Wednesday, March 6, 2019

What will you do for this patient transferred to you who is now asymptomatic?


A middle-aged woman with history of hypertension presented to another hospital approximately 2 hours after onset of chest pain and shortness of breath.

This ECG was recorded on arrival:

What do you think?








This is technically a STEMI, with 1.5 mm STE in V1 and 1.5-2.0 mm in V2. The current criteria only require 1mm in V1 and 1.5mm in V2 for a female. However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." The normal QRS complex with STE and large volume underneath the T-waves in V1-V3 confirm Occlusion MI (OMI). There is not technically STD in V6 and I, however the morphology looks similar to STD.

Here is the computer interpretation at the top:


Here is the calculation of the formula that differentiates benign anterior ST elevation from subtle LAD occlusion (OMI):
The most accurate cutoff is 18.2 (derived and validated).  20.21 is far above 18.2 and should be considered diagnostic of LAD occlusion
A baseline was available:
Within normal limits. Proof that all STE and hyperacute T-waves in the presentation ECG are new.

The practitioner at the outside hospital was concerned and called our cardiologists, who accepted the transfer but stated they would like to evaluate the patient on arrival before activating the cath lab.

They collected several repeat ECGs at the outside hospital before transport:



None of these three ECGs meet STEMI criteria. There is perhaps a hint of inferior STD (reciprocal). The T-waves, especially in V2, remain hyperacute and convincing for ongoing Occlusion despite lack of STEMI criteria.

By the time the patient arrived at our facility, she had received aspirin and nitroglycerin, and her pain had apparently completely resolved. She did not receive any opioids (which would mask her pain without affecting any underlying ACS). She was asymptomatic at the time of this ECG recorded on arrival to our ED:
What do you think? What will you do for this asymptomatic patient???







This ECG shows persistent Occlusion MI but does not meet STEMI criteria. V2 still has STE and hyperacute T-waves. There is a new Q-wave in aVL, with STE and large T-wave as well. Lead I has a definitively hyperacute T-wave without STE. II, III, aVF, and V6 have STD.

This patient has ongoing Occlusion MI, despite being asymptomatic. Even if OMI were not recognized, these ECGs are evidence of ongoing full thickness infarction despite aspirin and nitroglycerin. She requires maximal medical management per all current guidelines (including heparin and P2Y12 inhibitor per cardiology), as well as consideration for emergent cath in the case of persistent ischemia.


So what will you do for this patient?

Below are possible decisions by the receiving team (assuming the first team recognized that the first ECG meets STEMI criteria and decided to emergently transfer the patient in the first place!):

1) The receiving providers do not recognize persistent occlusion on the receiving facility ECG, and therefore interpret this as an improved ECG ("just some ST depression now") in an asymptomatic patient. In this situation there is no sense that there is an emergency happening, and the patient will be simply monitored in the ED until they are admitted to cardiology, probably without any further serial ECGs unless the patient complains of recurrent symptoms. I believe this is by far the most common outcome for this patient around the world in 2019. Although current guidelines do not recognize "Occlusion MI", this management would still be wrong according to current guidelines because there is active ischemia obvious on this ECG (new ST depression), therefore the patient has ongoing ischemia and must receive maximal medical management (and cath if the ischemia is not fully resolved).

2) The providers think of this patient as a "transient STEMI" (technically this is accurate, she had STEMI before and now doesn't). There is no guideline statement to my knowledge explaining what the ACC/AHA recommends for transient STEMI. Current practice ranges widely, but based on my short experience and reports from other institutions, most of these patients are not being taken emergently to the cath lab in 2019.


3) The providers are skilled at ECG interpretation and understand that this patient has evidence of ongoing transmural infarction due to Occlusion MI, despite the fact that she is asymptomatic and no longer meets STEMI criteria. There is no literature that fits this situation perfectly (a patient who had symptomatic OMI [STEMI(+)] who is now an asymptomatic persistent OMI [STEMI(-)].  Therefore we will have to extrapolate from common sense and the related literature.

The common sense part is easy - this patient has extremely high likelihood of Occlusion MI which is ongoing and causing full thickness infarction, and she would therefore benefit by going emergently to the cath lab to minimize her infarction, restore blood flow, and prevent complications. There is no literature specific to this situation refuting this common sense.

Other than using common sense, we do have very small amounts of literature for transient STEMIs (symptomatic STEMI[+] OMIs who become asymptomatic STEMI[-] reperfused OMIs) and one study for patients who have persisent STEMI on ECG despite complete resolution of pain. See the notes at the end of this post for full details, but basically there was a benefit for asymptomatic persistent STEMIs to go emergently, while there was no detected benefit for the transient STEMIs despite several patients who had reocclusion during the waiting period (but remember, these patients likely did not have ECGs showing persistent OMI like our patient here does, so these studies would not be applicable).



Back to the case:

The providers recognized persistent ischemia and likely occlusion, and discussed this with cardiology who took the patient immediately for cath. They found an acute, total, thrombotic occlusion of the proximal LAD.  They opened it. She also had non-acute CAD of the left main (50%) and LCX (75%).









Initial troponin T was 0.46 ng/mL (significantly elevated), and peak troponin T at around 8 hrs after arrival was around 7.80 ng/mL (VERY highly elevated). For reference, I have never seen a patient survive to discharge from my hospital if the troponin exceeds 20.00 ng/mL (in 2.5 years of my records, it seems that all 7 cases I have found with troponin greater than 20 due to OMI died in hospital), but this is a meaninglessly small sample size.




Echo showed anterior septal, anterior wall, and apical wall motion abnormalities, as well as an EF of 45%.

Here are her ECGs after reperfusion (check to see if you think she is truly reperfused downstream of the lesion, or if you think she has evidence of No-Reflow phenomenon):




They both confirm downstream reperfusion, showing terminal T-wave inversions in the previously affected leads.

The patient did well.



Learning Points:

You must become facile with ECG interpretation for Occlusion MI and advocate for your patients, because the current guidelines are insufficient.

There has never been any study refuting the common sense argument that persistent Occlusion MI causing ongoing ischemia benefits from emergent intervention, so you should use common sense until proven otherwise: if you can open an occlusion and prevent more myocardium from dying, you should do it as soon as possible.

Patients who had clear STEMI who then become asymptomatic but still have STEMI on ECG have been shown to benefit from emergent cath lab activation rather than delayed.

Patients who had clear STEMI who then become asymptomatic with total ECG resolution have been inadequately studied, and in those small studies have not clearly been shown to benefit. However some patients in the delayed cath groups have reocclusion and complications during the delay. Just because none of them had a disastrous outcome in a small, highly monitored study population does not mean they won't have bad outcomes in normal practice.  


Timing of revascularization in patients with transient STEMI: a randomized clinical trial


Thus, in our clinical experience and interpretation of the literature, patients with transient ST elevation should go to the cath lab emergently just as if they had not had resolution of ST elevation. If for some reason the angiogram is delayed, they should receive maximal medical therapy in an ICU setting with continuous 12-lead ST segment monitoring under the close attention of a practitioner with advanced ECG interpretation training. The same reasoning applies to patients with unequivocal ECG evidence of reperfusion from Occlusion MI (Wellens syndrome, e.g. reperfusion of anterior Occlusion MI without recorded ECG during occlusion). Both groups of patients are at very high risk of reocclusion, and reocclusion may be clinically silent or too late to prevent myocardial loss or death.


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




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Timing of Reperfusion Therapy in Asymptomatic Patients


Resolved symptoms with persistent ECG findings:


Occasionally patients may present with persistent ST elevation (or other ischemic findings) but resolved chest pain. This is surprisingly common, and several studies of continuous 12-lead ECG monitoring in the setting of admitted unstable angina report high rates (15%) of silent transient myocardial ischemia (ST elevation), and that these findings were strong independent predictors of MI or death during hospitalization.(Patel et al., Krucoff et al.)


Patel et al. Early Continuous ST Segment Monitoring in Unstable Angina: Prognostic Value Additional to the Clinical Characteristics and the Admission Electrocardiogram. Heart 1996.

Krucoff et al. The Portable Programmable Microprocessor-Driven Real-Time 12-Lead Electrocardiographic Monitor: A Preliminary Report of a New Device for the Noninvasive Detection of Successful Reperfusion or Silent Coronary Reocclusion. American Journal of Cardiology 1990.



After a careful interrogation ensuring that the patient is truly symptom free and has not received any pain-reducing non-ACS therapy (opioids) which may be obscuring the identification of ongoing ischemia without actually addressing the underlying ACS, the provider is left with the question of whether to treat the patient emergently, as if symptoms were persistent. One would reason that ECG evidence of ongoing ischemia means that the suspected occlusion is still causing ongoing infarction, and therefore there should still be benefit to emergent therapy. Thankfully, Schomig et al randomized 347 patients with at least one 20 minute episode of chest pain 12-48 hours before presentation with no persistent symptoms but unequivocal ST elevation on the ECG to either receive immediate angiogram with PCI vs later unplanned invasive evaluation if they developed recurrent angina or other worsening features. Most importantly, the study design highlights the fact that persistent symptoms would have clearly indicated emergent PCI. The patients who received emergent PCI had significantly smaller median left ventricular infarct size (8% vs. 13%, p=0.001) measured by single-photon emission computed tomography study, as well as non-significant but underpowered decrease in the composite of death, recurrent MI, or stroke at 30 days (4.4% vs. 6.6%, p=0.37). There is no other available evidence for the case of the patient whose symptoms have resolved but whose unequivocal ECG findings persist. Thus, the available evidence supports the common sense theory that even asymptomatic patients with persistent ECG evidence of full thickness infarction (Occlusion MI) should receive emergent angiogram and PCI.



Schomig et al. Mechanical Reperfusion in Patients with Acute Myocardial Infarction Presenting More than 12 Hours from Symptom Onset: A Randomized Controlled Trial. JAMA 2005.



Resolved symptoms and resolved ECG findings:


The decision is more difficult for the patients whose symptoms and ECG findings have both resolved completely. On one hand, this patient is clearly demonstrating an unstable thrombus that has the potential to reocclude at any moment (and which may be silent when it does(Patel et al.; Krucoff et al.)) to disastrous consequences that may deteriorate before the patient can be rushed to the cath lab. On the other hand, one could argue that the patient will most likely be safe if receiving aggressive ACS therapy and extremely close monitoring with continuous 12-lead monitoring or at least serial ECGs being read by an expert in the signs of reocclusion, and that very few patients will deteriorate between immediate recognition and emergent PCI, such that the burden of activating the cath lab overnight may be somehow comparable to the risk of patient harm. There are at least three studies that help us understand the risks and benefits of this situation:




Lemkes et al. randomized 142 patients with transient STEMI (whose symptoms and ST elevation had resolved) to emergent vs. next day angiogram and PCI, with all patients receiving aspirin, a P2Y12 inhibitor, and an anticoagulant. While the infarct size by MRI was the same in both groups, “4 patients (5.6%) in the delayed invasive strategy required urgent intervention due to signs and symptoms of reinfarction while awaiting angiography.” Each patient who suffers reocclusion while awaiting delayed cath runs the risk of lack of identification of reocclusion, worsened MI due to the added ischemic time during the delay, and a small but real risk of true deterioration and death between identification of reocclusion and PCI.

Lemkes et al. Timing of Revascularization in Patients with Transient ST-Segment Elevation Myocardial Infarction: A Randomized Clinical Trial. European Heart Journal 2019.



Ownbey et al compared the emergent angiography results of 18 prehospital patients with transient STEMI to 75 patients with sustained STEMI. Significant lesions (greater than or equal to 50%) were found in 94% and 97% of patients (p=0.6), and subtotal or total lesions (greater than or equal to 95%) were found in 63% and 85% (p=0.1), respectively. Thus, even those with full resolution of symptoms and ST elevation had 63% incidence of total/subtotal occlusion. No other clinical outcomes were reported.

Ownbey et al. Prevalence and Interventional Outcomes of Patients with Resolution of ST-Segment Elevation between Prehospital and in-Hospital ECG. J of National Association of EMS Physicians 2014.


Meisel et al. studied 1244 consecutive STEMI patients and found 63 (5%) with transient STEMI. These patients were treated aggressively with IV nitroglycerin, aspirin, clopidogrel, and heparin. Compared with sustained STEMI, transient STEMI was associated with less myocardial damage, less extensive coronary artery disease, higher TIMI flow grade, and better cardiac function. Blondheim et al. similarly compared transient STEMI to sustained STEMI and found that transient STEMI portended lower mortality, lower myocardial damage by troponin, and better cardiac function. This is not surprising, because reperfusion by any means (including spontaneous reperfusion) portends better prognosis, but it does not answer the question of whether the majority of unaffected patients outweighs the rare disastrous outcome that will inevitably occur if all transient STEMIs are treated in delayed fashion.


Meisel et al. Transient ST-Elevation Myocardial Infarction: Clinical Course with Intense Medical Therapy and Early Invasive Approach, and Comparison with Persistent ST-Elevation Myocardial Infarction. American Heart Journal 2008.

Blondheim et al. Characteristics, Management, and Outcome of Transient ST-Elevation Versus Persistent ST-Elevation and Non-ST-Elevation Myocardial Infarction. American Journal of Cardiology 2018.




Thus, in our clinical experience and interpretation of the literature, patients with transient ST elevation should go to the cath lab emergently just as if they had not had resolution of ST elevation. If for some reason the angiogram is delayed, they should receive maximal medical therapy in an ICU setting with continuous 12-lead ST segment monitoring under the close attention of a practitioner with advanced ECG interpretation training. The same reasoning applies to patients with unequivocal ECG evidence of reperfusion from Occlusion MI (Wellens syndrome, e.g. reperfusion of anterior Occlusion MI without recorded ECG during occlusion). Both groups of patients are at very high risk of reocclusion, and reocclusion may be clinically silent or too late to prevent myocardial loss or death.



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Comment by KEN GRAUER, MD (3/6/2019):
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Excellent discussion by Dr. Meyers that provides yet another example of: iHow the History and the initial ECG are all that is needed to justify clear indication for acute cath in this case — regardless of whether strict criteria for acute STEMI are satisfied; andiiHow comparison of the initial tracing with a baseline ECG then removes any doubt that the ECG findings in the initial tracing are real.
  • In the hope of enhancing appreciation for the initial abnormal ECG findings — I focus my comments on these first 2 tracings shown in this case (Figure-1).
Figure-1: The first 2 ECGs shown in this case. ECG #1 was obtained in the referral hospital, approximately 2 hours after the onset of chest pain. ECG #2 — is a prior tracing on this patient, that serves as a baseline” for comparison with ECG #1 (See text).
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COMMENT: In a patient with new-onset chest pain — ECG #1 should be all that is needed to justify acute cath.
  • Regardless of what subsequent tracings show — leads V1, V2 and V3 in ECG #1 indicate a need to consider acutely evolving OMI until proven otherwise.
  • While we often advocate for frequent serial ECGs during the early hours of a suspected acute cardiac event — the decision for immediate cath in this case should not depend on waiting around to see what a repeat ECG shows. Clearly, if repeat ECG showed more diffuse, increased ST elevation — a definitive diagnosis of a STEMI would more easily be made. But what if the next ECG showed less ST elevation in leads V1 and V2? How would we know if this reflects complete spontaneous reversal of an acute occlusion? — or, a transition ECG about to develop reperfusion changes (ST depression/T wave inversion) from a completed infarct? (On the way from ST elevation to T wave inversion — there may be “pseudo-normalization” of ST-T waves ...).
  • In addition — Serum troponin values should not be needed in this case to assist your decision about whether immediate cath is indicated. There is often a “lag time” until troponin increases with acute MI — so time shouldn’t be wasted waiting for troponin to rise. This initial ECG #1 in this patient with new-onset chest pain should be all that is needed to justify immediate cath.
  • Lead V1 — does not normally manifest ST elevation, especially not with the straight ST segment take-off that we see in Figure-1.
  • Support that the ST-T wave in lead V1 is truly abnormal in this patient with new-onset chest pain — is forthcoming from the disproportionately tall, peaked, and wide-based T wave that we see in lead V2. This is a hyperacute T wave.
  • In the context of neighboring leads V1 and V2 — the T wave in lead V3 is probably also hyperacute — in that it is relatively tall and wide-based given the modest amplitude of the R wave in this lead. NOTE: As an isolated lead — I would not interpret the T wave in lead V3 of ECG #1 as necessarily abnormal. BUT — in the context of the appearance of leads V1 and V2 in this patient with new-onset chest pain — I believe the ST-T wave in lead V3 is a continuation of this presumably acute process.
  • PEARL #1: One of the ways to distinguish between more proximal vs more distal LAD occlusion — is from ST-T wave appearance in the limb leads. Thus, with more proximal LAD occlusion — there is often subtle-but-real ST elevation in lead aVL — and reciprocal ST depression in the inferior leads. While ST segment deviation is not seen in the limb leads of ECG #1 (it was probably too early in the course of this OMI to show these changes …) — the ST-T waves in the inferior leads of ECG #1 are not completely normal! Instead, there is some ST-T wave flattening in these inferior leads.
  • PEARL #2: Sometimes it is difficult to tell from the 2 or 3 beats in the lead II of the 12-lead ECG whether there is or is not abnormal ST-T wave deviation. For example, in ECG #1 — there is baseline artifact that distorts the 2nd QRS complex in lead II. Don't forget that we have no less than 12 “looks” at lead II in the long lead II rhythm strip at the bottom of the tracing — and this clearly shows subtle flattening (straightening) of the ST segment in this lead.
  • BOTTOM LINE regarding ECG #1: The ST-T wave appearance in leads V1, V2 and V3 in this patient with new-onset chest pain suggests acute evolving OMI until you prove otherwise — regardless of what initial troponins and the next ECG show.
====================
At this point — a prior ECG on this patient was found ( = ECG #2 shown in Figure-1).What DYou See when you compare ECG #1 and ECG #2?
  • Both tracings show sinus rhythm at a rate between 70-80/minute. There is no significant change in frontal plane axis between these 2 ECGs — so comparison of limb leads between these 2 tracings is valid. Minimal nonspecific ST-T wave abnormalities are seen in both sets of limb leads — without significant change between ECGs #1 and 2.
  • BUT — there has been a marked change in the appearance of the chest leads between these 2 tracings. Transition occurred slightly earlier (between leads V2-to-V3) in the baseline tracing ( = ECG #2). Most important — there can be NO doubt that the Selevation we saw in leads V1 and V2 of ECG #is NEW since the baseline tracing was done! Similarly, the upright appearance of the T waves in the remaining chest leads of ECG #1 represents a new change from the baseline ECG. In a patient with new-onset chest pain — finding this baseline tracing all but confirms our presumptive diagnosis of acute LAD occlusion.
  • P.S.: In follow-up to the point I made earlier — the 1st ECG done in Dr. Meyers’ ED ( the 6th tracing shown in this case, recorded at 20:29— now shows clear ST elevation in lead aVL — with reciprocal ST depression in each of the inferior leads. These limb lead findings that are now seen in this ECG done at 20:29, are consistent with acute thrombotic occlusion of the proximal LAD that was found on cath.


14 comments:

  1. Very good case. NTTV1 and T in V1 larger than V6.

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    Replies
    1. @ Swagata — YES, if one had any doubt on the initial ECG about the ST-T wave appearance in lead V1 — the PEARL you mention (ie, that normally the T wave in V6 should be taller than the T in V1) can be very helpful. I chose not to mention this Pearl in My Comment above, because regardless of the height of the T wave in lead V6 — the ST-T wave appearance in lead V1 of ECG #1 is definitely abnormal — all-the-more-so given frank ST elevation + hyperacute T wave in neighboring lead V2. Thanks for your comment!

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  2. What is your impression about the T-waves on the baseline ECG ?
    The ST is almost coved, and the T-waves negative. I admit I would be bothered in front of such an ECG...
    Thank you

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    1. Good question
      In the perfect clinical scenario for possible reperfusion (a patient with classic ACS symptoms but now resolved), I would entertain the possibility that those are terminal T-wave inversions which could evolve to be more convincing. But it's hard to describe why I just don't think they are true reperfusion terminal inversions. Repeat EKGs would tell. More likely in my opinion they are the patient's baseline. A prior EKG would of course be helpful.

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    2. @ Yannick — My understanding from this case — is that details are missing about when this baseline ECG ( = ECG #2 in my Figure-1 above) was obtained. We also don’t know the circumstances surrounding this baseline tracing. So we fully agree with you that the ST-T waves in many of the leads of the baseline ECG are far from normal. Alas, acute cath showed multi-vessel disease, with indication that some of this was longstanding — and that is probably the reason the baseline ECG was so abnormal. That said — there clearly has been new change in the form of new ST elevation + hyperacute T waves in leads V1, V2 and V3 of ECG #1 compared to the last ECG on the chart (which was the “baseline” tracing) — so new OMI was presumed until proved otherwise in this patient who presented with new-onset chest pain. THANKS again for your comment!

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  3. Dr. Meyers...

    This is an excellent presentation of a very, very common situation where an emergency physician can certainly feel "between a rock and a hard place." The documentation was superb!

    What concerns me most as we (I am including myself also) push to spread the word about how the STEMI criteria are failing us and the need to move on to the concept of OMI, there will be the usual pushback from those who who look strictly at the financial bottom line and raise objections based on the idea that patients are being sent for expensive tests and procedures without more "acceptable" documentation of need. While I understand and support the concept of "Choosing Wisely" I see this being carried to extremes. I listened to a podcast the other day narrated by two well-known EM physicians in which they chuckled about a mere 2% miss rate for some lethal disease being worth the savings in costs made possible by following a "rule" and doing fewer tests. I still think we should have a 0% miss rate. That "2%" represents human beings who value their lives as much as we value ours. Using the concept of OMI instead of the STEMI criteria (plus an aggressive educational approach to advanced 12-lead ECG interpretation) may not get us to a 0% miss rate, but it WILL get us a lot closer than the traditional STEMI criteria.

    I look forward to more of your posts!

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    1. Thanks as always for your comment Jerry! I just now added My Comment. I think among the key points to emphasize is that in this patient with NEW-onset chest pain — ECG #1 shows worrisome ST elevation in several leads that needs to be considered indicative of OMI until you prove otherwise — and, that as soon as the prior ECG on this patient was found — you proved this. Worrying about “STEMI criteria” in this situation shouldn’t be needed given clear indication for cath. Again — THANKS for your always insightful comments!

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    2. But there are harms associated with some of these diagnostic tests/procedures so it is not so easy as just sending everyone for these tests to catch that extra 2% that are maybe more insidious presentations.

      There are risks to angiograms as well and I understand cardiology if they do not want to risk taking someone to the cath lab without their own literature and guidelines backing up the decision in case there is a poor outcome, especially in the US. What if the patient developed iatrogenic coronary dissection after a clean cath in an asymptomatic patient with an ECG that does not meet current STEMI criteria? If they're held the standard of best practice and their colleagues would have managed them medically then this outcome would not bode well for them in court so it's easy for us to say to take them for a cath but we're not the ones on the line for the negative consequences of the procedure.

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    3. There are many things problematic with this point of view and a response here is almost impossible. Read the OMI Manifesto. In short, they are not even following their own guidelines. First, the "critieria" for STEMI have a terrible evidence base. This ECG is diagnostic of LAD occlusion. It cannot be anything else. However, there is not enough ECG expertise to recognize it. My formula has been derived and validated by me, and externally validated (https://onlinelibrary.wiley.com/doi/abs/10.1111/anec.12568). It remains diagnostic even when her symptoms resolve. Second, even if the ECG was not diagnostic, the cardiologists are not even following their own guidelines. ESC guideline say that with high suspicion, the patient should go to cath within 2 hours REGARDLESS of ECG or BIOMARKER FINDINGS. At the very least, there should be an emergent echo to prove absecne of wall motion abnormality. Finally, your worry about coronary dissection does not happen with angiogram but with PCI; PCI would only be undertake if the angiogram showed something that needed fixing. STEMI criteria are clearly not best practice.

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  4. Thanks Ken. It's pretty much a given that STE up to 3 mm in V1 - V3 can be "normal" for some men, but anything greater than 1 mm in women OF ANY AGE is NOT "normal!"

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  5. Hi Jerry. Agree regarding the measurements you cite — but you have to agree that regardless if ECG #1 ( = the initial ECG in this case) came from a man or a woman, in a middle-aged or older adult with NEW-onset chest pain, that the SHAPE of these ST elevations in these 3 anterior leads is clearly cause for concern (and in this setting = acute ongoing cardiac event until proven otherwise) — :)

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  6. After having followed and read many of posts such as this, none should overlook the concerning ST-T waves in V1-V2 (V3), corroborating by the subtle ST-segment abnormalities in inferior leads. Therefore regardless of the availability of a prior tracing (an exception than the rule), cath lab should have been promptly activated at the time ECG#1 was interpreted (or at minumum, I/we should advocate our patient and discuss with the interventionist cardiologists).
    As to management of an asymptomatic patient with persistent ECG findings of ongoing ischemia (here occlusion), we should take into account the pain threshold of a given patient: it's common experience that there are patients with high threshold not complaining any symptoms...it's a less reliable finding, compared for example with persistent signs of ischemia. But in this particular case (and likely many others in the past and alas in the coming days), we should not wait the patient become asymptomatic after having seen the concerning (and diagnostic) repolarization abnormalities that suggest an OMI.
    Thanks for this superb case!

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