Chest pain and T wave inversion, NSTEMI?

Case submitted and written by Dr. Mazen El-Baba and Dr. Emily Austin, with edits from Jesse McLaren

A 50 year-old patient presented to the Emergency Department with sudden onset chest pain that began 14-hours ago. The nurse alerted the MD because the patient was still symptomatic, diaphoretic and “looking unwell”. What do you think?

 

 

 

 

 

 

ECG interpretation: sinus rhythm, normal conduction (PR, QRS, and QTc), normal axis, delayed R-wave progression, and normal voltages. There’s primary TWI inferiorly (aVF and III) and V6, with reciprocal tall T-wave in lead I/aVL, and a Q wave in III. There’s also a taller T wave in V2, which can be reciprocal to posterior TWI.(1) This ECG represents reperfused inferoposterior occlusion MI (likely from the RCA) but could also be seen in subacute and ongoing occlusion.

This doesn’t meet STEMI criteria so in the current paradigm there’s no urgency to getting an angiogram. But two features were concerning: 

1. An ECG showing reperfusion indicates high risk for reocclusion – either from a transiently open artery at risk of closing, or an artery that is still occluded but with perfusion tenuously maintained by collateral circulation

2. The patient had ongoing ischemic symptoms, suggesting ongoing occlusion. Even though they were passed the 12 hour mark traditionally associated with reperfusion benefits, ongoing ischemia requires emergent angiogram 

On assessment, the patient appeared uncomfortable, leaning forward in his chair. He shared that he experienced sudden onset left sided chest pain (initially 10/10) that lasted for approximately 20-30 minutes. The pain improved (6/10) but is persisting, which prompted him to visit the Emergency Department. Interestingly, he experienced a similar episode approximately three months ago, which self-resolved. However, he began experiencing chest pain with moderate cardiovascular activity (e.g., incline walking on a treadmill) thereafter. He denied experiencing any shortness of breath, palpitations, presyncope, or syncope. His initial vital signs were all within normal range and his cardiovascular exam was unremarkable. 

The initial ECG suggested either subacute or reperfused inferoposterior occlusion and clearly does not meet traditional STEMI criteria. However, given that the patient remained symptomatic, the decision was made to call cardiology to a STAT consult and activation of the cath lab. In other words, the patient’s history, presenting ECG, and ongoing symptoms were all concerning for a subacute but evolving RCA occlusion; there may have been enough reperfusion to manifest on the ECG but not enough to resolve the symptoms. The patient was given ASA 160 mg,  ticagrelor 180 mg, and started on a heparin infusion. He was moved to a monitored bed. The cardiology team came to assess the patient. Approximately 40 minutes later, another ECG was obtained: 

ECG #2 is notable for the following:

• Deeper Q waves inferiorly

• Deepening of the T wave inversion in inferior leads

• New taller R waves in V2, V3, which could be suggestive of new Q waves in the posterior leads

• PVC with a LBBB morphology, suggestive of electrical irritability from the right side of the heart

At approximately 2-hours post his arrival to the emergency department, the patient became pre-syncopal and had a run of ventricular tachycardia which self-aborted. So now there was ACS + electrical instability, another indication for emergent angiogram.

The initial troponin was 5300 ng/L (normal < 17), which corresponded to the symptoms and confirmed subacute occlusion. After the episode of VT and the troponin results the patient was taken to the cath lab: complete occlusion of the RCA with TIMI 0 flow, which was stented. He also had 70% lesion of his LAD. Peak troponin was 16,500 ng/L. Discharge diagnosis was ‘STEMI’, even though no ECG ever met STEMI criteria.

ECG done 12 hours-post cath-lab showed ongoing inferoposterior Q waves and T-waves inversion.  

Take away: 

1. Primary T-wave inversion with resolved ischemic symptoms can represent reperfusion, can be seen in any vessel territory, and is at risk for reocclusion. These T-wave inversions are often accompanied by reciprocal tall T-waves. 

2. Primary T-wave inversion with Q waves and ongoing symptoms suggests subacute occlusion, which requires emergent reperfusion

3. ACS with refractory ischemia and electrical instability are indications for emergent cath, regardless of the ECG

References 

1. Driver, B. E., Shroff, G. R., & Smith, S. W. (2017). Posterior reperfusion T-waves: Wellens' syndrome of the posterior wall. Emergency Medicine Journal, 34(2), 119-123.

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MY Comment, by KEN GRAUER, MD (8/10/2023):

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Today's case by Drs. El-Baba, Austin and McLaren — provides yet another superb example of how "clinical interpretation" of today's initial tracing indicates definite need for prompt cath despite not satisfying STEMI criteria.

• As readers of Dr. Smith's ECG Blog know well — by "clinical" interpretation, we mean temporal correlation between the presence and relative severity of new-onset CP (Chest Pain) with each of the serial ECGs obtained.
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• Clinicians still "stuck" in the outdated STEMI paradigm would have missed a golden opportunity to save valuable myocardium in today's case. This is because the ST elevation they would have been "waiting" for never arrived. Given this patient's episode of VT — application of the OMI paradigm in today's case may well have been a life-saving measure.

For clarity in Figure-1 — I've put together the first 2 tracings in today's case.

• I focus my comments on a few additional points to supplement the excellent presentation by Drs. El-Baba, Austin and McLaren.

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

MY Thoughts on Today's Case: 

As per Drs. El-Baba, Austin and McLaren — the deep, symmetric T wave inversion in leads III and aVF of ECG #1, with more subtle T wave inversion in lead V6 could represent: i) A reperfused infero-postero-lateral MI from RCA OMI; ii) Subacute occlusion in this distribution; and/or, iii) An ongoing OMI in this distribution.

• It is impossible to be certain which of these possibilities is the explanation in today's case from the initial ECG in Figure-1 alone. Instead — temporal correlation of this patient's ongoing history with today's initial ECG — comparing this with several follow-up tracings over the next hour — ideally with comparison to any prior ECGs that may have been done on this patient — all in association with serial troponins — would be needed to provide the answer.

To the above 3 possible interpretations — I'd add a 4th possibility:

• The History in today's case indicates that this patient presented to the ED because of sudden, severe CP that began ~14 hours earlier — and which was persisting at the time ECG #1 was recorded.
• The patient also related that he experienced "a similar episode" ~3 months earlier, which self-resolved — but which was followed thereafter by anginal CP!
• In view of this history of a prior "similar" episode ~3 months earlier (especially given subsequent CP on exertion) — I thought the wide QS complex in lead III of ECG #1 suggested a 4th possibility = that the patient already had an initial event 3 months earlier, and was now having a 2nd event (recurrence) in the same distribution.

Drs. El-Baba, Austin and McLaren emphasize the following:

• Prompt cath was indicated in today's case because regardless of which of the 4 possibilities suggested above reflects the actual events — ECG #1 clearly indicates high risk for reocclusion — in this patient with ongoing ischemic symptoms. CREDIT to them for ensuring that prompt PCI was accomplished!
• ACS with refractory ischemia and electrical instability are indications for emergent cath regardless of the ECG!

I'd add:

• For whatever may have occurred during the 3 months prior to this patient's presentation in the ED — Comparison in Figure-1 of ECG #1 and ECG #2, done just 40 minutes later — clearly shows dynamic ST-T wave changes (as well as deepening Q waves and taller anterior R waves). This highlights in different words the same concepts emphasized by Drs. El-Baba, Austin and McLaren.
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• PEARL: Did YOU notice the clearly abnormal ST-T waves for the PVC in ECG #2? ( = beat #6 in this 2nd tracing). While not needed for an imperative to perform prompt cath on today's patient — there are occasions when acute ST-T wave changes may not be evident in sinus-conducted beats — but which may only be seen in PVCs! The huge, disproportionately hypervoluminous T wave in lead V2 — as well as the clearly abnormal ST-T wave shapes for beat #6 in leads II and V5 of ECG #2 would be diagnostic of acute ischemia even if ischemic changes were absent in sinus-conducted beats on this 12-lead. It's good to incorporate the habit of always assessing ST-T wave changes in any PVCs that might be seen.