Sunday, July 8, 2018

Test yourself: how many hours between your diagnosis of OMI and positive STEMI criteria?

Written by Pendell Meyers, with edits by Steve Smith

A male in his early 40s presented with intermittent chest/abdominal pain. He admitted to several episodes over the past two days, including one episode several hours prior to presentation, described as severe (8/10), substernal "burning," non-radiating, associated with diaphoresis, described as "feeling food stuck in my throat," or "like I ate too fast," but not associated with eating, relieved by belching and flatulence, relieved by lying flat. The episode on the day of presentation was similar except he had the additional new features of "burning ears" and "blurry vision," which prompted him to finally go to the ED. His history included known CAD (prior cath two years ago showed a 60% mid-LAD stenosis and 60% 1st diagonal stenosis), as well as early CAD in several close relatives.

Upon evaluation in the ED, he states that his pain had completely resolved just before arrival of EMS.

Here is his first ED ECG (no priors available):

I read this as normal. I see no evidence of ischemia, no evidence of OMI.

I would not have applied the the subtle anterior OMI vs. early repol formula to this ECG, as the formulas were not designed for cases with no STE (early repolarization, otherwise known as "normal variant STE," implies that there is STE). 

Had this been my case prospectively, I would not have identified OMI at this time. This is supported by the patient's lack of chest pain at the time of the ECG, likely meaning that the ECG changes (if present during pain) are resolving. I would strive to obtain any available EMS ECGs, and I would order q30 min serial ECGs during his ED stay and give him (and best if present, his wife or family members) my spiel about the importance of notifying staff for ANY possible returning symptoms.  I would also obtain an ECG immediately if his discomfort recurs.

The patient remained pain free in the ED, had an initial undetectable troponin, and was admitted for further ACS rule out.

Three serial troponins (not high sensitivity) were undetectable. A stress test was ordered for the next day. No serial ECGs were performed.

Day 1, 0650: Nursing report states that the patient has recurrent "heartburn." Pepcid and maalox were administered, and no further symptoms are charted. No ECG was performed at this time. 

Comment: This is a mistake. A patient was admitted for for discomfort of possible ischemic origin.  He is admitted for suspicion of coronary ischemia. The discomfort had resolved. But when the discomfort recurs, no ECG is performed.    

Furthermore, no additional troponins were ordered at that time. This also is not acceptable, unexplainable, and unfortunately I believe (without hard evidence) a common occurrence in many institutions. Practice patterns like this are the reason that we advocate even transient occlusions undergo emergent angiogram, because there is just no reliable hospital unit to monitor for reocclusion given the standard practice patterns and standard skill of ECG interpretation.

Ideally, patients at risk for recurrent ischemia should be placed on continuous 12-lead ST segment monitoring.  See these cases:

1. Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

Case continued

His pain apparently resolved spontaneously, and later that morning he went for a regadenoson/sestamibi/SPECT imaging stress test, which revealed a "large perfusion defect involving the apex, inferoapex, anteroapex, apical septum, and mid-anterior walls." There were reportedly no electrocardiographic changes noted during the stress test.

This test result confirms that this patient is having myocardial ischemia of the LAD distribution and has a huge area at risk of infarction, or actively infarcting, or already infarcted.  This alone should prompt an emergent angiogram.

It seems that this result led the team to schedule an angiogram the next day (unclear why they chose not to perform immediate angiogram).

Day 1, 2230: Nursing reports state that the patient had "recurrent chest pain starting at 10:30pm after he reached over his head to lift the head of the bed up." Last vitals before onset of recurrent chest pain included HR 84 and BP 146/72, then repeat vitals during chest pain were HR 145 and BP 200/102. 

Another troponin was sent, and an ECG was immediately obtained:

Sinus tachycardia. There is unequivocal evidence of anterolateral OMI including STE in V2-V3 and aVL, reciprocal STD in III and aVF, even more diminished R waves and QRS amplitude in V2-V4, and hyperacute T waves in V2-V4, as well as I and aVL. To sum up all these changes in one visual description, there is a diagnostic increase in the ratio of: area under the ST-T wave (increased) to the QRS complex (decreased).

Dr. Smith often says that tachycardia should make you doubt OMI unless the patient is in cardiogenic shock. This case is NOT an exception to that rule, even if the patient has elevated blood pressure. In a patient who lacks an adequate stroke volume (in this case due to massive ischemic wall motion abnormality), the only way to maintain cardiac output is to make up for it with increase heart rate. This patient must be assumed to be in cardiogenic shock. There is no documentation of bedside ultrasound during this time, no documentation of peripheral perfusion or signs of acute pulmonary edema. The patient is in cardiogenic shock.

The anterior wall is now completely without blood supply and actively infarcting! 

But this went unnoticed, apparently because it doesn't meet STEMI criteria.

Troponin T from 22:30 returned undetectable.

It appears that they attributed his chest pain over the next several hours to his his elevated BP and HR (HR 120-130 and BP 170-190/75-90).

His pain persisted, and another ECG was ordered:

Obvious anterolateral OMI (but still not meeting STEMI criteria), with massively hyperacute T-waves in V2-V4, I, and aVL.  The HR is now less than 100.

He was given nitroglycerin several times with some intermittent improvement throughout the night, but overall his pain persisted. Around 4:20am his pain worsened with radiation to the left arm, when this repeat ECG was obtained:

Finally obvious enough to meet STEMI criteria.

A repeat troponin T at this time came back at 0.13 ng/mL (mildly elevated). The cath lab was finally activated at 4:45 am (~6.5 hours after first diagnostic ECG).

His cath images are shown below:

Non-obstructed RCA.

First obtained view of the left main and its branches. What do you see?

Normal left main. The LCX is non-obstructed, but the LAD on the top of the screen is acutely occluded (arrow). The angiogram reports this as a "99% thrombotic stenosis" with "TIMI-1 flow," however you can see for yourself that there is no flow distally. This is a complete occlusion, although it doesn't take 100% TIMI-0 flow to cause immediate, full thickness infarction.

In this view the LAD is now below the LCX on the screen. The wire is just proximal to the lesion in preparation for intervention.

Just after opening of the stent, the remainder of the LAD is starting to reperfuse.

TIMI-3 flow has been restored per report.

TIMI flow was improved to 3 after intervention, and the patient's chest pain resolved.

Repeat ECG after cath:

There is new RBBB, which is common in proximal-mid LAD occlusion, however somewhat unusual to develop after the cath unless there is no-reflow phenomenon (in which there is diffuse downstream small vessel occlusion despite open epicardial vessel on angiogram). There is persistent STE with inferior reciprocal STD, however some leads including V2 also have terminal T-wave inversion suggesting reperfusion. I would not be entirely certain of the efficacy of reperfusion therapy based on this ECG, however the resolution of chest pain would be very helpful.

See this post: Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

Another repeat later that day:

RBBB has resolved. V1-V2 shows QS waves of anterior infarction, and V3-V4 have very diminished R-waves and QRS amplitude. There are Q-waves in 1 and aVL with persistent STE and terminally inverted T-waves. Overall this ECG confirms severe and nearly completed anterolateral transmural infarction with LV aneurysm morphology remaining.

Take a look at our OMI progression diagram below and compare the ECGs from this case with the progression, to lock in your knowledge of the progression of anterior OMI resulting in LV aneurysm morphology!

Over the next 10 hours after cath, troponin T peaked at 4.67 ng/mL (large MI).

Repeat echo showed large anterior and apical WMA and EF 45%.

Here is his repeat ECG 1 month later:
Large completed anterior infarct.

Let's reiterate some of the the many issues in this case:

1) When the patient had recurrent symptoms, no ECG or troponin was measured.

2) The team ignored the abnormal results of the stress test.

3) When they finally got repeat ECGs during recurrent symptoms, it was diagnostic for OMI but did not meet STEMI criteria. This led to at least a 6.5 hour delay to treatment of acute coronary occlusion.

Learning Points:

1) Contemporary troponin T (and likely many other similar assays) will not become positive until at least 4-6 hours of onset of persistent acute coronary occlusion. Conversely, elevated troponin does not distinguish OMI from other pathologies. Troponin should have no role in the diagnosis of OMI unless you are both unable to learn ECG interpretation and you don't mind letting the patient lie in bed with crushing chest pain and a fully occluded LAD for 6 hours without intervention.

2) This case is an excellent example of how unstable angina is alive and well. There were 4 initial undetectable troponins in a patient with symptoms and LAD thrombus. This is unstable angina that progressed to completed transmural anterior MI, likely with severe long term consequences. It is a myth that unstable angina is a thing of the past. See this post:

Unstable Angina: Dr. Braunwald asks if it is time for a Requiem

Because of cases like this and a vast body of supportive literature, we have proposed a requiem for the STEMI/NSTEMI paradigm rather than a requiem for unstable angina. For more see the OMI Manifesto.

3) STEMI criteria often misses OMI, and in many cases such as this one the delay until positive STEMI criteria causes an unacceptable delay to intervention, during which time the entire affected wall may be lost. The only way to consistently identify OMI as soon as possible is to learn expert ECG interpretation.

4) The ECG confirms reperfusion more accurately than TIMI flow on the angiogram.  (TIMI myocardial perfusion grade or "blush" is an angiographic measure of microvascular perfusion which correlates very closely with ECG measures of reperfusion)

5) You must be familiar with the progression of OMI and the features of LV aneurysm morphology in order to prevent false positives and false negative activations for this patient in the future.

Comment by KEN GRAUER, MD (7/8/2018):
Excellent blog post by Drs. Meyers & Smith. I’ll highlight a few additional points:
  • The History in this case is critical. The patient is in his 40s, and he has known coronary disease proved on prior cath. He has been having several prior episodes over the 2 days before admission — with no less that 8/10 chest pain that occurred several hours before he finally presented to the ED. In the context of this worrisome history in a patient with known coronary disease — I did not interpret his initial ECG as normal (Top ECG in Figure-1).
Figure-1: Original ECG at Time = 0 (Top) — and 2nd ECG (Bottom), done 37 hours after presentation. (See text).
The importance of history in interpreting ECG changes cannot be overemphasized. Clearly, the initial ECG (Top in Figure-1) is not diagnostic of OMI (acute Occlusion-related MI). But lead aVL (within the RED rectangleshows a straighter-than-usual ST segment that leads up to a T wave that looks both taller and fatter-than-it-should-beat its peak given the tiny amplitude of the R wave in this lead.
  • We are then faced with asking ourselves which of the 2 complexes in leads V2 and V3 are “the real complexes” in these leads — “A” or “B”? Due to baseline wander — we just can’t tell what the “real” QRS in these leads would look like. That said — both “A” and “B” are not totally normal. In — the ST segment is again straight, whereas there should be a gentle upsloping that gradually blends into the T wave. In — the T wave in V3 looks like it might be taller-than-it-should-be given the tiny r wave in this lead. While fully acknowledging that none of what I describe above is in any way definitive — in a patient who you KNOW has coronary disease, and who tells you he had an 8/10 severe CP episode just several hours earlier — the TOP tracing in Figure-1 is both technically inadequate, and (in my opinion) — demands repeat ECG over the next 20-30 minutes.
  • I presume an ECG was done at the scene at the time the patient contacted EMS. We are told this EMS tracing is “unavailable”. Chances are that IF that on-the-scene ECG was available for comparison with the initial ED ECG — that there would have been serial change. The point to emphasize, is that in patients with coronary disease who present with fluctuating symptoms — the presence of dynamic ECG changes is diagnostic of acute ischemia. Usually this is enough of an indication for cath, regardless of whether “stemi criteria” are or are not present.
  • As per Dr. Meyers — No ECG was done on Day #1 @ 06:50 when the patient had recurrent “heartburn”. The point is that any change in symptoms in a patient with known coronary disease who is admitted for chest pain should mandate repeat ECG.
  • As per Dr. Meyers — the 2nd ECG (Bottom tracing in Figure-1) is clearly indicative of OMI — but apparently was not acted upon because “it doesn’t meet STEMI criteria”. The point is that there are dynamic ST-T wave changes (which are actually quite dramatic!) that have occurred between the time that the 2 ECGs in Figure-1 were obtained — and that is indication for acute cath regardless of whether “stemi criteria” are or are not present.
  • I see no valid reason for doing a stress test on this patient. Had either the EMS ECG been available — or had the 2nd ECG been done in a more timely manner (rather than waiting 37 hours) — it is almost certain that dynamic ECG changes would have been seen — and that should have sufficed to prompt acute cath. The reason for considering a stress test in this patient is not to determine if there is coronary disease — because that has already been proven. And, given that there are fluctuating symptoms with dynamic ECG changes — this should be all that is needed to justify prompt cath. It is hard for me to imagine any result on stress testing that would dissuade me from that conclusion ...
COMMENT: Soul-searching cases like this one is difficult! It is one of the reasons I always strive to assess the case (and associated ECGsbefore I read what happens. That’s why I fully acknowledge how easy it is to second-guess from the comfort of my easy chair in front of my computer. But it’s important to learn from mistakes made, with goal of more optimal performance the next time out.
  • We are all learning all the time … Thanks to Drs. Meyers & Smith for presenting this soul-searching case.


  1. Regarding the ecg the was done at 22:30 in day 1: Don't you think that its quite extra ordinary that the rate is 125 with that blood preasure? You said a lot of times that sinus thacycardia and OMI almost never present together unless there is cardiogenic shock. So assuming that the lungs are clear that's an exception

    1. Great question. During editing it seems we accidentally deleted the paragraph we wrote about this question preemptively. We replaced it. See above, just after that EKG.

      Basically, this case is NOT an exception to the rule. We believe this patient was in cardiogenic shock with elevated heart rate making up for very poor stroke volume given the proven large wall motion abnormality even before the re-occlusion. Thanks for the question!

  2. Hello Dr. Smith,

    I am an Italian fellow pratictioner in Internal Medicine and an ECG enthusiast who sistematically follows your brilliant blog. I have two questions/observation about this case and it would be great if you gave me your opinion:

    1. In ECG number 2 (obtained during relapsing chest discomfort), what I see is 1 mm STE in I and aVL, which is a peripheral leads STEMI criteria. Am i counting wrong? Or am I being misled by PR interval depression?

    2. It is definitey true that high BP can cause left ventricular strain with ECG changes such as anterior ST elevation and peripheral ST depression, but, besides the fact that this usually happens in the setting of an underlying LVH, in this case we see an ANATOMICAL DISTRIBUTION of ECG modificantions that should clue you in! An plus, as you've already stated many times, in case of chest pain ANY change should be interpreted as AMI until otherwise proven!!

    Thanks a lot for keeping this blog up!

    1. 1) I agree that there is some small STE in I and aVL. Probably 1mm in aVL, but I do not think most people would say that lead 1 meets 1mm (we have to admit that when people look at the same EKG they do not agree on the number of mm STE). So I do not think that this would meet "official STEMI criteria" in most peoples' eyes.

      thanks for the comment!

    2. @ UNKNOWN: I Agree with Pendell regarding his answer to your excellent question — which is precisely why “strict stemi criteria” is the wrong way to go in 2018. Of note, comparison of the 1st & 2nd ECGs done in this case (which I put together in Figure-1 in my Comment above) — shows us that the QRS complex in lead aVL is now predominantly negative in the 2nd ECG (it was predominantly positive in the 1st ECG). So, if anything — the T wave will often be inverted in lead aVL when the QRS complex in this lead is predominantly negative — yet, compared to ECG #1 (in which the ST segment in aVL was FLAT) — there is now >1 mm ST elevation with a broad more upright T wave in ECG #2 that occurs in association with reciprocal inferior ST depression … Grazie per la tua domanda. Spero che adesso sia chiaro (Thanks for you question; I hope it's now clear) — :)

  3. painful.
    interesting : when a patient complains of heartburn, his heart is doing exactly that. and worrisome is that , with a mentality by many that is chained to the STEMI strict criteria, by many ER docs and cardiologists, patients are allowed to crash and burn form their "heartburn".
    i agree with Ken on that first EKG (though i would never dare to disagree with wendell and steve!), that there are suspiciously appearing plump (in NY we might say "zaftig") T waves in aVL, V2 and V3. esp in comparison to their respective R waves. granted , i have the advantage of hindsight. if a tech from triage placed this under my nose while i was talking to a surgeon about another patient with ischemic bowel, i might be less impressed.
    but i whole-heartedly agree that we must be masters of the electrocardiogram.
    one ecg begets another , the bible says. and we need to see all the 12 leads done pre-hospital.

    i think its impossible to get continuous 12 lead monitoring in our ER. we are often so busy thats it's hard to get 3, but our techs are excellent.

    excellent, but unfortunate case, Wendell and steve. thank you, and to you also ken for your comments.

  4. Hi Dr Smith, I have just found your blog on the internet and I feel it will be a good source of knowledge, as well as a paradigm breaker for me. I would to ask a question, hoping it won’t be a silly one. In the first ecg of the case, I saw STE, although small, in inferior leads 2, 3 and aVF. Is my impression right or exaggerated?

    1. Hello Bruno. We are glad you are enjoying our ECG Blog! YES — In the very 1st ECG (above) — there IS slight ST elevation in EACH of the 3 inferior leads. The shape of this ST elevation is gently upsloping (ie, “smiley”-configuration) — and what is most important — there is NO reciprocal (ie, “mirror-image” opposite) ST depression in lead aVL. It is often difficult to distinguish between repolarization variants vs acute MI. In the inferior leads — there is a “magic” reciprocal relationship that is almost always present between opposite-lying leads III and aVL when there is acute OMI (occlusion-based acute MI) — and, that is ABSENT here. It’s good to note this slight inferior ST elevation that we see — and it would be important to follow on serial tracings. In this particular case — it turned out that on cath, the RCA was not obstructed; instead it was the LAD that was acutely obstructed (and that initial slight inferior lead ST elevation turned into reciprocal changes from acute LAD OMI. For MORE on that “mirror-image” magical lead III-aVL relatinship — GO TO — — and — — I discuss and illustrate this phenomenon in detail in My Comment at the bottom of the page for these 2 links — :)


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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