Which Chest Pain patient needs a CT scan?

Which patient needs a CT Scan?

Case 1: 20-something woman with chest pain

Case 2: 50-something man with chest pain

Case 1

A 20-something yo woman presented in the middle of the night with severe crushing chest pain.  It had begun 4 hours before arrival and was initially dull, but became severe and "unbearable" 2 hours prior to arrival.  She was a walk-in at triage. She has no SOB and no prior medical history.  Her initial BP was 203/124.

She had this ECG recorded:

Obvious massive anterior STEMI

She was quickly brought to the critical care area and the cath lab was activated.

The blood pressure was 170/100 in the critical care area.

Cardiology wanted a CT of the aorta to rule out dissection, presumably partly due to the very high blood pressure readings, but also because it is hard for people to believe that a 20-something woman could have acute thrombotic coronary artery.

They also recommended a NTG drip, after which she reported complete resolution of pain.  No ECG was recorded after pain resolution.  

Here is the ECG at 25 minutes:

Terrible LAD STEMI (+) OMI

So a CT scan was done which of course showed a normal aorta.  But it also shows a massive area of total ischemia in the LAD territory:

CT shows the infarct

The CT is with contrast, which increases density (which looks more white).  Myocardium that does not have blood flow does not get the contrast, and therefore looks more dark.  

See the dark area in the septum and apex, highlighted with the white circle:

First hs troponin I returned at 256 ng/L.

 Angiogram

Door to balloon time was 120 minutes (much too long) because of time taken for a CT.

Coronary angiogram showed 100% mid LAD occlusion for which she received a DES with excellent angiographic result.  This was ruptured plaque with thrombus.  It was not SCAD (coronary dissection)

Highest troponin I was 37,000 ng/L, but it was not measured to peak.

Echo:

--Normal left ventricular cavity size, mild to moderately increased wall thickness, and moderate LV systolic dysfunction.

--The estimated left ventricular ejection fraction is 37%.  (if she does not get a lot of recovery over the ensuing weeks, that is a lot of lost myocardium)

--Regional wall motion abnormality- mid and apical anterior, apical septum, apical anterolateral, apical inferior, and apex, hypokinetic to akinetic.

Important:

It is exceedingly rare for an anterior STEMI to be due to Aortic Dissection.  And almost all of them could be detected by bedside ultrasound.

Conclusion: you may take a few moments to look for dissection with your bedside ultrasound, but when it is a clear STEMI, do NOT waste time with a CT scan.

Case 2

A 50-something y.o. male who hasn't doctored in several years presented to the emergency department by ambulance for chief complaint of chest pain.  

Here is the prehospital ECG:

There is some minimal STE in inferior leads with reciprocal STD in aVL, and also minimal STE in lead V1.  

This is very suggestive of OMI, but not diagnostic. 

Queen of Hearts: "STEMI or STEMI Equivalent detected" (that is, "OMI detected")

The Queen is not wrong very often, so maybe it is an OMI?

History

Patient complains of a 24-hours of chest pain of sudden onset, sharp in nature.  Pain started day before and it started on the left side of his face, descended down his neck, and remained mainly in his chest before radiating down his back to his left lower extremity.   It persisted through the night (for at least 18 hours), and nothing made the pain better or worse. He had never experienced a similar pain at rest or upon exertion.  He reported chest pain 9/10 at the time of evaluation. Denies SOB. Vomited 3 times overnight, not currently feeling nauseous. He denies history of HTN, HLD, DM, smoking. He does not take any medications chronically. 

Vital signs were normal.

An ED ECG was recorded:

Very Similar

Mild ST elevations in leads II, III, aVF with reciprocal changes in the lateral leads, along with ST elevation in V1 raising concern for RVMI. 

This time the Queen of Hearts interpreted: No STEMI or Equivalent. (Interesting!)

Initial hs troponin I returned at > 60,000 ng/L

Cardiology was consulted and the cardiology fellow palpated both radial pulses and found that they were very assymetric.

They recommended a CT of the aorta.

Here it is:

Type A Aortic Dissection

Why was the troponin so elevated?  And why does the ECG show subtle signs of OMI?

See here that the dissection is very close to the ostium of the RCA.  Most dissections which cause coronary ischemia are into the RCA ostium 

("ostium" = locations of takeoff of the vessel).

Going from the upper left to farther upper left is the RCA, which is open.

   The CT showed extensive type A aortic dissection which starts at the ostium of the RCA and extends all the way to the left iliac artery.  

Trop > 60,000 ng/L

Thus, at the onset of the dissection, it almost certainly occluded the RCA and led to OMI that is now reperfused.  

Thus, it was a PROXIMAL RCA occlusion (at the ostium) which resulted in right ventricular OMI (RVMI, RVOMM) with ST Elevation in V1

A dissection can break through the flap and reperfuse the true lumen

Here you can see some ischemic myocardium:

The dark areas are not perfused with contrast.  Most of it is subendocardial in the septum, apex, and even lateral wall, but mostly posterior (bottom of image)

What if the patient had cath lab activation?

That could have been troublesome.  It would delay diagnosis and treatment and perhaps not resulted in the correct diagnosis at all.

There were many clinical clues to dissection.  

The assymetric pulses mandated a CT scan.

But what if pulses were symmetric?  The strange history also mandates CT scan.

But what if you did not have either of the above?

Ultrasound

Here is one easy way to look for it when you think there is OMI but want to be certain that it is not dissection.

Bedside Ultrasound by the emergency physician of the aortic arch through the sternal notch:

The bright line in the middle of the aorta is the dissection flap. This is easy to see.

This patient had symptoms all the way to his leg, so an abdominal view is likely to show something.  Here is the abdomincal aorta transverse view:

On the left is the IVC, on the right is the aorta with a dissection flap across the middle.

Learning Points:

1. When there is a slam dunk diagnosis of OMI on the ECG, it will almost always be a waste of valuable myocardium (time because time is myocardium) to get a CT scan.

2. It is not a waste of time to use bedside ultrasound to look for dissection

3. Dissection is rare.  OMI is common.  Pretest probability is important.

4. Most Dissection that causes OMI is in the RCA

5. Only ~1% of STEMI are due to dissection

6. Only about 5% of dissection result in OMI

7. Check pulses!

8. When there is an unusual history ("started in face, went down to leg"), pay attention.  Not all chest discomfort is the same.

9. Young women have large MI and the worst thing you can be if you have OMI is to be a young woman: no one will believe that you have OMI. 

Some Literature

1.3% of STEMI are due to Aortic Dissection.

Wang J-L, Chen C-C, Wang C-YW, Hsieh M-J, Chang S-H, Lee C-H, Chen D-Y, Hsieh I-C. Acute type A aortic dissection presenting as ST-segment elevation myocardial infarction referred for primary percutaneous coronary intervention. Acta Cardiol. Sin. [Internet]. 2016;32:265–272. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884753/   

The incidence of STEMI in the US is 100 per 100,000 per year (300,000 STEMI per year in the U.S.)

The incidence of Aortic Dissection in the US is 3 per 100,000  (maybe up to 6 per 100,000)

Yin J, Liu F, Wang J, Yuan P, Wang S, Guo W. Aortic dissection: global epidemiology. Cardiol. Plus [Internet]. 2022;7:151–161. Available from: https://journals.lww.com/cardioplus/fulltext/2022/12000/aortic_dissection__global_epidemiology.1.aspx   

5% of Aortic Dissection result in STEMI, and the majority are RCA occlusions.  When they are due to left coronary artery, the are left main, and rarely present as Anterior STEMI

Kawahito K, Adachi H, Murata S-I, Yamaguchi A, Ino T. Coronary malperfusion due to type A aortic dissection: mechanism and surgical management. Ann. Thorac. Surg. [Internet]. 2003;76:1471–6; discussion 1476. Available from: https://www.sciencedirect.com/science/article/pii/S0003497503008993   

Wang: Transthoracic echo is 85% sensitive for type A dissection.

Wang Y, Yu H, Cao Y, Wan Z. Early screening for aortic dissection with point-of-care ultrasound by emergency physicians: A prospective pilot study: A prospective pilot study. J. Ultrasound Med. [Internet]. 2020;39:1309–1315. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/jum.15223   

Good Review:

Loftus A, Abou-Arbid S, Marshall D, Suszanski J, Clark C. Resuscitative transesophageal echocardiography identifies aortic dissection intussusception as the cause of aVR STEMI. JEM Reports [Internet]. 2023;2:100029. Available from: https://www.sciencedirect.com/science/article/pii/S2773232023000251   

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MY Comment, by KEN GRAUER, MD (12/16/2024):

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Today's post features 2 highly insightful cases. I focus My Comment on Case #1. Dr. Smith’s discussion covers all aspects of Case #2 in fascinating fashion.

Regarding Case #1:

• It is insightful seeing how Aortic CTA (Computed Tomography Angiography) so clearly showed this patient's infarction — thereby confirming the diagnosis of acute MI prior to cardiac catheterization (even though the primary reason for aortic CTA was to rule out aortic dissection).
• It is humbling to realize that bedside Echo revealed normal LV function — whereas formal Echo showed significantly reduced ejection fraction with multiple regional wall motion abnormalities. The accuracy of bedside Echo is clearly a function of operator skill and experience — and at times it may be difficult to exclude the possibility of WMA (Wall Motion Abnormality) from bedside Echo alone.
• The clinical presentation of the patient in Case #1 qualifies as a hypertensive emergency (with the difference between HT "urgency" vs "emergency" being whether or not there is acute end-organ damage — which clearly was present given the large acute infarction).
• Sublingual NTG (nitroglycerin) X3 was no more than minimally effective in relieving this patient's CP (Chest Pain). As a result — IV NTG was started, with complete resolution of the patient's CP (and presumably significant improvement in her marked hypertension)! This raises the question as to how much this patient's hypertensive emergency contributed to her ongoing severe CP prior to initiation of IV NTG — vs — how much her acute MI contributed to her ongoing severe hypertension? (See below).
• And — this patient's initial ECG (that I've reproduced and labeled in Figure-1) shows some interesting findings (See below).

Hypertensive Urgency/Emergency and CP in the ED:

Although accurate data is hard to come by — true hypertensive emergency is rare (most probably well under 1% of ED visits).  

• As noted above — the presence of acute target organ damage in today's case (ie, acute MI) in association with marked sustained hypertension (this patient's BP at times exceeding 200 mm Hg systolic and >110 mm Hg diastolic) — qualifies her as a true hypertensive emergency (Janke et al — JAHA 5(12); 2016 — and — Cardiology Advisor — Feb. 29, 2024). Fortunately — today's patient rapidly responded to initiation of IV NTG.
• It is not always appreciated that chest pain is one of the most common associated symptoms of hypertensive crisis presenting to the ED (occurring in more than half of the patients with HT urgency — and in an even greater percentage of those with HT emergency in the study by Salkic et al — Mater Sociomed 26(1):12-16, 2014).
• PEARL: Case #1 in today’s post provides superb illustration of the synergistic effect that IV NTG may have in the patient who presents with severe CP in association with the combination of hypertensive emergency and acute MI.

Figure-1: I've labeled the initial ECG in Case #1.

The Initial ECG in Case #1:

The ECG in Figure-1 — shows sinus tachycardia at ~110/minute with markedly increased QRS amplitude and marked chest lead ST elevation.

• We have often made the point in Dr. Smith's ECG Blog that in general — it is not common to see tachycardia with an uncomplicated MI. As a result — the finding of sinus tachycardia in today's case should immediately suggest that something else might also be going on (which in today's case was this patient's severe CP and her hypertensive emergency).

QRS voltage is markedly increased in ECG #1 (with an S wave in lead V3 of 36 mm — as shown by the QRST complex outlined in RED in Figure-1). This extremely deep S wave is consistent with this patient's severe hypertension and increasd LV wall thickness on formal Echo.

• This degree of increased S wave amplitude made me initially stop to consider proportionality of the amount of chest lead ST elevation relative to the increase in chest lead voltage.
• Double RED arrows in leads V3,V4,V5 highlight what I considered the point of inflection defining the J-point for determining the amount of ST elevation. Even in lead V3 (in which the S wave attains a depth of 36 mm) — the 8 mm of J-point ST elevation is inappropriately increased, and indicative of acute MI in this patient with severe new CP.
• S wave depth is much less in neighboring leads V4 and V5 — which clearly show disproportionate J-point ST elevation (of 12 mm and 9 mm in lead V4 and lead V5, respectively) — compared to more modest S wave depth in these leads (ie, of 20 mm and 11 mm). As per Dr. Smith — the overall ECG picture in Figure-1 indicates an anterior STEMI in progress in this patient with acute hypertensive emergency.
• While difficult to know what to make of inferior lead ST-T wave appearance — the inappropriate T wave inversion in lead aVL adds further support to the diagnosis of an ongoing STEMI.

 

A man in his 50s with acute chest pain without STEMI criteria. Trop negative. Cath lab cancelled. But how about the ECG and echo?

Case submitted by Matt Tanzi MD, written by Pendell Meyers

A man in his early 50s presented with substernal chest pain and that started 1 hour prior to arrival. There was some radiation to the left jaw and diaphoresis. He had ongoing pain on arrival.

Initial triage ECG:

What do you think?

I sent this to Dr. Smith who immediately replied that it is diagnostic of OMI, but difficult to tell whether it is 1) anterolateral with de Winter morphology, or instead 2) A combination of Aslanger's pattern (inferior OMI with single lead STE in III and reciprocal STD in I, aVL, plus widespread STD of subendocardial ischemia) with posterior (V2 STD) and RV extension (V1 STE). In other words, does V2 indicate ST depression of posterior OMI? or is the ST depression and hyperacute T wave indicative of de Winter hyperacute OMI morphology of the anterior wall? It is difficult to tell, but either way: OMI needing reperfusion.

The ECG shows sinus tachycardia, grossly normal QRS complex, ST depression from V2-V6, and in I and aVL. There are possibly hyperacute T waves in V2 (maybe also V3 and V4), constituting de Winter morphology (hyperacute T wave taking off from depressed ST segment). V1 has a tiny amount of STE and a hyperacute T wave also. The ECG overall is diagnostic of OMI.

The cath lab was activated. He received aspirin and heparin bolus. The cardiologist immediately evaluated the patient and stated that the ECG did not meet STEMI criteria, so the cath lab was cancelled. The cardiologist stated that they should try nitroglycerin and see if that controls the pain. 

He was given sublingual nitro and then a continuous drip.

ED2 Post nitro:

Mostly similar, but ST segments in V3 and V4 have risen. Still de Winter morphology in V2, I, and aVL.

At this time, POCUS was performed by the ED team and is shown below:

I believe the POCUS clips above show a clear anterior wall motion abnormality.

The patient had ongoing chest pain. The ultrasound was reviewed with the cardiologist and together they reactivated the cath lab, about 25 minutes after the initial cancellation.

If you had waited for the initial (conventional prior generation) Troponin T, it was undetectable (less than 0.01 ng/mL).

Angiogram results:

Prox LAD 99%, thrombectomy (no TIMI flow listed)

"Distal nitroprusside administration and distal LAD thrombectomy performed with improvement in no reflow."

"Integrellin double bolus given in lab. Continue Integrelin for 18 hours."

Post cath ECG:

What do you think? What has changed?

Now there is RBBB (the right bundle is supplied by the LAD in all cases I am aware of), with persistent concordant STE in precordial leads, as well as Q-waves in V1 and V2. In the situation of LAD OMI, this ECG does not yet show significant signs of reperfusion, and may instead be concerning for No Reflow phenomenon, meaning lack of downstream perfusion despite epicardial intervention. 

Formal echo next day:

Severely reduced global LF systolic function, EF 25%

WMA: mid anterior, mid anterolateral, mid inferior, mid anterior septum, inferior septum, entire apex, all severely hypokinetic 

No evidence of clot with usage of echo enhancing agent. Swirling of contrast in LV apex consistent with low flow state

Normal RV systolic function

Peak Troponin T = 4.94 ng/mL (large MI, similar to the average STEMI+OMI in our data of 265 OMIs, using the same assay, which had mean and median peak troponin T of 5.50 and 3.78 ng/mL)  

Discharge ECG:

Persistent RBBB. The Q wave in V1-2 has widened, concerning for LV aneurysm morphology in RBBB. There is conspicuous lack of reperfusion T wave inversions in anterolateral areas, which would usually be present if there had been meaningful reperfusion. This ECG further supports No Reflow and long term poor outcome.

Learning Points:

When the OMI is most hyperacute, when there is maximal tissue to be salvaged by emergent reperfusion therapy, the troponin is lowest and there is very often insufficient STE to meet STEMI criteria. We have shown that, even in OMIs that DO meet STEMI criteria,  expert ECG interpretation can identify OMI hours sooner than STEMI criteria. Would you like your EM physician and cardiologist to be ECG experts? or just use STEMI criteria?

When the ECG is not diagnostic to a provider, immediate bedside echo can help to diagnose OMI.

The LAD supplies the RBBB and LAFB. New RBBB/LAFB in OMI is a sign of extremely dangerous LAD OMI.

No Reflow phenomenon indicates inadequate downstream reperfusion and is diagnosable by ECG.

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MY Comment, by KEN GRAUER, MD (9/22/2022):

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I liked this case — because it presents yet one more variation in the de Winter T Wave Pattern that we all need to recognize.

• For clarity — I have reproduced and show together in Figure-1 — the first 2 tracings in today's case.

Dr. Meyers showed Dr. Smith and myself the 1st ECG in today's case, initially without the benefit of any history. As noted above — Dr. Smith was immediately suspicious of, "de Winter, LAD OMI".

I focus my comment on my slightly different response. I replied as follows for my interpretation of ECG #1:

• "Sinus tachycardia — some potentially significant Q waves (in leads aVL, V1,V2) — and LOTS of ST depression, which interestingly is most marked in lead V2 (!), as well as in high-lateral leads I and aVL. In addition — there is ST elevation in “opposing” leads (ie, especially in lead aVR — but also in leads III and V1)."
• My Impression of ECG #1 was: "Diffuse subendocardial ischemia in a patient with multi-vessel disease (and probably some prior events). IF associated with a history of new chest pain — then this patient should clearly undergo prompt cath to define the anatomy."

The reason why I did not promptly recognize de Winter T Waves (as Dr. Smith immediately did) — was because I didn't see very tall T waves arising from the marked J-point ST depression.

• The "Take Home" point for me regarding today's case — was that the simple reason I didn't see the very tall anterior T waves usually associated with de Winter T Waves — is that we were seeing this extensive anterior infarction at a very early stage in the process before the T waves had a chance to enlarge.
• 
  
• I believe the process in today's patient did begin with diffuse subendocardial ischemia (supported by the diffuse severe hypokinesis on formal Echo done the following day). 
• Then followed initial marked J-point ST depression (in leads I, aVL and V2 — as seen in ECG #1 of Figure-1) — with development of terminal T wave positivity in these 3 leads.
• And as we look back on ECG #1 (after seeing the subsequent serial ECGs that evolved) — those Q waves I pointed out in ECG #1 were in fact early indicators of the infarction to come.
• 
  
• The follow-up ECG (ECG #2 — done a short while later) — then showed progression of extensive evolving infarction. Specifically — the amount of J-point ST depression in leads I, aVL and V2 is much less in ECG #2 (with reduction in the amount of ST depression in other chest leads) — and T waves in multiple leads (ie, leads I, II, aVL; V2,V3,V4) are becoming larger and "fatter"-at-their-peak (ie, more hyperacute).

Figure-1: The first 2 ECGs in today's case.

Additional Learning Points from Today's Case:

We continue to frequently review the gamut of de Winter T Wave "variants" in Dr. Smith's ECG Blog (See the May 2, 2019 post — among many others).

• I discussed in detail in My Comment at the bottom of the page in the July 11, 2022 post — how common it is to see "variations on the theme" of de Winter T Waves. In the interest of brevity — I'll simply reproduce in Figure-2, my adaptation from the original manuscript by de Winter et al, published in this 2008 NEJM citation — which shows you 8 selected ECG presentations from his series of patients.
• I've seen scores of other variations of de Winter T Waves. I have added to "My Mental List" — the additional ECG variation seen in ECG #1 from today's case, in which we catch a very early glimpse of de Winter T waves evolving from initial diffuse subendocardial ischemia.
• 
  
• P.S.: Clinically — the fact that I did not recognize de Winter T waves as soon as Dr. Smith did in today's case does not matter — because regardless of what you call the picture of ECG #1 in Figure-1 — in a patient with new-onset chest pain — prompt cardiac cath is clearly indicated. Unfortunately that was not done in today's case. 

Figure-2: The de Winter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See text).

OMI Confirmed by POCUS Echo in a 50 year man

Case submitted and written by Alex Bracey


A man in his 50s with no significant past medical history presented from a local beach with epigastric "burning" pain that had been intermittent for 4 days until this morning when it became constant at rest. He had associated nausea and diaphoresis, but overall looked well and had arrived by private vehicle to front triage. An ECG was performed there and brought to me for review:

What do you think?

STE in V2-4 that might just barely meet STEMI criteria
STE in aVL, and to a lesser extent lead I
Obvious reciprocal STD in II, III, aVF

Regardless of whether this ECG truly meets STEMI criteria, it is obviously diagnostic of OMI, most likely LAD occlusion. There is possible beginning of terminal T-wave inversion in V4 -5 possibly suggesting some reperfusion, but overall the ECG clearly shows active occlusion.



Since it was on the border of meeting STEMI criteria, a "heart alert" was activated. The heart alert pathway at my hospital summons a cardiology fellow and interventionalist to review the case and ECG without yet activating other cath lab staff, thereby allowing for rapid evaluation of the need for PCI without additional resource utilization.

The cardiology fellow presented to the bedside and reviewed the following additional ECG that had been obtained just before his arrival:

STE still present in V2-V4 and aVL, but to a lesser extent than the initial
Developing terminal T-wave inversion in V2-5, I, and aVL, implying reperfusion

He proceeded to review the ECGs and the case. He inquired as to the patient's recent alcohol intake, which had been increased compared to usual as he was on vacation. He had discomfort with deep palpation of the epigastrium.

At this point the fellow was concerned but not convinced that the presentation and findings truly represented OMI and wanted to wait for a troponin level before activating the cath lab.

The patient continued to have pain despite the reperfusion pattern, so we administered heparin 4000 U IV in addition to aspirin.

At our facility, we unfortunately do not yet have access to emergent high quality contrast enhanced echocardiography for our heart alert cases. So we immediately performed a bedside echo.

Despite imperfect quality, this shows severe hypokinesis of the anterior wall with reduced LV function.

I reviewed the images with the cardiology fellow who agreed that the constellation of symptoms and findings was concerning enough to activate the cath lab at this point. No troponin had yet resulted.

There was only a delay of perhaps 20 minutes between our diagnosis of OMI and the cardiologists' decision to take him for emergent cath.

Pre intervention: proximal to mid-LAD 100% occlusion (TIMI 0 flow).

Post intervention: stent placement with resultant TIMI 3 flow

The initial troponin T returned at 0.61 ng/mL.

5.5 hours later a repeat troponin T was 9.0 ng/mL, consistent with very large myocardial infarction.

At the 24 hour mark a formal echocardiogram was performed which revealed severe hypokinesis of the anterior wall, septum, and apex with an ejection fraction of 27%.


Teaching points:

You must learn to identify OMI so that you can advocate for your patients.

What is obvious to you may not be to your colleagues and consultants. Adjunctive tests such as point of care ultrasound to look for wall motion abnormalities may make the difference between an emergent or delayed cath lab activation (think of it as the FAST exam for ACS!). You should routinely perform these POC echos in order to practice identifying wall motion abnormalities. An easy exercise is to start by performing a POC echo on all STEMI activations where it is clear there is a wall motion abnormality; when there is STEMI, if you do not see a WMA, then you are missing it.

Although this ECG is completely diagnostic, there is utility in emergent echo looking for wall motion abnormalities in cases where the ECG is less diagnostic, or when the provider(s) do not recognize OMI on a diagnostic ECG. Only high quality contrast echo done by a trained echocardiographer and read by an expert can approach true rule-out of a wall motion abnormality. An echo of any lesser quality can of course be used, with the understanding that it is really only helpful if you find a wall motion abnormality, thereby increasing your suspicion of OMI and helping the decision to proceed with emergent cath.

Do not let POCUS convince you of absence of OMI if the ECG is diagnostic.  An inadequate echo, or one read by a non-expert, can be false negative.

Don't forget to obtain serial ECGs. Even if progression to STEMI is not seen, dynamic changes (e.g., development of reperfusion pattern) can help to expedite appropriate treatment.