Serial ECGs confirm initial suspicion of anterior STEMI (LAD occlusion)

A 52 yo man began having substernal chest discomfort and presented 2 hours later.  His prehospital ECG, which I cannot find, reportedly had some ST depression in precordial leads.  He had this ECG recorded at 0658:

There are hyperacute T-waves in V1-V4.  There is minimal ST elevation, almost 1 mm in V2 and less than 0.5 mm in V3, but this is diagnostic of anterior STEMI even without ST elevation.  Using the equation (which may not be applicable because there is not enough ST elevation to even qualify for early repol), and the computerized QTc of 424, the value is 25.995 (greater than 23.4 is LAD occlusion).

The clinicians who saw this patient do not, like me, spend their lives analyzing the minutiae of ECGs, so they were not certain of the diagnosis, but they did suspect it, so they did the entirely appropriate management of obtaining serial ECGs, and a repeat ECG was done at0713:

Still suspicious for hyperacute T's but no ST elevation or significant evolution.  The T-wave in V2 is less prominent, suggesting some reperfusion.  QTc is 436 and equation remains greater than 23.4

So another was recorded at 0720:

Now there is ST elevation in V2 and V3, diagnostic of LAD occlusion

 Another at 0726:

Not much changed

 Another at 0744:

Now it is unequivocal

 At this point, the cath lab was activated. 

This is the post cath ECG:

Cath showed a complete mid-LAD occlusion.  Peak troponin I was 120, even with a short door to balloon time, and even though the initial ECG was not striking.  The echo showed a large anteroapical wall motion abnormality.

I suspect the prehospital ECG had de Winter's ST depression and T-waves. 

Missed STEMI, spontaneously reperfused

Click here for other very instructive cases of missed STEMI.

This is a 48 yo female with no risk factors for CAD had sudden onset of arm numbness radiating to bilateral arms, followed by substernal chest heaviness that radiated to both sides of chest.  She had some associated SOB.  In previous weeks she had been having SOB when climbing 2 flights of stairs.  She called 911.  Medics arrived and recorded the following ECG at 1756:

There is sinus rhythm and a wandering baseline.  There is no ST elevation nor hyperacute T-waves, nor ST depression anywhere.   The ST segments are upwardly concave.  R-wave progression is normal.  It is a normal ECG.

The medics gave her sublingual NTG with some decrease in symptoms. They gave her an aspirin.



She presented to the ED at 1832 is some distress; the nurse's note mentions "grunting, mottled." 

This is the patient's first ED ECG, recorded at 1845:

There is now 1 mm of ST elevation in V2 and minimal STE in V3.  The ST segments are straight.  There is poor R-wave progression.  The T-waves are larger.  This description makes it sound like MI, but really, at a glance, it is not terribly remarkable on its own -- until you compare it with the previous.

The physicians caring for the patient were unaware of the prehospital ECG, and did not go look for it.  The patient remained in some discomfort, but no serial ECGs were obtained.  The first troponin was negative.  At 2016 the patient had no more grunting respirations.

With the ECG read as normal, a negative troponin, and a low risk patient, the providers did not have a high suspicion for ACS, so admitted her to observation with no further antiplatelet or antithrombotic therapy.  By the time of admission to observation, she had no more chest pain.  No more ECGs had been done.

Troponins

First trop at 1932 "normal" (negative)


Drawn at 2335: 34.8 (this returned at 0100, prompting the following ECG at 0111, 6.5 hours after the last one)

There are now Wellens' T-waves in V1-V5 and poor R-wave progression.

What happened?

One needs to view the prehospital ECG and the ED ECG side by side:

ED ECG is on the right.  Notice the T-waves are taller and fatter, the ST segments straight, and the R-waves have less voltage.  This is almost certainly a developing anterior STEMI.

Had this side by side comparison been done, the index of suspicion would have been much higher.  Perhaps a second, or third, ED ECG would have been recorded.  It almost certainly would have revealed more ST elevation and had indication for immediate reperfusion.

That her pain eventually spontaneously subsided indicates probable spontaneous reperfusion.

Subsequent troponins
0250: 41.7
0455: 35.6

An echocardiogram the next day showed an EF 55% and a regional wall motion abnormality in the distal septum, anterior and apex.

An angiogram later that day showed the culprit lesion at a 60% LAD stenosis (the patient did indeed have spontaneous reperfusion, but not before losing a significant amount of myocardium).

Learning points
1.  This is labelled a NonSTEMI, and shows one of the many ways in which a damaging coronary occlusion is called a NonSTEMI rather than a STEMI: the fewer ECGs you record, the less chance your STEMI is called a STEMI.
2. Always do serial ECGs in patients with ongoing unexplained substernal chest pain.
3. Always compare the ED ECG with the prehospital ECG
4. Beware of straight ST segments, and any ST elevation that is not accompanied by well-formed R-waves.  Early repolarization always has well formed R-waves.  This is the main reason why my early repol vs. MI equation works (although, in the study, I excluded any patients with straight ST segments).

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. 

3 hours prior to calling 911 he developed typical chest pain. 

The medics recorded this prehospital ECG at 1535:

There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression.  He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER).  But it could be anterior STEMI.  40% of anterior STEMI has upward concavity in all of leads V2-V6.

How can one decide whether this is ER or MI?  First, if an old ECG is available, then compare.  Only rarely does early repolarization change from date to date, though it is possible.

Second, I have developed a score that helps to differentiate the two.  His BER score, based on ST elevation at 60 ms after the J-point in lead V3, QTc (400), and R-wave amplitude in V4 is 23.9 (greater than 23.4 is likely anterior STEMI).

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm)

Third, one can do an immediate cardiac ultrasound.

Medics gave him nitroglycerine sublingual and his pain resolved.  He arrived in the ED and had this ECG recorded at 1544

It is essentially the same as the previous, and the score is again about 24 (MI more likely than early repol).  Also, compare with the patient's previous ECG below; concentrate on reciprocal leads III and aVL.  The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology).  The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL.  This rules out pericarditis, which essentially never has reciprocal ST depression.

A previous ECG was found:

This has no ST elevation, and T-waves are not tall.  Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology".  LV aneurysm is very different for inferior vs. anterior MI.

The patient remained pain free, and this ECG was recorded at 1606:

He remained pain free.  A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist.  They could see no anterior wall motion abnormality.  Diagnosis of ACS was in doubt.

His old angiogram was reviewed and it was known that his disease was not amenable to PCI.  He needed CABG.  He was therefore treated with eptifibatide, heparin, and aspirin, and referred for CABG, but not immediately.

The next AM, this ECG was recorded:

There is some residual ST segment elevation.  The T-waves are far less tall. 

8 days later.  All ST elevation resolved.

It is often difficult to see changes unless they are directly side-by-side.  Here are V1-V3 from start to finish.  I did not include the prehospital because it is identical to the first ED ECG:

Self explanatory, no?

All troponins were undetectable (less than 0.04 ng/ml). 

The patient had a critical LAD stenosis.  Flow had spontaneously been restored, perhaps aided by nitroglycerin.  He underwent CABG. 

Conclusions:
1.  Anterior STEMI can look very much like early repolarization.  There are means to distinguish the two.
2. Transient ST elevation is very hazardous.  Even when the serial troponins are negative, the ECG is critical to the diagnosis of ACS. 
3. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia.

4. This is not pericarditis because:

            a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)

            b. There is relative reciprocal ST depression in lead III.

                      Pericarditis does not have reciprocal depression.

            c. ST elevation of pericarditis  is maximal in leads II and V5, V6. 

                      Here the ST elevation is maximal in V2-V4.

            d. Pericarditis does not have hyperacute T-waves.

            e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

The development of an inferior-posterior STEMI, from prehospital to hospital

For other cases of inferior hyperacute T-wave click here and here.
For more on lead aVL, click here and here.  Also use labels on the right sidebar.

Case
A 65 yo woman called 911 for pain in her upper back (between the shoulder blades) and in the left shoulder and left biceps, and some "mild chest pressure" elicited by the medics.  Exam was normal. All but the back pain resolved with nitroglycerine

Medics recorded 6 prehospital ECGs.  Below are 3 of them:

1430

There are hyperacute T-waves in II, III, and aVF.  Note T-wave inversion in aVL, which is the earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement

 1432

No significant change

 1445

Now there is clear ST elevation in inferior leads.  T-wave inversions in aVL and V2 have evolved to ST depression.  

They arrived in the ED at 1503.  BP was 116/70.  CXR and cardiac and aortic ultrasound were done to look for any evidence of aortic dissection.  All were normal except for a possible inferior wall motion abnormality.

In the ED, the following ECGs were recorded. 

1512

ST segments have almost normalized. Hyperacute Ts are less prominent, as is T inversion.  There is probably some spontaneous reperfusion of the infarct-related artery.  The computer noticed only some "minimal" ST depression.

1532

Inferior ST elevation is more obvious, with 1 mm in II and III, but T-waves have normalized.  ST depression in V2 is clearly abnormal.  Computer did not read MI.

1542

Now the most obvious findings are ST depression in aVL and V2

Cardiology was consulted.  Again, a cardiology fellow opined that this was not a STEMI, and went to talk with the interventionalist. 

A posterior ECG was recorded:

Only aVL was of great concern.  There is no posterior ST elevation.

The interventionalist was very concerned and activated the cath lab.  The patient was taken to the cath lab.  The proximal RCA was 100% occluded.  It was stented.  Door to balloon time was 62 minutes.  Peak troponin I was 5.15 ng/ml.

Post PCI ECG

T-waves and ST segments are back to normal

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.

The Importance of Serial ECGs

If there is high suspicion for ischemia, do serial EKGs and pay attention to them!

Case 1)
This is the initial EKG of a 60 yo male with a couple days of stuttering chest pain. He is pain free at the time of the EKG at 2100.

At 2140, the patient had recurrent pain, and the following EKG was recorded:

If seen alone, this EKG would not look terribly abnormal. But compared to 40 minutes prior, there is ST elevation now where there was none before, and the T-waves are much taller.

This was not appreciated by the treating physician. Even with no change in the EKG, the patient should have at least been admitted for observation. Unfortunately, the patient was discharged and suffered significant loss of the anterior wall.

Case 2)
This is the initial ECG of another 60 yo man with chest pain that is now resolved.

There is left bundle branch block (LBBB) without any ST segment shift that would be suggestive of acute coronary occlusion (of LBBB with STEMI). Such shifts would be 1) concordant (same direction as QRS) ST elevation in inferior or lateral leads 2) concordant ST depression in leads V1-V3 (where the QRS is negative, ST depression would be concordant and this would be posterior STEMI) or 3) excessive ST elevation in leads with a negative QRS; excessive is greater than or equal to 20% of the preceding S-wave. This EKG has some T-waves that are suspicious for NSTEMI: in the presence of an upright QRS, these are positive T-waves in II and V6 and also biphasically positive (terminal portion upright) in I and aVL. T-waves, like the ST segment, should be opposite the QRS in LBBB without ischemia.

The patient was admitted to the CCU and had recurrent chest pain. The following ECG was recorded:

Now there is definite ST elevation, concordant with the QRS, in lead V5. There is also excessively discordant ST elevation in lead V2 (=25% the depth of the preceding S-wave). More importantly, these are all changes from the initial ECG. The patient's cardiologist did not see this change and the anterior wall was lost.

Acute MI from LAD occlusion, or early repolarization?

3 hours of chest pain. Is it STEMI or is it normal (or early repolarization)?

Read Answer Below



This ECG looks quite normal, with only moderate ST elevation, upward concavity, good R-wave amplitude.  There is no ST depression or T-wave inversion.

But one easily identified characteristic makes the ST elevation unlikely to be from early repolarization: the computerized QTc is 455 milliseconds. In my study of early repolarization (ER) (n=167), only 2 of 167 (2%) cases of ER had a QTc greater than 455ms. The mean QTc was 394ms, compared to 420ms for MI (n=125) from LAD occlusion. Conversely, only 4% of LAD occlusion, vs. 40% of ER, had a QTc less than 380 ms. These clues were not appreciated by the clinicians. A very astute interpreter would not that the T-waves are also too symmetric to be early repol, which should have a steeper downslope than upslope, as demonstrated here:

The clinicians did not appreciate these subtle differences.

The patient continued to have chest pain.  70 minutes later, they repeated the ECG, which is shown here:

Note that now there are tiny Q-waves in V2-V4, making this unequivocally diagnostic of acute STEMI. 

These subtle Q-waves were not appreciated, but the clinicians were astute and ordered a stat echocardiogram, which confirmed anterior wall motion abnormality. The patient was taken to the cath lab and had a 100% LAD occlusion.

After reperfusion, the patients baseline ST-T complex was revealed. This is probably what they would have looked like prior to the LAD occlusion:

For those who want some more detail on differentiating ER from MI, see below:

Also useful was the mean (from V2-V4) R-wave amplitude, at a cutoff of 5 mm, with values less than 5 mm likely to represent MI. Interestingly, mean ST elevation (no matter how it was measured) was not as good a differentiator as the mean R-wave amplitude, but if mean R-wave was less than 5 mm OR the mean ST elevation (V2-V4, as measured at the J-point, STEJ) was greater than or equal to 2 mm, then it was very likely to be MI and very unlikely to be ER.

Even better was a formula derived with logistic regression, which also included the QTc :
(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc in milliseconds) - (0.326 x RA in V4 in mm), where RA is R-wave amplitude and STE60 is ST elevation at 60ms after the J-point relative to the PR interval.

If the value of the formula is greater than or equal to 23.4, it is MI (Sens, spec, accuracy all around 90%); if less, then it's ER.

For the first ECG, STE60, V3 = 2.5mm, QTc = 455, and RA V4 = 17, so: (1.196 x 2.5) + (0.059 x 455) - ( 0.326 x 17) = 24.29; this is barely greater than 23.4, thus consistent with MI but also further illustrating that this ECG is very difficult.