Healthy 45-year-old with chest pain: early repolarization, pericarditis or injury?

Submitted by Dr. George Mastoras (Twitter @georgemastoras), written by Jesse McLaren

It’s a busy day in the ED when you’re sent another ECG to sign off from a patient at triage. A healthy 45-year-old female presented with chest pain, with normal vitals. The computer interpretation was “ST elevation, consider early repolarization, pericarditis or injury.” What do you think? Only one of these options is concerning, so should the patient stay in the waiting room until a bed becomes available, or do they need to be seen immediately?

There’s normal sinus rhythm, normal conduction, borderline right axis, and normal voltages. Anterior R waves are small, but leads may have been placed too high as P waves are inverted in V1 and biphasic in V2. There’s mild concave ST elevation and hyperacute T waves in V3 and especially V4, with more subtle hyperacute waves inferiorly. There’s TWI in aVL but this is concordant to its QRS.

The final cardiology interpretation confirmed the computer interpretation of “ST elevation, consider early repolarization, pericarditis or injury”. But which one is it? 

1. Early repolarization/normal variant has ST elevation and T waves proportional to tall voltages. But here the voltages are normal and the ST elevation and T waves are disproportionately large relative to the QRS – including a T wave almost as big as the entire QRS in V4 - so this isn’t normal

2. Pericarditis has primary diffuse ST elevation without affecting the T wave – but here there are hyperacute T waves localized to an antero-inferior distribution - so this isn’t pericarditis

3. OMI: the ECG was not marked as ‘STEMI’ because there is only borderline ST elevation, and no inferior reciprocal change often associated with anterior STEMI. But inferior reciprocal change in LAD occlusion is mostly seen when the occlusion is proximal to the first diagonal, whereas mid LAD occlusion often has no effect on inferior leads, and distal LAD occlusion can produce inferior ST elevation/hyperacute T waves as in this case 

So this patient with chest pain has hyperacute T waves in II, III, aVF and V3-V5, which excludes early repolarization and pericarditis and is diagnostic of OMI - with a distribution that suggests distal LAD. This is apical OMI -- both inferior and anterior, usually due to a distal LAD, often one that wraps around to the inferior wall, a "wraparound LAD".

Dr. Mastoras immediately recognized the hyperacute T waves, and brought the patient into a room for further assessment. The patient was previously healthy, with no atherosclerotic risk factors, and developed chest pain after an episode of stress. The pain was crushing retrosternal, radiated to the arms and was associated with lightheadedness. During initial assessment the patient received nitro and aspirin, with resolution of symptoms, and had serial ECGs:

The hyperacute T waves have deflated – proving this was transient OMI, and not early repolarization or pericarditis. 

Then the patient suddenly became unresponsive while another ECG was being recorded:

Polymorphic VT preceded by a normal QT interval. So not “torsades” (polymorphic VT + long QT) but ischemic polymorphic VT. The patient was immediately cardioverted back into sinus rhythm and regained consciousness.

Smith comment: Ventricular Fibrillation looks just like polymorphic VT. So whether it is one or the other would depend on 3 factors: 1) preceding long QT, 2) spontaneous conversion, and 3) presence or absence of pulses. An unconscious patient probably has no pulses and so this is VF. On the other hand, when there is not pulse, there is no difference in treatment: it should be difibrillation (not synchronized cardioversion).

Here is the post shock ECG:

Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm.

Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically. Echo showed EF of 50% with akinetic apex. First trop was 90 ng/L (normal <16 in females) and peak was 7,400 ng/L. Discharge ECG showed antero-inferior reperfusion T wave inversion:

Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. But because Dr. Mastoras recognized the hyperacute T waves, the patient was immediately seen, the polymorphic VT was immediately defibrillated, and the patient was rapidly diagnosed and treated. 

Without clinical context, the Queen of Hearts identified OMI with high confidence, based on the hyperacute waves.

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Take away

1. LAD occlusions can be missed when there is minimal and concave ST elevation and no inferior reciprocal change

2. Hyperacute T waves help exclude normal variant or pericarditis and identify STEMI(-)OMI

3. Distal LAD occlusion produces antero-inferior STE/hyperacute T waves
4. Young women without atherosclerotic risk factors are at risk for delayed diagnosis of MI, yet this is the classic group to develop MI secondary to SCAD

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MY Comment, by KEN GRAUER, MD (9/27/2024):

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Important question posed above by Dr. McLaren — namely, if working a busy shift in the ED and presented with the initial ECG in today's case (that I've reproduced in Figure-1) — Does this patient need to be seen immediately? 

To take Dr. McLaren's question to another level:

• How long should it take you to know that this previously healthy 45-year old woman with new CP (Chest Pain) is having an acute OMI — at least, until you can prove otherwise?

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

How Long Should It Take?

As per Dr. McLaren — OMI was correctly diagnosed in today's case. The point of my Comment — is that it literally took me less than 5 seconds to know that prompt cardiac cath was going to be needed. I based this on the following:

• The History is Worrisome: This previously healthy 45-year old woman developed sudden, crushing retrosternal pain radiating to her arms, with associated lightheadedness. 
• On learning this history, and then on seeing ECG #1 — my attention was immediately drawn to the ST-T wave in lead V3 (within the RED rectangle in Figure-1). We should instantly recognize that the shape of the ST-T wave in this lead is "off". That is — the T wave in V3 is overly large, "fatter"-at-its-peak and especially wider-at-its-base than it should be given relative size of the QRS in this lead. 
• To assure myself that the abnormal appearance of the ST-T wave in lead V3 was "real" (and not the result of artifact or a repolarization change) — my "eye was next drawn to the ST-T wave in neighboring lead V4 (within the BLUE rectangle in Figure-1) — which showed a clearly disproportionate ST-T wave large enough to "swallow" the modest-sized R wave in this lead.

Conclusion: 

• Given the history of severe, new-onset CP and the presence of hyperacute-looking T waves in leads V3 and V4 — I knew there was no way that this patient was not going to need full evaluation, and most likely prompt cath. 
• Total TIME to Reach this Conclusion: Literally, less than 5 seconds.

Clearly, there are other findings of concern in this initial ECG (that I review below). But the point of my Comment is that Dr. Mastoras (who provided us with today's case) — was quickly able to recognize the hyperacute T waves, that in a patient with sudden, new and severe CP — mandate immediate further assessment.

A Picture is Worth 1,000 Words:

Why then in this patient with new CP — are the T waves in leads V3,V4 of Figure-1 hyperacute? The answer should be immediately apparent on looking at Figure-2:

• The ST-T waves for leads V3,V4 on the left (GREEN border leads) — are from a normal tracing. There is slight J-point ST elevation, with a gently upsloping ST segment that ends with a slender, upright T wave.
• In contrast to the normal ST-T wave appearance in the GREEN border leads — is the appearance of the ST-T waves from leads V3,V4 of today's initial ECG (taken from Figure-1). Aren't the ST-T waves within the RED and BLUE rectangles obviously more "bulky", with a much wider T wave base than would be expected given modest QRS amplitude in these leads? In a patient with worrisome CP — these are hyperacute T waves suggestive of OMI until proven otherwise.

Figure-2: Comparison of normal vs hyperacute ST-T waves.

Return to Figure-1: What are the Other ECG Changes?

Hyperacute T waves are "hypervoluminous". They are larger than what we expect given relative amplitude of the QRS complex in the lead(s) we are looking at.

• Given the hyperacute changes we identified in leads V3 and V4 of Figure-1 — I like to look next at neighboring leads.
• If any doubt remained about the abnormal appearance of the ST-T wave in lead V3 — it should be removed on seeing how flat the ST-T wave is in neighboring lead V2. There simply is no way the transition between the flat ST-T wave in V2 — to what we see within the RED rectangle in lead V3 — is going to be normal.
• Given the hyperacute appearance in lead V4 — I thought the T waves in neighboring lateral leads V5,V6 were both "fatter"-at-their-peak than what is normally seen. And despite the tiny size of the QRS in lateral lead I — Isn't the T wave in lead I wider than you would expect? 
• To Emphasize: I might not think the ST-T wave appearance in leads V5,V6 was abnormal if everything else on the tracing was normal. But in the context of the hyperacute neighboring leads V3,V4 — Doesn't the appearance of the ST-T waves in leads V5,V6 look like a tapering off of the same process?
• Similarly — upright BLUE arrows in each of the inferior leads highlight "bulkier"-than-expected T waves.
• Finally — lead aVL shows reciprocal T wave inversion to the inferior lead hyperacute T waves. This is subtle — but isn't the inverted T wave in lead aVL wider-than-expected given small amplitude of the QRS in this lead. 

BOTTOM Line: In today's patient (who presented with severe new-onset CP) — recognition of hyperacute T waves in leads V3,V4 can be made within seconds. As described above — increased scrutiny elsewhere on the tracing reveals ST-T wave abnormalities in virtually all remaining leads. As capably recognized by Dr. Mastoras — the need for prompt cath quickly became obvious.

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P.S.: Of interest — the previously healthy 45-year old woman in today's case was found to have SCAD (Spontaneous Coronary Artery Dissection) of the distal LAD, with resultant 95% narrowing of the involved area.

• As per Dr. McLaren — the above demographic for today's patient is typical for a much higher-prevalence group for having SCAD as the cause of their acute event. Whereas SCAD is found in ~1-4% of all angiograms performed for ACS — this percentage increases to over 30% in middle-aged women. The risk of SCAD is even higher in pregnancy — accounting for over 40% of angiograms performed for ACS during the peripartum period.
• Clinically — the importance of recognizing SCAD as the cause of ACS — is that the approach to management is different, in that a conservative approach (without PCI) is often favored in hemodynamically stable patients with good TIMI flow. (For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog).