This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

A 38 year old with chest pain and SOB:

The answer can be found here (a different example of the same pathology, with explanation):

http://hqmeded-ecg.blogspot.com/2010/03/anterior-t-wave-inversion-due-to.html

Anterior MI: Ongoing STEMI, reperfused STEMI, or NonSTEMI?

 An 80 yo male presented with chest pain onset 1130 AM.  The prehospital ECG was reported to have some "ST depression", but is unavaliable.  His pain resolved with nitroglycerine.  Here is the first ED ECG, while still pain free, was at 1350:

There is 1.5 mm of STE in V2 and about 1 mm in V1.  There is an abnormal Q-waves (QR-wave) in V2 (a QS-wave in V1 may be normal).  The Q-wave in V2 is one clue that this ST elevation is not normal variant.  The other is some very subtle ST depression in V5 and V6.  The Q-wave could be due to old MI, but they prove that MI is present and thus one can NEVER diagnose "early repolarization."

At 1400, a second ECG was recorded:

There is now less STE in V2, 0.5 mm in V3, and a new Q-wave in V3.  The ST depression is almost gone.

Another ECG was recorded at 1418: it was identical to 1400.  First troponin I returned at 0.6 ng/ml (elevated).

The cath lab was activated.  A cardiologist came to assess.  He opined that the ST elevation was not due to ischemia.  The patient was admitted to the CCU.

At 3PM, an echocardiogram confirmed anterior wall motion abnormality.

Another ECG was recorded at 2257 that evening:

Now there is a PVC, and there are more prominent Q-waves, loss of R-wave in V2, and the T-wave has begun to invert.

 This one at 0027 is not much different:

The next AM this was recorded at 0703:

And at 0855

He was taken to the cath lab on the day after (48 hours) and had a 99% stenosis of the LAD.  Max troponin was 44 ng/ml.

Convalescent echo 3 weeks later showed normal EF and no wall motion abnormality.

Is it an ongoing STEMI? 

There was at least one ECG with 2 leads having at least 1 mm of ST elevation, so by some definitions, it was STEMI.  We don't have an old ECG, so we can't prove at the time of presentation that the STE is new.  But we do have subsequent evolution, with T-wave inversion.  This proves retrospectively that the STE was new.

T-wave inversion proves reperfusion, but we don't know when that happened: some time between 1418 and 2257.   Persistent ST elevation at later ECGs suggests


He did have a large amount of troponin (large MI), but we don't know if all that damage occurred before presentation.

He was pain free at presentation, so probably all the damage was done, but in some cases pain can be gone although ischemia continues.

He did have a significant wall motion abnormality (anterior); that can also happen with non-STEMI or reperfused STEMI, with an open artery.

The artery was open at angio 2 days later, but the TIMI flow was not listed in the cath report. 

Is is STEMI, reperfused STEMI, or non-STEMI?  At presentation, I would classify it as a reperfused STEMI.  Many would classify it as a non-STEMI.  The important question is: does he need immediate, emergent cath lab activation?  That is to say: will more myocardium die if he does not go to the cath lab immediately?  This can only be answered for certain in retrospect, not prospectively; even in retrospect, it will only be known for certain after a convalescent (weeks later) echo is done. In non-STEMI or reperfused STEMI, the wall motion should recover over time.

In fact, an echo was done 3 weeks later and showed no wall motion abnormality and normal EF, so the delay apparently was not harmful.  There was no later ECG done, so I can't say if the Q-waves resolved or not.

Thus, in RETROSPECT, it was not a true, ongoing, STEMI, defined as ST elevation MI that portends continued imminent loss of viable myocardium unless there is immediate reperfusion.

Since at presentation the T-waves were still upright, the best clue to this is the absence of chest pain, but I believe it is a big risk to count on this: 1) pain can be misleading and 2) such an unstable plaque can occlude at any time.

So what would I do??  I think there is some question on the initial ECG as to whether the ST elevation is definitely new (though I would highly suspect that it is).  I would get serial ECGs for a longer time, get an immediate formal echo, and ultimately I believe that these would be convincing of acute (probably reperfused) STEMI.  The positive initial trop would help, but this would be positive in a nonSTEMI also.  Once convinced that the STE is new, I would activate the cath lab because acute anterior STEMI, even if reperfused, is extremely unstable and dangerous.

LBBB with acute STEMI due to ruptured obtuse marginal, diagnosed with bedside ultrasound

This 74 yo male had just returned to his unit bed after successful PTCA of tight lesions of the first diagonal and obtuse marginal coronaries. He complained of chest pain. This ECG was recorded. The previous is below.

There is LBBB with concordant ST elevation in II and aVF (inferior STEMI) and V6 (lateral STEMI); also concordant ST depression in V2 and V3 (Posterior STEMI). There is also excessively discordant ST elevation in V5 (ST/S ratio 2:5 = 40%; excessive is > 20%). Compare with baseline ECG below.

Here, all ST segment are appropriately discordant; none excessively so. Maximum discordant ST elevation is in lead V2, (at 4 mm; but this is only 7% of a 60 mm S-wave)

Suddenly, the patient became hypotensive. The physician (one of our fine EM residents) caring for the patient did an immediate bedside ultrasound. This showed a loculated hyperechoic pericardial fluid (blood with clot).

Patient returned immediately to cath and this confirmed a ruptured coronary artery with pericardial bleeding. A balloon pump was placed and the patient went for immediate CABG.

The circumflex was dissected and will be bypassed any moment now.

Classic Evolution of Wellens' T-waves over 26 hours

A middle-aged patient presented with resolved chest pain.

t = 0, presentation to ED: Initial ECG of 50 yo woman who had prehospital chest pain, now resolved.  There is old inferior MI (and the nonspecific minor T inversion in aVL may be due to this, or may be new).  
There is subtle ST elevation in V2 and V3 with reverse R-wave progression and subtle ST depression in V5 and V6.  
This ST elevation should not automatically be attributed to normal variant early repol because there is also reverse R-wave progression and the afore-mentioned STD in V5 and V6, neither of which occur with normal variant ST elevation.
Therefore, this is suspicious for resolving LAD occlusion.

Serial ECGs are critical, especially if chest pain persists or recurs. 

The patient remained pain free, and did not get another ECG for 110 minutes:

t = 1.83 hours. There are now the beginnings of T-wave inversion in aVL, V4 and V5.

t = 4.75 hours.  Now there is the beginning of T-wave inversion in V2, with more in V3, and progressive T-wave inversion in aVL, V4, and V5.

 t = 6 hours.  Still more T-wave inversion, becoming symmetrical in V4 and V5.

t = 8.5 hours.  Still more T-wave inversion and increasing symmetry.

t = 23 hours.  Deepening T-waves with increasing symmetry.

t = 27 hours.  Diffuse symmetric T-wave inversion.  The patient had positive troponins and a tight LAD stenosis that was stented.

Reperfusion through collaterals associated with nitroglycerin, lead reversal mimics T-wave inversion (and fooled me)

This 69 yo male with a history of HTN, but no h/o CAD, presented with chest pain at an outside hospital at 1700 hours with chest pain onset at approx 3 PM.  Here is the first ECG, at 1720:

There is a negative T-wave in lead III, but this is not necessarily abnormal: the T-wave (18 degrees) and QRS (+9 degrees) axes are very close to each other.  The negative T-wave in aVF also looks suspicious, especially since the QRS appears to be upright. Otherwise, the ECG is normal

The patient received nitroglycerin, and became pain free.  A second ECG was recorded at 1739:

Thanks to Christopher for noticing that the leads were switched from the previous ECG, with this ECG having correct lead placement.  Now the inferior T-waves are upright because the leads are correctly placed and the axis is more normal.  Nevertheless, there is now T-wave inversion in aVL.  Additionally, ST depression can now be seen in leads V2 and V3, suggesting posterior MI.  These highly suggest posterolateral MI, probably circumflex, with reperfusion due probably to nitroglycerin.

The patient was put on heparin and eptifibatide and transferred to our institution.  Here, he remained pain free.  His initial Troponin I was 16 ng/ml.  A 3rd ECG was recorded at 2202:

The ST depression in precordial leads is gone.  The biphasic T-wave in aVL remains, with an abnormal reciprocal ST segment in lead III.

At 0032 another ECG was recorded:

This shows enlarged T-waves in V2-V3, an example of a heretofore never described (except on this ECG blog) phenomenon of what I call "posterior reperfusion T-waves."  Reperfusion T-waves are inverted, but if one makes an anterior (precordial) recording of inverted posterior reperfusion T-waves, then one gets enlarged anterior T-waves.

Here is another example of posterior reperfusion T-waves:
http://hqmeded-ecg.blogspot.com/2010/12/computer-misses-again-two-cases-one.html


The next AM the patient went into atrial fib with RVR:

The tachycardia has resulted in recurrent ischemia.  Now there is ST elevation in aVL (and reciprocal ST depression in lead III) and ST depression in precordial leads (posterior subepicardial ischemia).

He was taken for cath and had a 100% occlusion of a large 1st obtuse marginal (circumflex).  Ultrasound confirmed a posterolateral wall motion abnormality.  The troponin peaked at 74, went down, then went back up to 180 after the atrial fib, and down again.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

This 38 yo male presented with chest pain with activity for 4 days, worse on the day of presentation, and associated with SOB.  He has a h/o Renal failure and has a transplant, lately struggling with CMV infection.  His exam was negative.  Here is the ECG:

There is sinus rhythm at a rate of about 100 (faster than normal for ACS).  There is T-wave inversion in V1-V3, with some inversion also in lead III.  

The patient had an initial troponin I of 0.22 ng/ml (+) and an NT-proBNP of 3200 ng/ml (elevated).  He was diagnosed with NSTEMI and admitted to the hospital on heparin.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely.

Here is a quote from this study, "negative T waves in leads III and V₁ were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V₁ allows APE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Later, the patient had an echocardiogram which showed hyperdynamic LV fct (EF = 80%) and a dilated RV.  PE was diagnosed by CT, with bilateral pulmonary emboli.

If this were ACS, it would be Wellens' syndrome, and this just does not look like Wellens' (difficult for me to explain why, but compare with other Wellens' cases on this blog).

Compare with a classic Wellens' with biphasic T's: 

Anterior T-wave inversion, when accompanied by T-wave inversion in lead III, especially if tachycardic, should make you think of PE.  A simple emergency physician performed bedside ultrasound would have confirmed this.  Troponin will not help you in this diagnosis because, when there are T-wave inversions in either situation, the troponin is positive.