A Tale of 2 Occlusions in the Same Patient: one with Expert ECG interpretation, the Other Without

Submitted by Nic Thompson, Written by Pendell Meyers, edits by Steve Smith

This is a long post, but well worth the read because it clearly delineates the difference in patient outcomes between advanced ECG interpretation and STEMI criteria!

Dr. Thompson evaluated a male in his 40s with history of CAD s/p MI with PCI years ago, active smoking, HLD, HTN, who presented with chest discomfort and diaphoresis starting when the patient woke up a few hours prior to arrival. The pain waxed and waned until EMS arrived and gave him 325 mg aspirin en route, and had significant relief just prior to arrival. 
Here was his presentation ECG with approximately 2/10 discomfort and improving:
What do you think?
This ECG is not diagnostic of anything by itself. However, the morphology of lead aVL is slightly suspicious with a subtle down-up T-wave (terminal positivity) which suggests that perhaps there is reperfusion of the inferior wall. The T-waves in the inferior leads are neither definitively hyperacute nor clearly reperfusing. Thus, they are within normal limits if you don’t have a prior for comparison. Remember that T-waves appear normal briefly between transitions from occlusion to reperfusion and vice versa.
Dr. Thompson documented concern based on the patients history as well as suspicious ECG abnormalities including “broad T-waves II, III, aVF with subtle depression in aVL…High suspicion for acute coronary occlusion with some perfusion (probably 2/2 ASA en route).”
Again, I would not be able to say that the T-wave in the inferior leads are hyperacute based on this ECG alone. A prior ECG would be helpful.
Here is the prior ECG for comparison:

The T-waves in the inferior leads on the presentation ECG are slightly larger and more upright than the baseline. However, this is complicated by the slight axis change between the two ECGs. Lead aVL has a positive T-wave at baseline, but a negative T-wave on the presentation ECG. The R-wave progression is similar to prior.

These two ECGs interpreted together provides higher suspicion of OMI affecting at least the inferior leads. But it is not clearly diagnostic.

The patient became completely pain free during Dr. Thompson’s evaluation, and so the cath lab was not immediately activated because there was clinical reperfusion, lack of chest pain, and only subtle findings which would not generally be accepted by the cardiologist. A bedside US was performed  which did not show any clear wall motion abnormality (this is not unexpected in reperfusion).

Dr. Thompson was concerned by the subtle findings above and kept a close eye on the patient. Sure enough, 40 minutes later, his pain returned.

Here is his repeat ECG:

Similar to initial ECG, but the T-waves in II, III, aVF, and V3 are slightly larger, and the T-wave inversion in aVL is slightly different. This is still non-diagnostic but suspicion is growing for possible hyperacute T-waves.

Dr. Thompson activated the cath lab now that pain had returned with findings suspicious for OMI. At this time she documented “dynamic T-waves in II, III, aVF with more obvious depression in aVL.”

As the cardiologist was evaluating the patient, the pain increased further, and this repeat ECG was performed 12 minutes later:

This meets STEMI criteria, yet the hyperacute T-waves are the most obvious aspect in the anterior and inferior leads.

Luckily, the inferior OMI was subtle enough not to manifest large amounts of STE, because in these cases providers often will be confused by “diffuse” STE and are more likely to doubt the validity of the OMI pattern.
The patient was taken emergently to the cath lab. 
Dr. Thompson was correct about there being OMI:
This was documented as a 95% acute thrombotic lesion of the proximal LAD with TIMI-1 flow.

Remember: Thrombi are constantly lysing and propagating, so that unless one has another identical 12-lead at the exact same time as the angiogram, one cannot know for certain what the state of the artery was at the time of the ECG. 95% occlusion, depending on flow state and many other factors (especially presence of downstream platelet-fibrin fragments and also collateral flow) can show many morphologies. No matter whether fully occluded or not, the ECG (and the pain) were dynamic, proving an unstable thrombus that could propagate and fully occlude at any time. It is possible there was 100% occlusion at the time of the ECG, but one cannot say for certain. In any case, although there is an open artery with flow, the artery is at risk of complete occlusion at any moment.

See how the LAD wraps around the apex, explaining how it is able to register as OMI even in the inferior leads.
Post-intervention with TIMI 3 flow.

The patient’s pain resolved completely.

Here is the post-intervention ECG:

OMI findings resolved. Beginnings of terminal T-wave inversion in lead III. Make sure to compare this ECG with the first few presentation ECGs to convince yourself that there was, retrospectively, concerning area under the ST segment and T-wave in the inferior leads.

Resolution of pain and reperfusion on ECG are definitive evidence of true reperfusion.

The patient was admitted to the CCU and observed while modifying risk factors and titrating medications.

Thanks to Dr. Thompson’s early recognition, his troponin T peaked at only 0.51 ng/mL (relatively small compared to the area at risk) and started to drift back down.

Here is his ECG on day 2 (there is no documentation as to why this ECG was ordered, or whether he has returning pain):

Similar to last ECG, with more leads showing evidence of terminal T-wave inversion of reperfusion.

One hour later (they usually do not record ECGs this frequently on day 2 unless the patient complains of something), here is his ECG (1545 on day 2):

What do you think? 

This is definitively diagnostic of re-occlusion at 15:45. The terminal T-wave inversions have been obliterated by recurrent upright, hyperacute T-waves in the same distribution as last time. There is recurrent STE in V2-V4, but is does not meet “STEMI criteria.”
Nothing is documented during this time period. 
This patient should immediately receive emergent angiography and reperfusion, but he did not for unclear reasons.
Another repeat ECG is performed 1 hour later:
Findings are improved compared to 1 hour ago. Some terminal T-wave inversions are trying to form again.

This patient clearly has an unstable thrombus occluding, reperfusing, and re-occluding in the LAD again. It seems as though this was not noticed, as there is no documentation.

Finally, about 6 hours later it is documented that he complained of recurrent chest pain, as well as nausea and diaphoresis. It is documented that he described it as “exactly like” the chest pain he had in the Emergency Department.

Here is his ECG at that time:

Obvious re-occlusion with hyperacute T-waves. It might even meet STEMI criteria in V3-V4.

Apparently the team did not see any evidence of STEMI and did not activate the cath lab at this time.

Instead, he is given morphine at 22:15.

Shortly thereafter, his pain improves but does not fully resolve.

Here is the ECG at 22:30:

OMI progressing down the occlusion pathway of findings: increasing STE, conversion from concave (smiley face) to straightened ST segments, increased area underneath the massively hyperacute T-waves. This clearly meets STEMI criteria.

Still no cath lab activation. He was given nitroglycerin at 22:31 with no change in symptoms.

Another 30 minutes goes by. Repeat ECG at 23:00:

Persistent occlusion.

Still no cath lab activation. More morphine given.

41 more minutes goes by. Repeat ECG at 23:41:

Persistent occlusion.
At this time, when the next troponin returned at 0.33 ng/mL (which was barely higher than the most recent troponin which had previously been downtrending), they activated the cath lab.
They of course found recurrent occlusion of the proximal LAD:
100% thrombotic occlusion with TIMI 0 flow.
Restoration of TIMI 3 flow with PCI.

The procedure was complicated by “mid-distal rupture of the LAD after dilation with 3.0 mm balloon, covered with 3.5 graftmaster covered stent.”

He ended up with a total of 5 overlapping stents within the proximal to mid LAD in order to fix the perforation and original lesions.

Believe it or not, this event was documented as an NSTEMI involving the anterior wall.” 

Repeat ECGs show successful reperfusion, but with significant anterior completed infarction with worsened R-wave progression and LV aneurysm morphology.

Troponin T peaked around 2.25 ng/mL (quite high).

This demonstrates left ventricular aneurysm (LVA) morphology with precordial Q-waves, very poor R-wave progression for the leads with remaining R-waves, persistent STE and T-wave discordance to the Q-wave.
Please note: just because the ECG shows LVA morphology now does not mean that it will stay this way over the convalescent period or that a true anatomic LV aneurysm will develop. According to Dr. Smith’s experience, one must wait at least two weeks to find out if that will happen.

Unfortunately for the patient, he suffered a much larger MI than his initial occlusion 2 days previously. His troponin profile and new LV aneurysm morphology show how much bigger his MI was when there was a 2 hour delay to cath.

In effect, this patient underwent a N of 1 randomized controlled trial. He had acute coronary occlusion (or near occlusion) at least twice. The difference between the two events was the ECG interpretation.

Occlusion #1
The first time, he was randomly assigned a provider who happened to have training in advanced ECG interpretation (Dr. Thompson has undergone several years of self-training using Dr. Smith’s ECG blog and has practiced ECG interpretation with me on many occasions). During this event, there were less than 10 minutes between onset of pain and the decision to proceed with emergent reperfusion.

11:10 – recurrent pain
11:12 – expert ECG suspicion of OMI and decision to activate the cath lab
11:24 – STEMI criteria positive

Time from pain to decision to cath: less than 10 min
Peak Troponin T: 0.51 ng/mL
Change from baseline QRS complex to post-intervention QRS complex: no significant new Q-waves or LVA morphology, essentially unaffected QRS

Occlusion #2
The second time he suffered proven OMI of the LAD, he happened to have providers who use the classic STEMI criteria to decide who needs emergent reperfusion therapy. During this event, there was one hour and 41 minutes between onset of pain and the decision to proceed with emergent reperfusion. This is in spite of the fact that they had the advantage of knowing for certain that he had acute LAD pathology with a new stent (much higher pretest probability).

22:00 – recurrent pain
22:04 – STEMI absent per team (ECG clearly shows OMI)
22:15 – morphine given with improvement in pain but persistent OMI on ECG
22:30 – STEMI criteria clearly positive, possibly missed by team
23:41 – Troponin elevated from last measurement, decision to activate the cath lab

Time from pain to decision to cath: 1 hr 41 minutes
Peak Troponin T: 2.25 ng/mL
Change from baseline QRS complex to post-intervention QRS complex: new LV aneurysm morphology indicating full thickness anterior wall infarction

If I had been in charge of this patient, I would have activated the cath lab at 15:45 on Day 2 (EKG 6 reproduced below), as that ECG is absolutely diagnostic of re-occlusion at that time. In this imaginary scenario, I believe he would have been found to have either total occlusion or an unstable non-fully-occlusive thrombus a full 6 hours prior to his re-occlusion at 22:00. Ideally, his more severe re-occlusion event could have been mitigated or prevented all together.

The results of this N of 1 study are quite clear. Which type of provider would you prefer to have for your family member???

We are currently collecting data in a blinded retrospective case-control study to evaluate just how much better advanced ECG interpretation is compared to the STEMI criteria. Ideally, this study would trigger further research, eventually justifying interventional studies one day which might prove that early recognition of OMI by advanced ECG interpretation results in improved outcomes.

Learning Points:

Dr. Thompson and many other readers who have contributed to the blog are a testament to the fact that Dr. Smith’s educational content can be learned reliably if you take the time to practice.

Expert ECG interpretation is superior to the current STEMI paradigm. Patients deserve to have their acute coronary occlusion recognized and treated as soon as possible.

Opioids likely delay recognition of OMI among providers without advanced ECG interpretation due to decreasing symptoms without affecting the occluding thrombus. Avoid opioids in patients with possible ACS unless the decision to go emergently to the cath lab is already made, or else the patient is at risked for missed or delayed coronary occlusion.

Hyperacute T-waves often precede STE and portend even greater benefit to emergent reperfusion therapy than STEMI criteria, because there is more myocardium to save.

Comment by KEN GRAUER, MD (9/2/2018):
Superb sequential treatise by Drs. Meyers and Smith on this highly insightful case submitted by Dr. Nic Thompson. In view of the clinical history reported — serial ECGs in this case provided ample indication of events as they were transpiring — but early recognition, and then failed recognition of events turned out to be clearly dependent on ECG interpretation ability of the provider charged with patient care at the time. I’ll suggest a few additional thoughts to the excellent discussion by Drs. Meyers and Smith:
  • More than just suboptimal ECG interpretation — problems in management after reocclusion occurred include: ifailure to document why several ECGs were done on Day #2 (which almost makes me wonder IF the team even looked at those ECGs …); iifailure to listen to the patient (who described recurrent chest pain “exactly like” that experienced on admission) — and apparent failure to appreciate that pain recurrence might signal reocclusion; and, iiifailure to use the post-intervention ECG ( = EKG 4) as the “new baseline tracing” for lead-to-lead comparison with subsequent serial ECGs — which reveal unmistakable acute ST elevation that could not be missed if lead-to-lead comparison had been made.
  • NOTE: I fully acknowledge that retrospective analysis from the comfort of my reclining chair is far easier than being on the “front line”. My point is that simple steps like documenting why additional tracings are ordered — increasing your index of suspicion for the possibility of acute reocclusion when there is recurrence of severe chest pain — using the post-intervention tracing as your new “baseline” ECG — and then getting into the habit of lead-to-lead comparison between “baseline” ECG and subsequent tracings obtained at the time of chest pain recurrence — go a LONG way toward giving you the answer as to when recath becomes urgently needed.
  • It is interesting that the subtle ECG abnormalities astutely picked up by Dr. Thompson did not suggest the LAD as the “culprit” artery. We later learned from cath that the reason for this was “wraparound” of the LAD, accounting for acute limb lead changes. The point is that initial ECG findings suspicious for ongoing OMI will not always point to the true “culprit” artery. What counts is that in the setting of the “right history” (ie, new-onset cardiac-sounding chest discomfort) — that subtle abnormalities in a series of leads IS indication for concern, regardless of whether or not stemi criteria are initially met.
  • Finally — I would add that in addition to leads II, III, aVF and aVL — leads V2 and V3 are also clearly abnormal in the initial ECG ( = EKG 1 = the MIDDLE tracing with red border in Figure-1). This is another subtlety that should be identified from the initial ECG. That is, the ST segment in lead V2 is straight — whereas it virtually never normally is so straight. And, the T wave in lead V3 is disproportionately tall compared to the small r wave in this lead. While these findings alone might not be enough to cause concern — in the context of the subtle abnormalities already pointed out in 4 of the limb leads, these abnormalities in leads V2 and V3 should clearly add to our concern.
  • Once we are given the prior ECG (from 2 years earlier = TOP tracing in Figure-1) — there can be NO doubt that the straightening in lead V2 and the disproportionately tall T wave in lead V3 are new findings in EKG 1.
  • In EKG 2 ( = BOTTOM tracing in Figure-1) — note the T wave in lead V3 is now even taller (as is the T wave in V4). This pattern of excessive T wave peaking in lead V3 (and in other anterior leads) continues serially in this case in EKGs 6, 8 and 9. Some patients do this — that is they develop a series of reproducible changes when acute ischemia/reocclusion is occurring. Awareness of a certain “pattern” that some patients have can be a key CLUE that immediately tells you “the event (ie, ischemia or occlusion) is happening again!”
Figure-1: Comparison of the prior ECG with EKGs 1 and 2 in this case (See text).

Our thanks to Dr. Nic Thompson for submitting this highly insightful case!

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