Tuesday, June 11, 2024

What if your system adopted the recommendation that a computer "normal" ECG need not be shown to the doctor?

Written by Pendell Meyers with edits by Smith.  Sent by anonymous

A man in his 40s with no previous heart disease presented within 30 minutes of onset of acute chest pain that started while exercising. There was associated shortness of breath and left arm radiation. 

This Triage ECG (ECG #1) was recorded on a chest pain patient at triage at 1906 (top highest quality image, bottom photo including computer algorithm interpretation):

"Sinus rhythm, normal ECG" (This was performed on a Mortara machine, most likely using Veritas algorithm, but I do not have perfect confirmation of that)

This ECG shows an obvious inferior acute coronary occlusion (OMI).  It is clearly missed by the conventional algorithm.  

Many systems now refrain from showing computer "normal" ECGs to the busy emergency physicians at triage because of very poorly conceived articles that say that if the computer algorithm says "normal," the emergency physician should not be bothered.  

Luckily, this institution does show all triage ECGs to the physician, who in this case immediately recognized OMI and activated emergent transfer to the local PCI center.

Here is the ECG interpreted by the Queen of Hearts:

Click here to sign up for Queen of Hearts Access

Here is ECG #2 at 1959 (I believe this is the time of arrival to the PCI center): 

Again, outrageous conventional algorithm interpretation!
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral
But at least it does not call it "Normal."

Queen of Hearts:

The initial troponin (high sensitivity troponin I) returned less than 6 ng/L.  Below the limit of detection.

Angiogram findings included:

95% mid RCA stenosis with occluded distal right PDA secondary to thrombus (peristent OMI). Successful drug-eluting stent placement opening up 95% mid RCA stenosis to 0% residual

Nonobstructive left system disease. 

Left-ventriculogram showed severe infero-apical hypokinesis with LV ejection fraction 50 to 55%. LVEDP 25.   This is a significant loss of myocardium and ejection fraction.  Some function might possibly recover over weeks.

Medical therapy for thrombotic occlusion of distal right PDA.

Formal echocardiogram:

Systolic function is at the lower limits of normal. The ejection fraction is 50% +/- 5% , calculated using biplane MOD. Severe hypokinesis of the mid-apical inferior and inferoseptal myocardium.

Troponin trend:
less than 6 ng/L
933 ng/L
13,386 ng/L, typical of STEMI
(none further measured -- it might have peaked at a much higher level if it had been measured to peak)

Repeat ECGs after PCI:

These are diagnostic of reperfusion.

The patient was discharged home the next day. No further follow up is available.

Learning Points:

You cannot trust conventional algorithms even to find STEMI(+) OMI, even when they say "normal ECG." We have shown many examples of this on this blog.

Queen of Hearts is available and performs well.

Click here to sign up for Queen of Hearts Access

You should not wait for the troponin when the history and ECG is diagnostic. Even in obvious STEMI(+) OMI, the initial troponin can easily be negative in the initial short time from onset of OMI.

The Queen of Hearts diagnoses almost all of these so called "Normal" ECGs with are in fact OMI and she does so with High Confidence:  

See this post of 10 cases:

When the conventional algorithm diagnoses the ECG as COMPLETELY NORMAL, but there is in fact OMI, what does the Queen of Hearts PM Cardio AI app say? (with 10 case examples)

See other relevant posts:

An undergraduate who is an EKG tech sees something. The computer calls it completely normal. How about the physicians?

Three patients with chest pain and “normal” ECGs: which had OMI? Which were normal? And how did the Queen of Hearts perform?

Four patients with chest pain and ‘normal’ ECG: can you trust the computer interpretation?

And literature:

McLaren, Meyers, Smith and Chartier. Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review. Acad Emerg Med 2024;31:296-300


MY Comment, by KEN GRAUER, MD (6/11/2024):
Recognition of repolarization variants can be challenging. At times, the distinction between a repolarization variant vs the early stage of acute OMI may not be possible solely on the basis of a single ECG.
  • To add to this complexity (as per My Comment in the August 22, 2020 post in Dr. Smith's ECG Blog) — the ST-T wave appearance in repolarization variants may be dynamic! On occasion — ST-T wave appearance with repolarization variants may change from one-hour-to-the-next — or, ST-T wave appearance may change due to a difference in heart rate, performance of exercise, or variation in vagal tone — and, sometimes even without any obvious explanation.
  • Finally — there is the clinical reality that a patient who has a "baseline" ECG that manifests a repolarization variant — may at some point develop acute coronary occlusion that in part is masked by benign-appearing ECG characteristics of the underlying repolarization variant.
It is for the above reasons that I was at first uncertain about the ST-T wave appearance in the inferior leads of the initial ECG in today's case (within the light BLUE rectangles in leads II,III,aVF in Figure-1).
  • Although the amount of J-point ST elevation in leads II,III,aVF in Figure-1 is more than is usually seen with repolarization variants, and the peak of the T wave in these leads seemed "bulkier" than usual — the upward-concavity shape of the ST segment (ie, "smiley"-configuration) was not unlike that seen in many repolarization variants.
  • Small and narrow q waves are seen in each of the inferior leads of ECG #1 — but in this patient with a relatively vertical frontal plane axis, narrow inferior lead q waves are a common normal manifestation of septal depolarization.
  • BOTTOM Line: I would not have diagnosed an acute OMI on the sole basis of inferior lead appearance in today's initial tracing.

KEY Point: Despite what I felt was the nondiagnostic picture presented by the ST-T wave appearance in leads II,III,aVF — Definitive ECG diagnosis of an acute OMI is present in ECG #1 for the following reasons:
  • The clinical history immediately places today's patient in a higher-prevalence group of patients likely to be evolving an acute OMI (ie, a middle-aged man who presents to the ED for new-onset CP [Chest Pain] that occurs during exercise, and lasts for at least 30 minutes!).
  • There is no way the ST-T wave appearance in lead aVL can be normal (within the RED rectangle in this lead). True reciprocal ST-T wave depression does not develop with repolarization variants. While some T wave inversion may normally be seen in lead aVL when the QRS is predominantly negative — there should not be J-point depression in such cases (the RED arrow in lead aVL) — and the inverted T wave should not be as "bulky" as it appears to be in lead aVL of ECG #1.
  • Once we know in this patient with new CP that the ST-T wave appearance in lead aVL is definitely abnormal (and consistent with reciprocal ST depression) — we then have to presume that the upward-concavity ST elevation in each of the inferior leads is not simply due to a repolarization variant — but instead, must be interpreted as an acute inferior OMI until proven otherwise.
  • PEARL: Acute posterior involvement is a common accompaniment of acute inferior OMI. Therefore, the fact that the limb leads show an acute inferior OMI — should prompt us to carefully scrutinize anterior leads for any suggestion of posterior involvement.
  • Having said this — there is no way the ST-T wave appearance in lead V3 of ECG #1 can be normal (within the RED rectangle in this lead). As we often emphasize on Dr. Smith's ECG Blog — there is normally slight, upward sloping ST elevation in leads V2 and V3. The RED arrow in lead V3 highlights the isoelectric (ie, non-elevated) baseline of the J-point in this lead — which in the context of the above ECG findings, strongly suggests acute posterior OMI until proven otherwise.
  • By the concept of neighboring leads — I strongly suspected that the ST-T wave appearance in lead V2 was also abnormal because: i) There is no more than the most minimal J-point elevation in this lead; and, ii) The T wave appears more pointed than expected (potentially suggesting some posterior reperfusion).
  • To EMPHASIZE: I would not perceive lead V2 by itself to be abnormal (especially given how deep the S wave is in this lead) — but because the history and limb lead appearance are diagnostic of acute inferior OMI — and — because lead V3 truly suggests associated acute posterior involvement — I suspected that the subtle changes in lead V2 were probably also abnormal.

Figure-1: I've labeled the initial ECG in today's case — and compare it with the repeat ECG done 53 minutes later.

What Do We Learn from ECG #2?
The diagnosis of acute infero-postero-lateral OMI becomes obvious with the evolution seen in ECG #2: 
  • The ST elevation in the inferior leads of ECG #2 has increased — and the shape of this ST elevation has clearly taken on a more acute appearance.
  • There is more ST depression in lead aVL — and the shape of this reciprocal ST depression has taken on a "shelf-like" appearance.
  • The peaked T wave previously seen in lead V2 has been replaced by ST depression. The upright T wave seen in lead V1 of ECG #1 is also gone.
  • There is now frank ST segment straightening, with some definite ST elevation in leads V3-thru-V6.
At this point — a STEMI was diagnosed, and cardiac cath with PCI was performed.
  • Given the history of new-onset worrisome CP — the initial ECG in today's case was diagnostic of acute infero-postero OMI for the reasons detailed above.
  • The fact that the initial troponin was normal does not in any way rule out acute OMI — as the initial troponin is not always elevated.
  • KEY Point: The comparison between ECG #1 and ECG #2 done just 53 minutes later — shows a dramatic change! Significant ST-T wave abnormalities may evolve over a period of minutes in an actively ongoing OMI. If either the initial ECG in today's case was not recognized as diagnostic of acute OMI — or — the interventionist cardiologist On-Call could not yet be convinced of the need for prompt cath from the initial ECG — it is likely that a repeat ECG done much sooner than 53 minutes later would have satisfied their criteria for cath.
  • In cases like this — repeating the ECG every ~10-20 minutes until there are ECG changes sufficient for the patient to be accepted for cath is advised.

Sunday, June 9, 2024

Prehospital "Altered mental status and hypotension due to probable DKA" (everyone must know this ECG diagnosis)

A patient presented with hypotension and altered mental status and presumption of DKA.

As the medics arrived, they handed me this ECG:

What medication did I call for IMMEDIATELY when I saw this?

This is obviously severe hyperkalemia and the patient is near cardiac arrest.  The medics had no idea.

I called for 2 grams of Calcium Chloride.

There was no IV access, so we obtained intraosseous (IO) access, but she arrested before we could give her all the calcium.

Over the next 10 minutes we resuscitated with high doses of Calcium, Epinephrine, and Bicarbonate.

We also gave insulin and furosemide (which take much longer to have their effect)\

First K returned at 7.7 mEq/L.

After episodes of asystole, VF with defibrillation, and VT, she obtained ROSC and this 12-lead was recorded:
The monitor around this time was NOT showing a very wide complex
What do you think?

Here is the transesophageal echo (TEE) which was placed during arrest (and which is great for real-time assessment of resuscitation) at the same time as this 2nd ECG:

Excellent LV Function.  
How could that be with such a 12-lead?
I have had many cases of severe Hyperkalemia with wide complex that show good cardiac function.

The ECG above is bizarrely wide.  It is nearly a sine wave.  One might think that it is all due to hyperkalemia, but the K returned at 4.0 and the monitor around this time was not showing a very wide complex.  

This is actually Accelerated Idioventricular Rhythm (AIVR).  There are no P-waves (this can also happen in hyperkalemia due to sino-ventricular rhythm), but here is it slow and even wider than

9 minutes later:

The patient eventually did well and fully recovered.

Learning Point:

You MUST learn the many morphologies of hyperkalemia.  See the cases below in order to learn them.

Hyperkalemia and Cardiac Arrest

Large calcium doses for hyperkalemia, and VT in hyperkalemia.

Weakness, prolonged PR interval, wide complex, ventricular tachycardia

Very Wide and Very Fast, What is it? How would you treat?

This patient with VT in the context of hyperK required both defibrillation and 13 g of Calcium Chloride (CaCl):

A middle aged man with unwitnessed cardiac arrest

See this amazing case in which hyperK was not initially diagnosed:

This shows on serial ECGs the effect of Calcium:

Sine wave, or nearly so, due to hyperK:


ADDENDUM — by KEN GRAUER, MD (6/10/2024):


Did the 2nd ECG show AIVR?
I found the 2nd ECG in today's case to be especially interesting. For clarity in Figure-1 — I've reproduced and labeled this tracing.
  • As per Dr. Smith — the rhythm in ECG #2 is almost completely regular with extremely wide complexes, simulating AIVR. 
  • That said — the BLUE arrow in the long lead II rhythm strip highlights a vertical spike that confused me. RED arrows are seen throughout this long lead II, regularly occurring at the same interval after each of the wide complexes.
  • Vertical dotted BLUE lines suggest that similar spikes are seen in other simultaneously-recorded leads at the same point in time.

  • Could these regularly-occurring, small-amplitude vertical spikes be QRS complexes?
  • If so — Does that mean that rather than the QRS complexes of AIVR — that the wide complexes are artifact?
  • If so — then this would explain why serum K+ was normal — and why the QRS on the monitor at around this time looked to be narrow.

  • BUT — still unexplained, is what would (could) produce these bizarrely wide but surprisingly regular complexes that are seen before each of the small-amplitude vertical spikes on this tracing? This patient does not have a pacemaker — and these small-amplitude vertical spikes are not P waves. These wide complexes also do not represent PTA (Pulse-Tap Artifact) — because none of the standard limb leads are normal, and these wide deflections occur before the small-amplitude vertical spikes (whereas PTA occurs after the QRS since it is a systolic phenomenon).

As I like to do in problematic cases like this — I sent ECG #2 to David Richley for his expert opinion. Dave agreed that the shape of the wide deflections looked very unusual to be QRS complexes — but he could not explain why, if the wide complexes were artifact — they would occur before (and not after) the QRS. Therefore:
  • We will never know for certain what the rhythm in ECG #2 was. The "good news" — is that clinically this turned out not to be important because the 3rd and final ECG in today's case (done just 9 minutes later) showed sinus rhythm with a normal (narrow) QRS complex — and the patient did well and fully recovered.

  • KEY Point: It is sometimes exceedingly difficult to recognize artifact. As a result — the BEST approach when you suspect that there may be a "technical misadventure" — is to go to the bedside and LOOK at the patient! Surprisingly often — looking at the patient will reveal some obvious movement or tremor that clarifies the source of artifact. 
  • If not — check out your suspicion regarding a possible technical misadventure by replacing the electrode leads, verifying their correct placement — and repeating the ECG to see if the unusual deflections have now disappeared.

Figure-1: I've labeled the 2nd ECG in today's case (See text).


Friday, June 7, 2024

Chest pain with serial ECGs – can you guess the sequence?

 Written by Jesse McLaren

A 45-year-old presented with 24 hours of intermittent chest pain. Below are serial ECGs focusing on the inferior leads and aVL. Can you guess the sequence?


First, what’s the interpretation of each ECG on its own?



There’s T wave inversion in III/aVF and a taller T wave in aVL and V2. On it’s own this is nonspecific, but in the right context this could be diagonal occlusion (if active chest pain) or infero-posterior reperfusion (if resolved chest pain).



Normal ECG




There’s discordant T wave inversion in aVL, which is reciprocal to inferior T waves that are tall relative to the QRS but not bulky. On it’s own this is nonspecific, but in the right context this could be inferior OMI (if active chest pain) or reperfused high lateral (if resolved chest pain).




Obvious infero-postero-lateral STEMI(+)OMI, regardless of context



Now let’s put them in order: what was the sequence?


The most likely would be #2) initially normal, then #3) subtle OMI, then #4) obvious STEMI, and then #1) reperfusion:

In other words, the patient with an initially normal ECG develops an acute coronary occlusion, with ECGs that progress from subtle to obvious, and then reperfuse after angiography. But that’s not always the case.


Now let’s look at the actual sequence, with the addition of clinical context, and see how the patient was managed:


The patient received aspirin from EMS and arrived at triage painfree (ECG #1). But 90 minutes later troponin returned at 70ng/L (normal <26 in males and <16 in females), and a repeat ECG was done (ECG#2) for recurring chest pain. The patient received nitro but the pain persisted, and the ECG was repeated 10 minutes later (ECG#3). The patient received more nitro, but the pain continued, and another ECG was done just 6 minutes later (ECG#4).

So the patient arrived with spontaneous reperfusion(ECG#1). When the pain recurred the ECG normalized(ECG#2), but this is pseudonormalization: the coronary artery has spontaneously reoccluded, and the T waves are on their way up. Just 10 minutes later the repeat ECG showed subtle OMI(ECG#3), with rising T waves and reciprocal STD in aVL. Looking at each ECG in isolation and without clinical context, the Queen of Hearts called the first 3 ECGs ‘not OMI’. But in sequence and with the clinical context of resolved and then recurring and refractory chest pain, the ECGs show subtle spontaneous reperfusion progressing to reocclusion. With serial ECGs that are ‘STEMI negative’ the physician could have waited for serial troponin levels or referred the patient as “non-STEMI”. But with ongoing pain despite nitro and dynamic subtle ECG changes, a fourth ECG was repeated just 6 minutes later, showing obvious STEMI(+)OMI (ECG#4), and the cath lab was activated.


What was the outcome and final diagnosis?

By the time of angiography 20 minutes later the RCA had spontaneously reperfused again: it was 90% occluded and had normal TIMI 3 flow. The patient had a 5th ECG after angiography, which was normal (this time truly normalized, not pseudonormalized):

Post-cath trop was 300ng/L but was not repeated after. There were no follow up ECGs, which would have shown infero-posterior reperfusion TWI like the first ECG.


The discharge diagnosis was STEMI based on the STEMI positive ECG and code STEMI activation, with culprit lesion on angiography. This is one of the 20% of true positive STEMI that have open artery and normal flow by the time of the angiogram, showing that STEMI paradigm does not require a totally occluded artery at angiography.

And yet more than a quarter of ‘non-STEMI’ have an occluded coronary artery on delayed angiography, and yet are still discharged with a diagnosis of ‘non-STEMI’. So neither STEMI ECG criteria nor angiographic findings on their own sufficiently identify the pathology of acute coronary occlusion. Whereas the OMI paradigm incorporates, ECG, troponin, echo and angiographic findings to capture the dynamic nature of occlusion/reperfusion.


If acute MI is a movie, what film are we watching?


ECGs are 10 second snapshots in time, and with 4 columns on a page each lead only shows 2.5 seconds – so these are like still shots from a movie. The angiogram is a longer shot but does not represent the entire movie, and is separated in time from when the earlier scenes when the initial ECG was done. But if MI is a movie, what film are we watching?


In the STEMI paradigm there are only two possible films, which are completely different from each other: ‘STEMI’ depicts on artery that is totally occluded until it is reperfused on emergent angiography, while ‘non-STEMI’ shows a non-occluded artery that can wait to be seen on delayed angiography. But many STEMI spontaneously reperfuse while many ‘non-STEMI’ have totally occluded arteries. Bizarrely, the STEMI/Non-STEMI films are named not after how they end (the patient outcome) but how they begin (whether ECGs meet STEMI criteria, or whether code STEMI is activated), with STEMI(-)OMI still called ‘non-STEMI’ regardless of outcome. This is like categorizing a film that ends in tragedy as a comedy based on an earlier scene.


Occlusion MI is a dynamic process that can fluctuate between occlusion, spontaneous reperfusion and spontaneous reocclusion. Each patient with acute MI has their own film (with Non-occlusive MI, or Occlusion MI with or without spontaneous reperfusion or reocclusion), presents at a different time in the show (with acute or subacute presentations), and have corresponding ECGs that show subtle STEMI(-)OMI, obvious STEMI(+)OMI, or no ECG signs of OMI at all (for NOMI or electrocardiographically silent OMI). All these scenes can be missed by STEMI criteria, but looking through the lens of OMI allows us to see much more. By interpreting each still shot, looking at their sequence, and applying them in context, we can piece together the film for each patient.



Take away


1. OMI is a dynamic process that may spontaneously reperfuse or reocclude, and all phases can be missed by STEMI criteria

2. Just as true positive STEMI may have normal flow by the time of the angiogram, OMI is not based exclusively on the angiogram but also incorporates ECG, echo and trop

3. Serial ECGs applied in context can show subtle changes from reperfusion (resolved chest pain with reperfusion T wave inversion) to spontaneous reocclusion (recurring chest pain with pseudonormalization), and reciprocal change is often the more obvious initial change

4. Acute MI is like a film and ECGs are still shots: interpreting each ECG still shot through the lens of OMI, looking at their sequence and applying them in context, can help show each patient’s film and at what stage you are watching


MY Comment, by KEN GRAUER, MD (6/7/2024):

Fascinating clinical dissection of today’s case by Dr. McLaren! My thoughts as I read his excellent discussion are simple — namely, that depending on the history (ie, depending on the presence and relative severity of chest pain at the time each of the 4 ECGs shown was done) — a different logical sequence for these 4 tracings could have been proposed!
  • For example — the ECG showing inferior lead T wave inversion would logically occur after chest pain resolves (because this ECG is showing reperfusion T waves) — but whether this ECG was the 1st, 2nd, 3rd or 4th tracing in the sequence might depend on when this sequence of recorded ECGs began (ie, Had this patient’s CP already resolved by the time EMS arrived on the scene to record their 1st ECG — or was CP slowly increasing — or maximal – or gradually or rapidly decreasing at the time that EMS arrived?).

The BOTTOM Line in Today’s CASE:
Realistically — Optimal clinical ECG interpretation is not an attainable goal in the absence of correlation to the presence and relative severity of CP at the time each serial ECG is done. Despite this clinical reality — all too many clinicians still fail to document the presence and relative severity of CP at the time each serial ECG is recorded
  • As is shown in expert fashion by Dr. McLaren throughout his discussion of today’s case — the result is that too many ECGs are erroneously interpreted as “nonspecific”, and too many acute OMI’s are either overlooked or diagnosed only after significant (avoidable) delay.
  • Correlating events (symptoms) at each point in the story (ie, at the time each ECG is recorded) — is essential for appreciation of “dynamic” ST-T wave changes that expedite early recognition of an OMI in progress.

  • SUGGESTION: There is a very simple way to ensure that this critically important correlation between the presence and relative severity of symptoms to each ECG that is done in a patient with chest pain is not lost: Simply write down for every tracing — on the actual ECG recording on a scale from 0-to-10, what the patient's "pain score" is at that time. Then sign this notation, and write down the time. 
  • Adherence to this simple suggestion will instantly facilitate review of serial tracings — and make it so much easier to "put together" a cohesive story that will invariably enhance clinical interpretation.

Wednesday, June 5, 2024

Normal angiogram one week prior. Must be myocarditis then?

Written by Magnus Nossen

The patient in todays case is a 50 year old male. He has a medical hx notable for hypertension, hyperlipidemia and previous tobacco use disorder. The patient presented due to chest pain that was typical in nature, retrosternal and radiating to the left arm and neck. He denied any exertional chest pain. 

The below ECG was recorded. It is unclear if the patient was pain free at this time. 

The ECG does not show any definite signs of ischemia. In fact, the ECG was described as normal, and without serial ECGs or prior ECGs for comparison it could be. Initial high sensitivity troponin I returned at 6ng/L (normal <34ng/L) repeat troponin at 3 hours was 13, later peaking at 15 the following day.

Due to the nature of the symptoms (in spite of absence of a single troponin value above the 99th percentile URL), the patient was suspected to have unstable angina and referred for a coronary angiogram the following day. The angiogram did not reveal any obstructive coronary artery disease. The IC stated that "another cause for the patient’s complaint must be sought."

Smith: there was no intravascular ultrasound or optical coherence tomography, both of which could be used to find rupture plaque that does not show up as stensosis on the angiogram.  Nor was there a challenge to look for coronary spasm.  I think none of these a commonly done in cases in which the troponin is not elevated since the probability of ACS is low.

The patient was discharged only to present with chest pain again within one week. The below ECG was recorded during chest pain. What do you think?

The above ECG demonstrates obvious significant ST changes. How would you proceed in handling this patient? Do you think this patient needs another cath lab activation? What will you say if the IC declines arguing the recent CAG was normal one week prior? What if the IC states that this is myocarditis, will you accept that as a plausible explanation?

The ECG shows ischemic looking ST elevation in the inferior leads (II, III and aVF) and lateral leads (V5-V6). There is ST depression in leads V2-V3 signifying posterior involvement as well. 

But this patient had a normal coronary angiogram one week prior! It must be myocarditis then right? 

No! Even though this patient had a normal angiogram one week prior that is no guarantee he is not experiencing a type I MI. In fact, with the typical chest pain and the presenting ECG type I MI is the absolutely the most likely cause of the patient's symptoms. This patient needs emergent coronary angiogram. An erroneous assumption of not OMI could be devastating.

  • This patient could have a conventional type I MI from plaque rupture despite having no significant stenosis one week prior. 

  • The patient could be having an embolic coronary artery occlusion.

  • The patient could be having SCAD or extension of an aortic dissection to a coronary artery.

  • Also on the list of differentials are myocarditis, takotsubo, coronary artery spasm.

Just prior to the angiography the patient became unwell with a heart rate in the 30’s. At the same time massive ST elevation in the inferior leads were noted. Almost instantaneously after intubation of the RCA ostium with the diagnostic catheter the ST elevation rapidly disappeared. Below is a still image obtained of the RCA angiogram. The yellow arrow pointing at the proximal portion of the RCA that shows significant narrowing.

How can this be? Angiography was normal a week prior. A CT angiogram of the aorta was obtained, no dissection was found. Below is an image from the CT scan showing the aortic root and RCA. The cardiac chambers are denoted with the yellow arrow pointing to the proximal segment of the proximal RCA. 

This patient was having a type 2 acute MI from coronary artery spasm of the proximal part of the RCA. The angiography still image and the CT angiogram both show severe narrowing of the pRCA. This explains ST-elevation and bradycardia. Most episodes of chest pain were of short duration (minutes). The slight troponin release a week prior, typical symptoms, angiographic, electrocardiographic and radiologic investigations are all consistent with variant angina as a cause of the intermittent ST elevation. Troponin T during the second visit peaked at a modest 83 ng/L. The patient was prescribed calcium channel blocker and extended release nitroglycerin. Long term follow up is not available.

Learning points:

  • The ECG does not lie and sometimes patients need a second cath lab activation.
  • Listen to the patient, if the symptoms are typical in nature an ECG during pain must be obtained.
  • Plaque rupture cannot be ruled out by angiography alone.  When there is such "Myocardial Infarction with Non-Obstructive Coronary Arteries" (MINOCA), there are ways to look for plaque rupture beyond standard angiogram (which is only a "lumenogram".  The best of these is optical coherence tomography.  Intravascular ultrasound is also acceptable.
  • Variant angina has typical symptoms that may be of short duration and not related to activity. 

See this case and this case for more examples of "Prinzmetal's" variant angina.


MY Comment, by KEN GRAUER, MD (6/5/2024):
Today's case provides insight for assessment of the patient with new CP (Chest Pain) — for whom recent cath is negative for obstructive coronary disease. Should cardiac cath be repeated on such a patient IF days later the patient returns with another episode of CP?
  • As per Dr. Nossen — the fact that today's patient so recently had a normal cath does not rule out the possibility that recurrence of CP could indeed be due to new acute coronary occlusion.
  • Another reason for our interest in today's case — is that this patient was found on his 2nd admission to have coronary artery spasm with massive inferior lead ST elevation and marked bradycardia with positive troponin — all in the absence of underlying coronary disease. This evidence for pure coronary spasm without underlying coronary disease is not a common occurrence.

I focus my comment on a few additional aspects of today's case.

Was the Initial ECG "Normal"?
As per Dr. Nossen — the 50-year old man in today's case presented for new CP. Despite negative troponins and ECGs interpreted as unremarkable (I've labeled in Figure-1 the only ECG we are shown from his 1st admission) — it was this patient's description of his CP that prompted the need for diagnostic cardiac catheterization.
  • To EMPHASIZE: Persistent symptoms in a patient with new worrisome CP is sufficent justification to perform diagnostic cath, even when serial troponins are negative and ECGs are interpreted as unremarkable.

The above said 
— I'll offer another perspective on the initial ECG in today's case.
  • Given that this patient's history of new CP was worrisome enough that it alone served as the reason for cardiac cath — My threshold for interpreting an ECG as "not normal" was immediately loweredBy this, I mean — even seemingly minimal ECG findings in this clinical context should be interpreted as potentially suspicious.
  • Comparison with prior ECGs is extremely important in such cases (Given this patient's past medical history — it is clear that prior tracings had to have been done).
  • As noted by Dr. Nossen — it was unclear if the patient did or did not have CP at the time ECG #1 was recorded. As we have emphasized in numerous cases — correlation between the presence and relative severity of CP at the time an ECG is done is critical (albeit all-too-often-neglected) information for optimal ECG interpretation (ie, "Pseudo-normalization of ECG findings may be seen if CP has resolved by the time the ECG is recorded).
  • Serial ECGs (recorded in close succession) are an essential component of evaluation when looking for "dynamic" ECG changes that may occur if the initial ECG was recorded during the period of pseudo-normalization.

To EMPHASIZE: ECG #1 is clearly not diagnostic of acute OMI. But in a patient with new worrisome symptoms — I interpreted this initial ECG as not "normal" because of the following:
  • The T wave in lead III looked "bulkier"-than-expected given small size of the R wave in III (within the BLUE rectangle in this lead).
  • The T wave in lead aVL is usually not inverted when the R wave is all positive (as it is within the BLUE rectangle in this lead).
  • Given these findings in leads III and aVL — the ST segment straightening in lead I is not "normal".

  • There is more than the usual amount of ST elevation in lead V1 (BLUE arrow in this lead) — and the taller-than-expected T wave in this lead suggested "T wave imbalance" given the greater T wave size than seen in lead V6 (See My Comment in the June 1, 2022 post in Dr. Smith's ECG Blog).
  • There is "early transition" — with an R wave already greater than the S wave by lead V2 (which while clearly a nonspecific finding — taller-than-expected anterior R waves can be a sign of posterior infarction).
  • While the amount of upsloping J-point ST elevation in lead V2 is not abnormal (BLUE arrow in this lead) — I wondered WHY this J-point elevation was abruptly lost by lead V3? (slanted RED line in this lead).

  • BOTTOM Line: I fully acknowledge that all of the above findings are exceedingly subtle and nonspecific. BUT, taken together in this patient with a history of worrisome new CP — careful correlation with the presence and severity of CP symptoms in association with serial ECGs over the ensuing minutes would be needed to know if the above described findings might be real.
NOTE: I believe that ECG #2 obtained days later during CP supported my suspicion about the subtle findings I describe above for ECG #1 — because during coronary spasm (ie, at the time ECG #2 was recorded): i) Lead III now manifests marked ST elevation; ii) Lead aVL now manifests marked reciprocal ST depression; andiii) The J-point ST depression in leads V1,V2 now clearly indicate posterior involvement; andiv) There is a marked contrast in ECG #2 between the ST depression in leads V1,V2 and the beginning of marked ST elevation with lead V3 — just as there was that inexplicable loss of J-point elevation between leads V2 and V3 in ECG #1

Figure 1: I've labeled the initial ECG in today's case.

What are the ECG Findings in ECG #2?
I've labeled in Figure-2 the one ECG we are given from this patient's 2nd admission. As per Dr. Nossen — ECG #2 shows inferior lead ST Elevation — J-point ST depression in leads V1,V2 — and J-point ST elevation in all chest leads that show predominant R wave positivity ( = leads V3,V4,V5,V6).
  • We are told this patient developed more severe bradycardia a bit later on during his evaluation, with a heart rate in the 30s (no tracing available).
  • We see 8 consecutive beats in ECG #2 (albeit there is no long lead rhythm strip).

  •  What is the likely mechanism of the rhythm in ECG #2

Figure 2: I've labeled the 2nd ECG in today's case.

While access to a long lead rhythm strip and additional monitoring would be helpful — we still can draw clinically useful conclusions regarding the likely mechanism of the rhythm in ECG #2:
  • There is sinus bradycardia with marked sinus arrhythmia.
  • There is marked baseline artifact — which makes identification of atrial activity challenging. That said — Beat #6 occurs unexpectedly early. However, rather than being a PAC — I believe the RED arrows that are seen in lead V1 suggest a marked sinus arrhythmia.
  • My caliper measurement of the PR interval preceding beats #5 and 6 in lead V1 — suggests that the PR interval increases. However, unlike Mobitz I 2nd-degree AV block — P waves are not regular, and there is no dropped QRS after beat #6.
  • All 8 beats in ECG #2 appear to be conducted (ie, preceded by a PR interval that is constant for all beats except #6).
  • There is 1st-degree AV block (ie, PR interval clearly >0.20 second).

  • IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block (See My Comment in the October 9, 2020 post in Dr. Smith's ECG Blog).

  • PEARL: Increased vagal tone is highly likely to be the cause of the abnormal rhythm in ECG #2. Given CP, increased troponin and inferior lead ST elevation — this is the ideal situation for which atropine in modest dose may be optimally effective (ie, during the early hours of acute inferior MI when vagal tone is most likely to be increased and responsive to judicious atropine).
  • Especially later on during evaluation of this patient when heart rate continued to drop (ultimately attaining a rate in the 30s) — readiness to administer atropine might prove lifesaving.

Why Was Cardiac Cath Negative for Coronary Disease?
As noted by Dr. Nossen — this patient qualified as MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries) — since troponin was positive on his 2nd admission, yet there was no evidence of obstructive coronary disease on cath. As per my review of this subject (Check out My Comment at the bottom of the page in the November 16, 2023 post in Dr. Smith's ECG Blog) — the 3 most common Causes of ACS (Acute Coronary Syndrome) with a "negative" cath are: i) Myocarditis; ii) Takotsubo cardiomyopathy; andiii) MINOCAWith regard to today's case:
  • I thought acute myocarditis to be unlikely given the lack of a viral infection — and the anatomic localization of ECG findings (suggestive of acute infero-postero-lateral MI on ECG #2).
  • I thought the complete lack of QTc prolongation and anatomic localization of ECG findings made Takotsubo cardiomyopathy unlikely.
  • This left MINOCA as the most likely cause of this patient's symptoms. Although important to always consider the possibility of an acute OMI that spontaneously reperfused, such that thrombus is no longer evident by the time cath is performed — today's patient turned out to have coronary artery spasm in the absence of underlying obstructive coronary disease.

Final Thoughts:
Today's patient was discharged and treated with a calcium blocker and extended release nitroglycerin. This combination is often extremely effective for maintaining good longterm outcome (Lanza and Shimokawa — Eur Cardiol 18: e38, 2023).
  • Uncontrolled coronary spasm may be associated with serious arrhythmias, including cardiac arrest (Looi et al — Postgrad Med, 2012; Tan et al — Eur Heart J Case Rep, 2018Chevalier et al — JACC, 1998Rodriguez-Manero — EP Europace, 2018). As a result — an ICD may need to be considered in selected cases.
  • Use ß-blockers with caution (as they may aggravate coronary spasm).
  • Today's patient was noted to be "a previous tobacco user". Given the potential triggering effect of smoking on coronary spasm — absolute abstinence from smoking is essential!

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