtle but truly diagnostic dynamic changes. Sometimes I can tell them apart, sometimes not, but I get better with more and more experience.

Regardless, I do not see any ECG in this patients history that looks even remotely close to his presentation ECG.

Was this cocaine induced Na channel blockade, causing brugada pattern? That's the best guess I have.

Was it LAD spasm enough to cause enormous anterior STE for at least a half hour, but without causing ANY rise at all in serial high sensitivity troponins? Is that even possible? I think probably not.

Was it some kind of bizarre pulse tapping artifact? I doubt it.

See Dr. Balasubramanian's comments at the end!

Learning Points:

Saddleback STE morphology is usually considered unlikely to be due to OMI. But we have seen a few rare cases break this rule.

Brugada pattern can be seen in a wide variety of scenarios other than Brugada syndrome. Especially hyperkalemia and sodium channel blockade.

The diagnostic portion of the angiogram is not very dangerous, compared to the risks of the actual intervention if OMI is found (in which case, the benefits are probably worth the risks!). For a patient with possible ACS symptoms and an ECG like this, it is a very reasonable plan to take an emergent look with emergent angiogram. I still think this was a correction option at the time of the decision, with the information available.

The concept of OMI is not all about the ECG. The ECG is just one (very) important part of the decision.

Below I have reproduced some very interesting commentary sent to us about this case by Dr. R Balasubramanian from India:

 

Reg:  Blog Thursday   9^TH SEPTEMBER 2021

Dr Smith,

Brugada syndrome (BrS) and  Early Repolarization Syndrome (ERS) are two major phenotypic expressions of the same J wave family and this ECG is unique, because  both these syndromes are manifested in the same ECG of the same patient, incidentally solving the mystery of “what is the cause of the massive ST elevation, with the coronary angiogram drawing  a blank.”

In the first ECG ( Triage ECG ), of course, there is Brugada pattern in V1 & V2. Concurrently, there is also J wave lying near the baseline in each of the inferior leads ( II , III & aVF ). Now, please note the third ECG showing climbing up of the J wave along with mild  ST elevation. In the fourth ECG, the J wave has climbed up to two thirds of the R wave with about 5 mm of STE, with concave morphology and upright T wave. Thereafter, serial ECGs show J waves gradually climbing down with STE also settling down. So, the ST elevation in the anterior leads also must be on the same lines -a manifestion of pseudo-myocardial  hyperacute infarction pattern of ERS.

Occurrence of both BrS and ERS in the same ECG and same patient has given an incontrovertible  evidence that they are indeed similar in  patho-electrophysiology. That way this ECG is priceless and is likely to grab the attention of the scientific community.

With regards,

Dr.R.Balasubramanian.

Professor Emeritus in Medicine

SLIMS 

 Pondicherry - INDIA

A 76 Year Old Female With Recurrent Syncope, Lightheadedness, Palpitations and Negative Stress Test

Written by Lucas Goss MD, peer reviewed by Meyers, Smith, Bracey

A 76 year old female with a history of arial fibrillation not on anticoagulation, non-obstructive CAD found on coronary CTA 2 years prior, HTN, HLD, recurrent lightheadedness, and syncope status post loop recorder placement, presented for another episode of feeling lightheaded, diaphoretic, and feeling like she “was going to die.” She was discharged just the day prior for her second hospitalization for similar episodes. She was actually at the pharmacy to pick up her medicines the day after discharge when this episode occurred, and pharmacy staff sat her down in a chair while they awaited the ambulance. Her symptoms were mostly gone by the time of arrival.

Vital signs on arrival: BP 143/89, HR 63, RR 18.

During her recent hospitalizations she had a negative CT pulmonary angiogram (CTPA), negative nuclear stress test, normal echo, and her loop recorder did not identify any concerning findings when interrogated. During the first of two prior recent hospitalizations for similar symptoms, her troponin I rose from undetectable to 219 ng/L and trended back down, and the notes seem to attribute this to her blood pressure which was in the 200/110 range. During her second hospitalization (from which she was just discharged yesterday), she had multiple troponins all undetectable, less than 6 ng/L. 

A note on Loop Recorders, thanks to our electrophysiologist: 

They only record if:

1. The HR meets the programmed criteria (eg, pause over 3 seconds, HR<30 bpm, HR>*** etc). It’s unusual to program this “automatic recording trigger as HR of 50 or 40. 

2. The patient triggers recording when they have symptoms. In those scenarios it records a loop of several minutes before and a minute or so after (variable depending on company).

So if the patient did not trigger a recording when she had symptoms, then people usually don’t program automatic recording with HR in 40’s or 50’s otherwise decide memory will be full and there would be a lot of recordings that will be overwritten. 

Smith comment on troponins: the definition of myocardial infarction is 2 of the following:

1. Troponin rise and/or fall with at least one value above the 99th percentile reference range

2. Plus one or more of the following: A. Symptoms of MI; B. ECG evidence of ischemia;  C. Development of pathologic Q waves; D.  Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology; E. • Identification of a coronary thrombus by angiography or autopsy (not for types 2 or 3 MIs).

This patient had 1. and 2A., so she had a myocardial infarction.  

Now one needs to decide which type of Acute MI (usually type 1 or 2).  If type 2 MI, one must find an etiology of supply demand mismatch, or identify coronary dissection or spasm or a few other entities.  Syncope is the result of temporary loss of perfusion to the brain, and there are many etiologies, all of them are bad.  One must find the etiology.  More likely, this is a type 1 MI and the patient needs an angiogram regardless of ECG findings.

Here is her ECG on arrival (symptom free):

Initial ECG#1: (1159) 

ECG from 2 days prior (not "baseline," during prior admission):

Initial interpretation:

Sinus rhythm, normal QRS, no clear signs of ischemia, no signs of hyperkalemia, normal QT.

Meyers note: I read this ECG in real time, compared it to the prior, and did not see any clear signs of ischemia or OMI. In retrospect, I think perhaps the TWI in aVL is slightly more abnormal, and the ST segment and T wave in V3 slightly more "pushed down" than in the ECG from 2 days ago, but it is still not diagnostic to me. 

Case Continued

Labs demonstrated an unremarkable CBC and BMP, however her HS troponin I that was obtained in triage was mildly elevated at 23 ng/L. A repeat was obtained after she was seen by the physician at 1700 and had increased to 138 ng/L. Again, the combination of troponin rise and fall with symptoms is diagnostic of acute MI.

 

ECG #2: (1707)

There is baseline movement and artifact in critical leads such as II, III, aVF, and aVL where there is likely new STE and enlarging T waves in the inferior leads, with slight reciprocal changes in aVL.

The ECG should be immediately repeated to confirm or deny this suspicion, but it seems that it was not repeated at that time. 

Cardiology was consulted for admission and definitive coronary imaging. They accepted the patient, however while she was awaiting a floor bed, she became hypotensive and bradycardic.

 

ECG#3: (1834) 

 

This repeat ECG demonstrates a junctional escape rhythm with a rate of 36, however no definitive signs of OMI. At this time the patient was ill-appearing, lightheaded, and diaphoretic. Her blood pressure was 80/40. She was given 0.5mg of atropine while pads were being placed and shortly after her junctional rhythm resolved with improvement in her blood pressure and symptoms:

 

ECG#4: (1851)

She is now back in sinus rhythm on repeat ECG. There may be the tiniest hint of STE in lead III, and aVL shows the tiniest bit of reciprocal STD and increase in size of the negative T wave. There is a tiny amount of reciprocal STD in I, and there is a barely-perceptible amount of STD in V2 and V3 compared to prior. These findings are all highly suspicious for inferoposterior OMI.

Interestingly enough, her loop recorder was interrogated again and did not identify this event.

She was admitted to cardiology with plan for non-emergent cath the next day as well as EP evaluation for potential sinus node dysfunction. 

Overnight her troponins rose from 23 to 138 to 390 to 668 to 1,000 to 1,219, then they stopped measuring them at 2am in the morning (we are clearly committed to ignoring them anyway, so why wake us up for them?!).

While awaiting catheterization an EKG was obtained due to worsening symptoms:

 

ECG#5 (Hospital day 2)

This ECG shows sinus bradycardia with signs of inferoposterior reperfusion. Leads III and aVL are diagnostic of acute MI, but, because of the T-wave inversion, it is probably with an open artery (or collateral circulation). There is some STE in inferior leads leading into T waves with terminal inversion, which is reciprocally mirrored in aVL. There are posterior reperfusion T waves in the precordial leads, much taller than on the most recent ECG. 

Another repeat ECG was obtained a few hours later (just prior to catheterization):

ECG#6 (Hospital Day 2)

This ECG is slightly confusing as to the state of the vessel, as there is newly worsened STD maximal in V2-V4, but ongoing terminal T wave inversion in the inferior leads. I would assume that there is ongoing ischemia until proven otherwise.

Smith note: 3 possibilities: 

1. The artery is open but with TIMI-2 flow, enough to perfuse vessels to the inferior wall, but not to the posterior wall.  

2. TIMI-2 flow can be enough to result in T-wave inversion (apparent reperfusion) even though there is ongoing ischemia. 

3. There is collateral flow that is robust enough to result in T-wave inversion in the inferior, but not the posterior, wall.

 

Cardiac catheterization findings:

RCA: 100% stenosis from lesion described as “complex, noncalcified, consistent with atherosclerotic disease as well as a filling defect consistent with thrombus” supplying the inferior and posterior walls, which was successfully stented.

LAD: Mild luminal irregularities

Circumflex: Minor luminal irregularities

 

The patient afterwards underwent dual chamber pacemaker implantation due to sick sinus syndrome, as she continued to revert back into a junctional bradycardia.

 

What was interesting about this case is that she had multiple presentations for similar progressive symptoms, but had both negative stress test as well as echo within 2 weeks of this presentation. Additionally, after her episode of junctional bradycardia her loop recorder was interrogated and did not identify the event.

 

Learning Point #1: Recent Negative Stress Tests Do Not Rule Out ACS

Do not rely on a recent negative stress test to rule out acute coronary syndrome or high risk coronary lesions. A stress test has nothing to do with ACUTE coronary syndrome. A stress test is ostensibly designed to help detect symptomatic, chronic, stable coronary disease, in hopes that a patient's chronic stable exertional symptoms may be attributed to that stable coronary disease. Acute coronary syndrome can arise from small unstable atherosclerotic lesions that can rupture and cause OMI. These lesions may not be picked up on stress testing (because they are not yet ruptured and occluding!), as was the case above.  Several studies have demonstrated concerningly high percentages of patients experiencing acute MI with recent negative stress testing.^{1,2,3, 4} The supposed utility of stress testing is to identify critical, chronic, stenoses causing reduced coronary blood flow which reproduces a patient's stable angina symptoms. Coronary lesions not significant enough to be detected on stress testing can still undergo plaque rupture and thrombosis causing acute MI.

See Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations -- A Case from Salim Rezaie (R.E.B.E.L. EM)

 

Learning Point #2

Be able to recognize posterior reperfusion T waves as demonstrated here with large tall upright T waves with associated subtle ST depression.

See Series of Prehospital ECGs Showing Reperfusion

       A woman in her 70s with bradycardia and hypotension

      

 ^{References on evaluating patients in the ED who had a recent negative stress test:}

1. Walker J et al. Coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
3. Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 
4. Engineer RS, Lauer MS, Emerman CL. Chest pain after recent stress test: Is there a warranty? Ann Emerg Med [Internet] 2004;44(4, Supplement):S47. Available from: https://www.sciencedirect.com/science/article/pii/S0196064404008765