How do you explain these inferior hyperacute T-waves?

Alberto Pinsino, a cardiology fellow from Milan, Italy, sent this case:

Dr. Smith,

I would be interested in knowing your opinion about this case..

The Case

A 59-year-old Asian woman with hypertension and hypercholesterolemia and no past history of CAD came to the ED of a major teaching hospital with waxing and waning chest pain worsened by minimal efforts which had been ongoing for 5 days.  

She had visited the same ED two days before for the same reason.  The EKG is not available but described by the on-call cardiologist as “non specific repolarization abnormalities.”  The troponin was negative and she was discharged on ibuprofen with a diagnosis of pericarditis.

My comment: you diagnose pericarditis at your (and your patient's) peril!  It is relatively rare and usually when the ECG diagnosis of pericarditis is made, it turns out, in retrospect, to have been MI and a misread ECG.  Remember that unstable angina still exists.

At presentation, this EKG was recorded: 

Alberto's interpretation: "Inverted biphasic T waves in V1-V4, inverted T waves in D1-aVL."
Smith comment: I agree, consistent with Wellens' syndrome of the anterolateral wall, due to proximal LAD ACS.

Bedside echo was normal. First troponin was 16 ng/L (0.016 ng/mL), second 22 ng/L, third 28 ng/L (so, just barely positive: cut-off at our institution is 13 ng/L).

In the telemetry ward, 18 hours later, the patient had chest pain and another EKG was taken as shown in image 2 

Alberto's interpretation:  "There are deeply inverted T waves with minimal ST depression in V2-V3 and D1-aVL, hyperacute T waves in the inferior leads, especially III and aVF, long QT. Looks like Wellens' Syndrome." 

The crux of Alberto's inquiry:  "Why are there "hyperacute T-waves" in inferior leads??"

Smith answer: The Wellens' syndrome has evolved as it normally does, with increasingly inverted T-waves in the affected anterolateral territory.   These large upright and fat T-waves in inferior leads, especially lead III, are NOT hyperacute inferior T-waves.  These T-waves are reciprocal to the large inverted T-waves in aVL (high lateral).  III and aVL are 150 degrees opposite each other.  When there is a large Wellens' inverted wave in aVL, added to the already upright inferior T-wave, there MUST be a large upright T-wave in lead III.

So this large upright T-wave in lead III is analogous to what I call posterior reperfusion T-waves: tall, wide, upright T-waves in lead V2 after reperfusion of the posterior wall.  They are reciprocal to what would be recorded from the posterior part of the heart (inverted Wellens' waves), and added to the upright anterior T-waves.

Question: How can you tell if a large upright wave is hyperacute or if it is reciprocal to an inverted wave?  

Answer: You can tell mostly based on the state of the patient.  If the patient is symptomatic (should usually be chest pain), then the large fat T-wave is hyperacute.  Serial ECGs should show evolution to STEMI in that lead.   If, on the other hand, the patients is now pain free, then the ischemia is in the territory of the inverted T-wave and that is a reperfusion T-wave.  The hyperacute T-wave is only a reciprocal view.

The remainder is the Case Continued.

During the night, she experienced other episodes of chest pain – image 3 is an EKG while on chest pain at time 22 hours – and was put on iv nitrates.

In the morning, another EKG was collected while pain free as shown in image 4, time 33 hours. 

Troponin at this time was 7 (negative) In the cath lab, patient had a tight LAD stenosis which was stented and noncritical stenosis on the ostium of PDA (right dominance) and LM.

Here is the angiogram:

EKGs 5 and 6 below show, respectively, EKG after cath lab (time 37 hours) and EKG collected the day after the procedure (inverted T waves still present but less deep, shorter T waves in the inferior leads). Patient was pain free after stenting.

She was discharged three days later, still pain free.

I would be interested in knowing your opinion about this case. I think it is clearly a Wellens syndrome, but I am really having a hard time to explain the hyperacute T waves – if they really are hyperacute - in the inferior leads.  

Kind regards,

Alberto Pinsino

Here is a comment from Ken Grauer:

Our thanks to Alberto Pinsino for submitting this case. GREAT explanation by Dr. Smith as to why the  ST-T wave changes seen in leads III and aVF are reciprocal to the deep T wave inversion elsewhere rather than primary hyperacute changes. I’d simply add that 2 additional clues why these ST-T wave changes in leads III and aVF are much more likely to reflect reciprocal changes rather than primary hyperacute T waves are: i) that lead II shows no more than minimal ST-T wave changes. With acute evolving inferior STEMI, we’d expect a similar ST-T wave appearance in lead II as in the other 2 inferior leads; and ii) With acute inferior STEMI, we often see accompanying anterior ST depression consistent with posterior involvement. But instead of the usual “shelf-like” ST depression that is most commonly seen with acute posterior MI in these anterior leads — there is deep, symmetric T wave inversion that is different than the typical morphology of a posterior stemi-equivalent pattern. On the other hand, this anterior deep T wave inversion is consistent with a Wellens pattern from a tight LAD lesion. Molto grazie to Drs. Pinion and Smith for posting this case!