A 20-something with intermittent then acute chest pain

This was sent to me by a partner:

"Curious what you think of this one we had overnight.  Healthy male under 25 years old with a pretty good story for acute onset crushing chest pain relieved with nitro.  He had another episode the day before after exerting himself.  No pericardial effusion on ultrasound."

What do you think?

First, many on Twitter said "Pericarditis".  This is NOT pericarditis, which virtually NEVER has ST depression any where except aVR.  When there is ST depression (as in aVL, V2, V3), then top on the differential is OMI or myocarditis.

See our publication: ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

There is STE in inferior leads, high lateral leads, and V4-V6.  And there is ST depression in V2 and V3, all but diagnostic of posterior OMI.

My response was: "OMI until proven otherwise"

#PMCardio AI Bot (AKA: "The Queen of Hearts"): OMI

• You can sign up to be on a list to receive the PM Cardio AI App here.  It was trained by Drs. Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI.

The young age always makes one suspicious of myocarditis.  The STE in II ＞III is also suggestive of myocarditis.  But the stuttering pain and sudden onset suggest acute coronary occlusion (Occlusion MI, or OMI).  And it would be dangerous to assume this is myocarditis.   

Therefore, emergent cath is indicated, and the cath lab was activated.

Angiogram:

"Acute onset chest pressure with diaphoresis." 

"ECG diffuse ST elevation, but lacking pericarditis features, and very concerning for acute injury."

"Cath lab activation by the ED and I agree with coronary angiography emergently."

Result: no angiographically significant obstructive coronary artery disease .

Medical Rx. Aggressive risk factor modification.

The initial hs troponin returned at 6700 ng/L.  It peaked at 21,000 ng/L

Post angiogram ECG:

The fact that there is near normalization suggests that this may have been a thrombus with complete lysis.  

How would the ECG findings of myocarditis resolve rapidly and nearly completely?

Formal Echo:

The estimated left ventricular ejection fraction is 47 %.

Regional wall motion abnormality-distal septum anterior and apex .

Regional wall motion abnormality-distal inferior wall .

Stress induced cardiomyopathy (Takotsubo like LV dysfunction) possible 

The appearance of wall motion abnormalities in some apical views suggest possibility of stress mediated cardiomyopathy.

A normal angiogram does not necessarily mean that there was no OMI.  There can be non-obstructive lesions that fissure and thrombose, with complete lysis of the thrombus. So MRI is necessary to confirm myocarditis.  Especially with resolution of the ECG findings, OMI is more likely that it otherwise would be.

MRI confirmed Myocarditis.  Viral studies were positive for Rotavirus.

MRI summary:

1) Mildly decreased LV function with no wall motion abnormalities 

2) Normal dimensions of all cardiac chambers 

3) Patchy mid-myocardial and epicardial delayed enhancement in a 

non-coronary distribution, consistent with myocarditis. 

Don't assume that young people don't have OMI!!  2 cases here:

A teenager with chest pain, a troponin below the limit of detection, and "benign early repolarization"

And even more here:

Dr. Smith's ECG Blog: young (hqmeded-ecg.blogspot.com)

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My Comment by KEN GRAUER, MD (4/25/2023):

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Today's case is illustrative of the diagnostic path for determining the etiology of new-onset, severe chest pain in a young adult in his 20s. Even after repeat ECG, Echo, troponins and cardiac cath — a definitive diagnosis was not yet attained — with considerations including: i) Acute OMI (with rapid spontaneous reperfusion accounting for the failure of cath to show obstructive coronary disease in this young adult); ii) Takotsubo (Stress) Cardiomyopathy; or, iii) Acute Myocarditis.

PEARL: Most patients who present with new chest pain + ECG changes + positive troponin — will not need Cardiac MRI. That said — today's case serves as an insight-providing reminder of the important selective minority of cases in which Cardiac MRI tells us the answer that had alluded us prior to ordering this test.

• We've previously discussed the all-too-often ignored entity known as MINOCA ( = MI with Non-Obstructive Coronary Arteries) — which we detailed in the November 30, 2022 post in Dr. Smith's ECG Blog (See My Comment at the bottom of the page). But cardiac MRI ruled out MINOCA in today's case — because cardiac MRI did not show infarction.
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• Cardiac MRI ruled in acute Myocarditis in today's case — by finding a suggestive acute inflammatory pattern on LGE (Late Gadolinium Enhancement).
• 
  
• NOTE: For detailed review regarding use of Cardiac MRI in acute chest pain evaluation — See the extensive article by Broncano et al (RadioGraphics 41:8-31, 2021). 

Today's Initial ECG:

For clarity and ease of comparison — I've put the 2 ECGs in today's case together in Figure-1.

• We've shown on a number of occasions in Dr. Smith's ECG Blog how difficult it may sometimes be to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and the clinical history (See My Comments in the July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).
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• To Emphasize: Definitive diagnosis was not attained in today's case until cardiac MRI study. That said — there are some ECG findings in the initial tracing that are worthy of mention. These include: i) An unusual distribution of ST-T wave changes (ie, While ST elevation in inferior and lateral chest leads with ST depression in V1-V3 suggest acute LCx OMI — it's unusual with acute OMI to see more ST elevation in lead I than lead III, at the same time there is no ST elevation in aVL); and, ii) The ST/T wave ratio in lead V6 far exceeds 0.25, consistent with what may be seen with pericarditis (See My Comment in the December 13, 2019 post in Dr. Smith's ECG Blog). ECG findings somewhat atypical for acute OMI in a 20-something year old adult increase suspicion for acute myocarditis.

The Post-Cath ECG: 
Despite an initial ECG picture consistent with acute myocarditis — Uncertainty returned for the follow-up ECG done after cardiac catheterization.

• As per Dr. Smith — marked reduction in ST elevation and depression so quickly in the post-cath ECG was clearly unexpected in this patient who turned out to have myocarditis! Although there has been a change in the frontal plane axis (which in ECG #2 is now consistent with LPHB, with predominant negativity in lead I) — I don't think this axis shift is enough to explain the resolution of ST elevation in the limb leads.
• I don't know the significance (if any) of the new Q waves in the inferior leads in ECG #2.
• In the chest leads — there is no longer anterior lead ST depression. 
• Lateral chest leads now show narrow Q waves that were not previously present — and the abnormal ST-T wave ratio is no longer present.

 

BOTTOM Line in Today's Case:

• Cardiac MRI proved invaluable for determining the diagnosis in today's case.

Figure-1: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECGs using PMcardio).