Friday, May 7, 2021

A man in his 30s with greater than 12 hours of chest pain

 Written by Bobby Nicholson MD, with edits by Meyers

A man in his early 30s presented at 7:35am to the ED with chest pain (7/10) beginning suddenly at 7:30pm the night prior. The note did not specify whether the pain had been truly constant for 12 hours, or whether it had been intermittent. He had associated nausea, vomiting, hot flashes, chills, dyspnea, and cough. He had uncontrolled type 1 diabetes and smoking history. Vitals were normal. Physical exam was unremarkable. No prior ECG was on file.

At 0742, this ECG was obtained in triage:

What do you think?

Raw Findings: 

 - Sinus rhythm

 - QRS is narrow with normal frontal plane axis, but with deep QS waves in V2-V4, and small Q waves in V5 and V6

 - STE in V1-V5, meeting STEMI criteria in multiple leads

 - Also a tiny amount of STE in I and aVL (with terminally inverted T-wave in aVL), with tiny reciprocal STD in III

 - Upright and large T waves in leads with STE


Assuming he did not have a prior LAD territory OMI, this ECG shows acute LAD Occlusion MI, with a very significant amount of damage already done (very deep QS waves in multiple leads), but also with ongoing viable tissue that is actively infarcting (this is known because of the large upright hyperacute T waves in the same leads).

The pitfall I see for this ECG is that many providers will believe that there is no benefit to emergent reperfusion due to the presence of Q waves and the description of pain that started 12 hours ago. This ECG makes me certain that there is still remaining salvageable myocardium, and the patient should get emergent reperfusion as soon as possible.

Should the patient get emergent PCI according to the ECG? YES

Should the patient get emergent PCI according to the current ACC/AHA STEMI guidelines? YES

The ACC/AHA guidelines state that

Immediate PCI is recommended if available for STEMI patients with ischemic symptoms for <12 h in duration (class I, level A) and those with ongoing ischemia at 12-24 h after the onset of symptoms (class IIa, level B).

Below is some reference information from our EMRAP Corependium chapter regarding the acuity of OMI, hyperacute T waves, and Q waves:

  • Hyperacute/tall T waves
    • “Tall” T waves are an independent marker of benefit from thrombolytics, such that STEMI patients who received thrombolytics with tall T waves had a lower 30-d mortality than patients who did not (5.2% vs. 8.6%, = .001), and were less likely to develop heart failure (15% vs. 24%, < .001) and cardiogenic shock (6.1% vs. 8.6%, = .023).
    • The mortality after thrombolytics in patients with positive T waves is the same for those who have >2 vs. <2 h of symptoms.
    • These data, combined with common sense and the ECG progression of occlusion MI (above), leads to the logical conclusion that the benefit would be even greater in the presence of hyperacute T waves before the stage of ST segment elevation, when the ratio of salvageable to infarcted myocardium is maximum, although this has never been studied.
    • Unfortunately, hyperacute T waves have never been formally defined.
  • Q-waves
    • Although Q waves may be indicative of lower acuity, it is important to note that QR waves are present in 50% of anterior MI within the first hour of symptom onset, representing ischemia of the conduction system rather than completed infarction.
    • Patients with pathologic Q waves already present within the first hour have a larger final infarct size but benefit equally from thrombolytic therapy.
    • Armstrong et al. more recently showed that Q waves on the “baseline” ECG (first ECG recorded during the event) were an independent marker of a worse outcome, and “after multivariable adjustment, baseline Q-wave but not time from symptom onset was significantly associated with a 78% relative increase in the hazard of 90-d mortality and a 90% relative increase in the hazard of death, shock, and CHF.”
    • Therefore, QR waves alone should never be used as a reason to withhold immediate reperfusion therapy.

Back to the case:

The cath lab was activated and the patient was found to have 100% occlusion of the mid-LAD, which was stented successfully.

The initial hs troponin I returned at 2,478 ng/L, and would later peak greater than 25,000 ng/L (our lab does not report higher). 

His echo showed EF 42%, "akinesis of the mid-apical and apical inferoseptal myocardium."

At 9:00, after his cath and stent, a repeat ECG was obtained:

Consistent with initial reperfusion compared to the presentation ECG. STE has reduced, and there is expected terminal T wave inversion.

Later that afternoon at 1400:

Similar to prior.

Next day at 0700:

Progression of reperfusion. Again, there has been significant anterior wall loss, but also a significant amount saved (if not, there would not be such significant reperfusion progression).

Learning Points:

Young people can have classic type 1 ACS and OMI.

The timing of OMI is much more complicated than the time since onset of symptoms reported by the patient. The ECG is much better at estimating acuity and viability.

Q waves can be present in the first hour of OMI, but deep QS waves usually are not present in the first few hours of persistent OMI.

The viable but at-risk myocardium shows up in the T wave. Upright T waves mean there is still viable tissue to save or lose.

Persistent symptoms or persistent ECG ischemia is an indication to perform primary PCI even after 12 hours of reported symptoms per the ACC/AHA guidelines (with other guidelines around the world being even more aggressive). 


  1. I am not really seeing an reciprocal changes on this EKG besides the TWI in aVL. As a paramedic, our particular protocol explicitly states "STE with reciprocal changes." I think a lot of medics I work with would recognize this as a STEMI, especially when correlated with clinical presentation. I guess my question is, is it common to have lack of reciprocal changes in an LAD OMI?

    1. I see just a hint of reciprocal STD in III, so little that many would disagree with me on that. I believe it is very common not to have reciprocal changes in and LAD OMI. I do not have the numbers on the top of my head, but in my experience the inferior leads could commonly have STE (from apical involvement and/or wraparound extension of the LAD), STD (from reciprocal changes from high lateral involvement), or neither (both of the previous two cancelling each other out).

      The only two walls of the LV that have (almost) perfect reciprocal partners on the standard 12 lead ECG are high lateral and inferior walls. If OMI in aVL or III, the other will show reciprocal findings, because of the spatial relationship between these two leads. No other standard lead has such a perfect and useful reciprocal partner present on the standard 12 leads as far as I know.

      If there is OMI in the anterior wall, no one can say there "are no reciprocal findings" - did you check the posterior leads for reciprocal findings? Of course they didn't. They assumed that all OMIs are supposed to show some reciprocal findings on the standard 12 leads that we created. That's not how it works. Long story short, I think many LAD OMIs do not have clear reciprocal findings present. Hope that helps!

  2. Agreed about the urgent angio.
    Also, I noticed the Q-waves in I and aVL got smaller in the 2nd and 4th ECG. which is very interesting.
    In the 3rd ECG, however, aVL looks different and I guess there is some electrode displacement.

  3. aVL is quite artifactual in the 4th ECG, making it hard to be sure, but based on what I think is there, I agree that the 3rd ECG may have some differing lead placement. Thanks for your comment!


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.