A woman in her 30s with sudden chest pain, nausea, and diaphoresis. Was her cardiology management appropriate?

Case written and submitted by Brandon Fetterolf MD, edits by Meyers

A woman in her early 30s with multiple autoimmune disorders including vasculitis presented with 2-3 hours of mid-left side chest discomfort with radiation to neck and left arm and associated with nausea, diaphoresis and dizziness. 

Initial ECG on presentation at 1554 (no prior for comparison):

What do you think is happening to his 30s woman?

 

The ECG shows NSR with a normal QRS except for poor R wave progression and pathologic QS-waves in V2-3. There is STE and hyperacute T waves in V2, I, and aVL with reciprocal STD in II, III, and aVF. 

This is the South African flag pattern. 

There is also the impression of slight STE in V1 and slight STD in V6, which is seen in LAD OMI. The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion). There is clearly sufficient STE for STEMI criteria in leads V2 and aVL, but lead I has less than 1.0 mm of STE - thus, technically this ECG does not meet STEMI criteria, although it is a quite obvious OMI.

This ECG was immediately discussed with the on-call cardiologist who said the ECG was "concerning but not a STEMI." They refused emergent transfer and advised further ED workup.

Initial hs-troponin I: elevated at 101 ng/L (upper reference limit for women is 12 ng/L for this assay).

Smith comment: one does not even need an ECG for this case, even though it is diagnostic of OMI.  There is a patient with persistent chest pain and an initial troponin I over 52 ng/L; 52 ng/L has an approximate 70% PPV for acute type I MI in a chest pain patient.  Any patient with type I MI and persistent symptoms should go to the cath lab within 2 hours of arrival, according to both the American and European guidelines.  In reality, cardiologists do not follow their own guidelines. This is something we have always known by anecdote, but not there is a study showing that only 11% of patients who meet this guideline go to angiography in a timely way.  

Lupu L, Taha L, Banai A, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin Cardiol [Internet] 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781

ECG 2: 35 minutes after arrival

Ongoing OMI. Several worsening features include new STE in V3 and V4 with likely hyperacute T waves, and increasing STE in V1 and STD in V6. It still does not meet formal STEMI criteria by my measurement.

Pain was severe and persistent.

CT angiography chest assessing for PE and dissection negative.

The patient was given a dose of hydromorphone for severe chest pain, then was noted to be pain free after.

Heparin drip was initiated.

ECG 3: 2 hours after arrival

What is this?

There is acute new RBBB morphology, with persistent findings of active anterolateral OMI including concordant STE in V2, and excessive STE in I and aVL. There are no obvious P waves, making this likely a junctional or ventricular rhythm such as AIVR. In my prior experience with AIVR, it usually does not mimic RBBB, but it certainly could. My best guess is that this is likely AIVR that has RBBB morphology. But it is unlike any AIVR I have seen before (see other AIVR cases below).

Amiodarone was given for "question of nonsustained V. tach and intermittent accelerated junctional rhythm which improved."

Smith comment: antidysrhythmics are NOT indicated for AIVR and can result in asystole.

2nd hs-troponin: 1165 ng/L.

Bedside echo: hypokinesis septal/apical locations, RV chamber size grossly normal in appearance (no available images).

ECG 4: 2.5 hours after arrival

Beginning of anterolateral reperfusion pattern and Wellen-type biphasic pattern V2, I, aVL.

 

The ED provider again called the on-call interventional cardiologist, but a new interventionalist answered. The ED provider explained the history, ECG findings septal and apical WMA, and stated "I would like to treat her as OMI and activate STEMI protocol with concern for acute occlusion possibly in the LAD distribution."

The cardiologist stated "I don't think the latest EKG is a "STEMI" nor do I think it represents deep T wave inversions typically seen with Wellen's syndrome. If she's improving which it sounds like she is, resolving pain and no further arrhythmia I think probably best to treat as UA/NSTEMI as you are doing."

No troponins ordered overnight.

ECG 5: the next morning, around 13 hours after arrival

Ongoing anterolateral reperfusion.

In the morning a new troponin returned at greater than 25,000 ng/L. (the maximum reported by the lab)

Formal echo:

Moderately to severely reduced systolic function, EF 30%. Severe hypokinesis of the anteroseptal, anterior, inferoseptal, and apical myocardium. Normal RV function.

Cath report later that afternoon, around 25 hours since arrival:

"There was a 70% proximal LAD stenosis secondary to a spontaneous coronary dissection with narrowing of the proximal LAD to at least 50% stenosis. There was normal TIMI-3 antegrade flow noted. Aspirin 81 mg daily. Plavix 75 mg daily for 12 months. Recommend coronary CT angiogram in 1-2 months to evaluate for resolution of spontaneous coronary artery dissection." 

Final Diagnosis: NSTEMI

She survived the hospitalization and was discharged home. Her long term outcome (with very large LAD MI and EF of 30%) is unknown.

Learning Points:

Many cardiologists and physicians of all specialties do not yet understand these ECG findings of obvious acute coronary occlusion, even when they almost meet formal STEMI criteria. There is likely no specialist or radiologist who has your back on ECGs in your practice, so currently you must be the one who learns and understands these patterns.  You must be the one who knows the ECG and indications for angiography, and who knows it well enough to be confident to push for angiography.

MI of many etiologies happen in young patients. Especially young patients with inflammatory/autoimmune problems like this patient.

Currently, SCAD is a diagnosis that can only be established emergently in the cath lab with angiography. Type 1 ACS OMI should be ruled out as it is the most common and most treatable cause, and only with angiography will type 1 ACS be ruled out and SCAD be diagnosed instead. Persistently occlusive SCAD (as this one was for at least several hours) is sometimes intervened on, even though it is more complicated and riskier than intervention for typical type 1 ACS.  (Otherwise it results in a terrible outcome, as in this case, with devastating permanent loss of myocardium).  If SCAD is not fully occlusive and causing ongoing myocardial damage, then many times it may be managed medically. See this case for one that was intervened upon: 

A woman in her 40s with acute chest pain

AIVR can occur in several clinical settings, including reperfusion from OMI. It should not be treated, as it signifies reperfusion and it will be brief and uncomplicated.

See these other cases of AIVR:

Getting It Right Despite the Wrong Paradigm

The cardiologist disagreed with cath lab activation. What do you think?

A Wide Complex Rhythm in an Intoxicated Patient

I saw this on the computer. Most physicians, at first glance, get this wrong. What is it?

What is the rhythm? And is there new left bundle branch block (LBBB)?

Is this Left Bundle Branch Block? Is there STEMI?

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

See these other cases of SCAD:

Acute Chest pain which then resolves spontaneously

A young peripartum woman with Chest Pain

A completely healthy 30-something woman with acute chest pain -- this post is loaded with info !!!

An athletic 30-something woman with acute substernal chest pressure

A woman in her 40s with acute chest pain

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MY Comment, by KEN GRAUER, MD (4/8/2022):

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Insightful — but frustrating case, with excellent discussion by Drs. Fetterolf and Meyers. I found this case to be insightful for reminding us that the ECG alone is unlikely to distinguish between SCAD (Spontaneous Coronary Artery Dissection) vs an acute Occlusion-based MI (OMI). On the other hand, I found it frustrating to read about this case — because the interventionist refused to proceed with cardiac catheterization for a number of hours despite persistent chest pain — and despite clear ECG evidence of acute MI.

I focus my comments on 2 clinical points that are illustrated by 2 of the 5 tracings shown in today’s case. For clarity — I have put these 2 ECGs together in Figure-1.

Figure-1: I’ve put together ECG #1 ( = the initial ECG in today’s case) — together with ECG #3, in which there is QRS widening (See text).

POINT #1: The Initial ECG in Today’s Case:

As noted by Drs. Fetterolf and Meyers — the initial ECG in today’s case brings to mind the color pattern of the South African Flag, in that the leads with the most prominent ST-T wave changes in ECG #1 are leads I, III, aVL and V2 — which correspond to the arrangement of GREEN coloring in the horizontal "Y" of the South African flag (upper most portion of Figure-1).

• As discussed in the November 21, 2020 post in Dr. Smith’s Blog (My Comment at the bottom of the page) — the ECG picture of ST elevation limited to lead V2 in the chest leads (with ST depression in other chest leads) — when seen in association with ST elevation in lead aVL (and sometimes in lead I) — should suggest acute OMI of either the 1st or 2nd Diagonal Branch of the LAD (I've reproduced below in Figure-2 from this Nov. 21, 2020 post — Optimal Use of Lead aVL for predicting the "culprit" artery).
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• As is seen in today’s case — the "South African Flag Pattern" is especially marked in ECG #1 by distinct hyperacute ST-T waves in leads I, aVL and V2 — in association with equally pronounced reciprocal ST-T wave depression not only in lead III, but also in lead aVF. More modest (but nevertheless-still-real) ST-T wave depression is also seen in the 3rd inferior lead ( = lead II).
• Although frank ST depression is not seen in other chest leads in ECG #1 (ie, the ST segment baseline appears essentially isoelectric) — the lack of clearly hyperacute ST-T waves and ST elevation in chest leads other than lead V2 — should suggest possible acute OMI of either the 1st or 2nd Diagonal Branch of the LAD.
• NOTE #1: It is sometimes difficult to distinguish early on, between acute OMI of the 1st or 2nd Diagonal vs an ongoing LAD occlusion, in which ST elevation has not yet evolved to include chest leads other than lead V2. This is clinically relevant to today's case — because the main objection to performing prompt cath was failure to satisfy strict "STEMI criteria". But, the well accepted 1st or 2nd Diagonal Occlusion pattern of ST elevation in leads aVL and V2, but not in other chest leads — by definition, might not manifest ST elevation in 2 "continguous" leads.
• 
  
• NOTE #2: We see in ECG #1 that infarction Q waves are already present. A QS is seen in lead V1. There appears to be an ever-so-tiny-but-real initial positive deflection (r wave) in lead V2 of ECG #1 — with loss of R wave between V2-to-V3 (ie, a QS complex is again seen in lead V3). A tiny r wave again develops in lead V4 — with transition (where height of the R wave becomes greater than the S wave is deep) not occurring until lead V4-to-V5. Careful review of this patient's history reveals that her symptoms actually began the night before — so whether there is now superimposed new infarction on top of a previous infarction in this woman with vasculitis (and no prior ECG available for comparison) — or — whether QS complexes (and loss of r wave) developed the night before, or anytime thereafter was unknown at the time ECG #1 was obtained.
• P.S.: The acuity and extent of ECG findings became obvious shortly thereafter, with persistence of severe chest pain — a marked increase in the 2nd troponin value — and, development of ST elevation in other chest leads seen on the 2nd ECG that was done 35 minutes after ECG #1 (shown above).

POINT #2: The Interesting AIVR Tracing:
Two hours after arrival in the ED — ECG #3 was obtained (bottom tracing in Figure-1). The rhythm is fairly (but not completely) regular at ~80/minute. This is AIVR (Accelerated IdioVentricular Rhythm).

• The 1st reason I know that the rhythm in ECG #3 is AIVR — is that we should always be looking for AIVR in the setting of acute coronary occlusion — and that is the setting in today's case! This slightly accelerated ventricular rhythm most often manifests a ventricular rate between ~60-110/minute (with an area of "overlap" between AIVR and "fast VT" at ~110-130/minute).
• Additional reasons why we know the rhythm in ECG #3 is AIVR — are that: i) P waves are absent; ii) QRS morphology looks nothing like the QRS appearance in the previous 2 ECGs done during sinus rhythm; and, iii) QRS morphology in ECG #3 manifests numerous distinctly ventricular-origin characteristics. The QRS is very wide (at least 0.14 second — as measured between the vertical BLUE and RED lines placed at the beginning and end of the QRS). The QRS is all negative in lead I — all positive in lead aVR — and almost all negative in leads V3-thru-V6. QRS morphology in leads II and III is contradictory for LAHB (both leads should be predominantly negative if there was LAHB conduction). Finally, the amorphous QRS complex in lead V1 is not suggestive of RBBB conduction given the all-negative lead I and almost-all-negative lead V6.
• 
  
• What is especially interesting about this AIVR tracing reflects a phenomenon that we have commented on many times in the past — namely, that on occasion ventricular beats may manifest even more prominent acute changes than sinus-conducted beats. While not as accurate for localizing the area of acute evolving infarction — ST-T wave changes in virtually all 12 leads of the ventricular rhythm in ECG #3 are clearly abnormal, and increasingly accentuated compared to the previous 2 sinus-rhythm tracings that were done on this patient.
• In the setting of evolving infarction — development of AIVR often heralds the onset of reperfusion (following thrombolysis, acute angioplasty, or spontaneous reperfusion). In this setting — this rhythm is usually transient. Although difficult to know from the history presented above — I wonder if this patient's chest pain decreased somewhat around the time that ECG #3 was obtained? In any event — I suspect that the disproportionately deep T wave inversion seen in leads V1,V2 of ECG #3 marked the beginning of anterior reperfusion (beginning before ECG #4 was obtained).
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• The final point to emphasize about AIVR — is that it is often an "escape" rhythm — in that it often arises because both the SA and AV nodes are not functioning. IF treatment is needed (because loss of the atrial "kick" results in hypotension) — Atropine is the drug of choice (in hope of speeding up the SA node to resume its pacemaking function). AIVR should not be shocked nor treated with antiarrhythmic medication such as Amiodarone/Procainamide — since if AIVR is functioning as an "escape" rhythm — such treatment might result in asystole by removing the patient's only viable rhythm.

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ADDENDUM:
As noted above — I wanted to add information I previously posted in Dr. Smith's ECG Blog regarding use of lead aVL to assist in predicting the "culprit" artery.

Figure-2: Optimal use of lead aVL for predicting the "culprit" artery with acute OMI (From My Comment in the November 21, 2020 post in Dr. Smith's ECG Blog).