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.