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


Interpretation:

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). 


Tuesday, May 4, 2021

Let's Use Aslanger's simplified formula on this case (simplified Smith LAD occlusion/early repol formula)

This was posted in August 2019:  Acute Chest pain in a 50-something, and a "Normal" ECG

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent this case

A 50-something man presented with acute chest pain.

Here is his ECG:
As you can see, the computer said "normal" and it really does have a normal appearance to those who have not been reading this blog regularly.
The ST Elevation in precordial leads does not meet STEMI criteria.  Both V2 and V3 are less than 2 mm, which is the cutoff for males over age 40.
We discussed this at the time (and I have copied and pasted that discussion below), and we used the 4-variable formula to show that it is an LAD occlusion.

But Aslanger has modified and simplified my formula, and I have not discussed it enough.

The primary benefit of the modification is that the QT need not be corrected.  This is particularly important because the computerized QTc is different on different computers, with any one of the 4 correction formulas used, and the choice of formula is not obvious.  On our EKGs, I had to reverse engineer to find out that it uses Hodges formula, not Bazett. 

Aslanger E et al.  A Simplified Formula Discriminating Subtle Anterior Wall Myocardial Infarction from Normal Variant ST-Segment Elevation.  American J Cardiol 122(8):1303-1309; Oct 2018.

Here is that simplified formula: (RAV4 in mm + QRSV2 in mm) - [(QT in mm) + STE60V3 in mm)

In this case:
QT = 360 ms (QTc = 385).  360 ms =  9 mm.
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18


A value less than 12 corresponds to LAD occlusion; a value greater than 12 to normal variant STE

Let's plug the numbers into the formula:
18 + 6 = 24; 9 + 4 = 13;  24 - 13 = 11, which is below 12, so LAD occlusion.


Previous Discussion:

An interpretation of "normal" could, of course, deceive many providers.

Analysis

This could be normal variant ST Elevation in V2 and V3.  There is 1.5 mm STE in at the J-point in lead V2 (relative to QRS onset, otherwise known as PQ junction).  There is 1.0 mm in V3.

So this is a normal amount of STE in V2 and V3, defined by Universal Definition of MI as up to 2.0 mm in men over age 40.  So there is definitely no STEMI, and the STE is normal.  So the computer is correct in calling it normal.

But after reading this blog, you all know that most OMI do NOT meet STEMI criteria.  Some patient's baseline ECG has zero STE.  Some patient's baseline has normal variant STE.  You don't know which kind of patient this is.

Some normal STE is actually due to OMI.  Some normal STE is not due to ischemia at all.

It is your responsibility to determine if STE is ischemic or not.

How do we do so?

Use the formula.

QTc = 385
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18

Formula value = 19.94 (very high, indicating LAD occlusion).

Any value greater than 18.2 is likely to be LAD occlusion.

For graphs of sensitivity, specificity, and accuracy at various cutoffs, see this post:

More precise interpretation of the results of the 4-variable formula.


12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


Chris Mondie's note:

"My read: Acute proximal LAD occlusion. Hyperacute T waves which tower above the preceding R waves, poor precordial R wave progression. Large T in V1.  Smith subtle LAD equation indicative of acute LAD occlusion. 

"Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI. 

"Cardiology agreed to take the pt to the lab but thought it would likely be negative. 

"100% proximal LAD successfully stented. 
Defibrillated out of v fib in the cath lab. 
Initial TnI was negative. 

"I thank you for constantly updating your blog and allowing free open access education on EKG interpretation. I recognized this as a STEMI immediately and I was only able to do so solely because of your blog."















Monday, May 3, 2021

See this: Occlusion/Reperfusion/Re-occlusion/Reperfusion/Re-occlusion/Reperfusion

A 60-something y.o. male presented with intermittent left-sided chest and shoulder pain that is achy in nature and lasted a few minutes or sometimes just a few seconds.  

"The symptoms come and go, not associated with any exertion or history of trauma.  Patient does have a history of hypertension and has been taking his medications.  Prehospital EKGs appeared consistent with anterior tombstone ST elevation with pain." 

Prior to arrival the patient was given full dose aspirin, as well as nitroglycerin, which relieved his pain, after which T wave inversions were noted in the anterior precordial leads.  

These 2 prehospital ECGs are not available.

On arrival, the patient had recurrent chest discomfort and had this ECG recorded:

LAD STEMI


His pain quickly resolved and 6 minutes later, this was recorded:
Reperfusion "Wellens'" waves


His pain quickly recurred and another ECG was recorded at 12 minutes (6 minutes after the 2nd one)
Re-occlusion

The patient's pain resolved again and this was recorded 19 minutes after the 3rd one (t = 31 minutes)
Reperfusion again


He went to the cath lab and the angiogram showed a thrombotic LAD culprit with normal (TIMI-3) flow.

The lesion was stented.

The initial high sensitivity troponin I returned at  96 ng/L.

The patient did well.

Comment:

This is a nice illustration of what occurs with occlusion and reperfusion, and a demonstration of how thrombus can lyse and propagate, lyse and propagate. This can occur with or without nitroglycerin and/or aspirin.  

We all have an ongoing delicate balance between thrombosis and thrombolysis, using our own endogenous tissue plasminogen activator. 

Large upright T-waves are a sign of a large amount of myocardium at risk, but also that it is all viable and salvageable.  So it is a bad sign that there is so much at risk, but a good sign that the vast majority is salvagable.

Large inverted T-waves are a sign that a large amount of viable myocardium is now reperfusing.   It is a sign that there was still a lot of viable myocardium at the time of reperfusion -- reperfusion was NOT too late.

As more fully ischemic time passes, T-waves become smaller, and when there is reperfusion, the size of the inverted T-wave is also smaller.

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