Wednesday, May 31, 2023

Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mass delusion (and Opiate pain relief).

I received the following text message with these 3 EKGs (providers text me ECGs all day every day; most are false positives; many are subtle true positives):

"Hi Steve, here are 3 EKGs for you (my colleague's case).  A 67 yo f developed chest pain this morning."

EKG #1

Followed 15 minutes by this #2 EKG:

Then the patient received aspirin and Dilaudid (hydromorphone, same effect as morphine) and the pain went away and there was this 3rd ECG:

Smith comment: hydromorphone will make any pain go away (or improve) without any improvement in the underlying pathology.  Do NOT give it unless you are committed to the cath lab!!

"Cath attending is aware.  I think it is OMI; am I right?  Cath lab declined as it is not a STEMI."

Smith Interpretation: there is diffuse ST depression followed by a hyperacute T-wave. This is classic de Winter pattern, and here it involves both anterior and inferior walls, so this is probably OMI of the mid LAD that also supplies the inferior wall (a "wraparound," or "Type III," LAD because it wraps around to the inferior wall).  There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves).

I sent the last one to the Queen of Hearts #PMCardio app and here is the verdict:

My response: 

"It’s not even subtle.  It is one of the few OMI patterns that is really well described: de Winter’s T-waves. And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! They are simply Hyperacute T-waves with depressed ST takeoff.  Even described in the New England Journal.  This is one that even cardiologists with no knowledge of subtle OMI should know.  LAD Occlusion.

Often, with this pattern, there is a trickle of flow through the LAD. So I doubt it was 100% Occluded. But the flow was greatly diminished and the infarct will be large.

So I encouraged her to be sure the patient goes to the cath lab emergently.

Many hours later, I asked what the angiogram showed.  

Here is her astonishing reply:

"Well, they still haven’t taken her to the Cath Lab yet!!!!  Trop at 5000 by now."

I asked: "Is this at the University of YYYYYYYY?"  

She answered: "I am so embarrassed to say that yes it is. I was not the attending, but I feel very bad for this patient who couldn’t defend herself." 

Smith Comment: This is all too common.  Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset.  It is a mass delusion.  

The patient did finally go to the cath lab and had a 99% Mid LAD Occlusion.

My response was: "This interventionalist should find a job that he/she enjoys doing."

This cardiologist has directly violated the ACC Guidelines on STEMI equivalents, and the patient will likely suffer increased morbidity and mortality as a result.

Opiates are associated with worse outcomes in Myocardial Infarction.

See this case: A man his 50s with chest pain. What happens when you treat with morphine rather than with reperfusion?

----See this study showing an association between morphine and mortality in ACS:
Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4. Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149:1043–1049.

And Another that we wrote:

----Bracey, A.  Meyers HP.  Smith SW.  Wei L. Singer DD.  Singer A.  Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion Myocardial Infarctions. Academic Emergency Medicine 27(S1): S220; May 2020.  Abstract 556.
Main result: STEMI(-) OMI Patients

65 (23.9%) patients were found to have STEMI(-) occlusion myocardial infarction (OMI) at the time of cardiac catheterization. The 45 patients with STEMI(-) OMI without pre-cath opioids had a door-to-balloon time of 75 minutes, vs. 684 minutes for the 25 STEMI(-) OMI with pre-cath opioids.

My Comment by KEN GRAUER, MD (5/31/2023):
I focus my comment on counting the ways that today's case should have been recognized as clear indication for prompt cath immediately on seeing the initial ECG — and at the very latest, 15 minutes after this when the 2nd ECG was recorded.
  • For clarity in Figure-1 — I reproduce today's initial tracing.

Figure-1: The initial tracing in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The Need for Prompt Cath: — Way #1 —
In a 67-year old patient with several hours of new chest pain — ECG #1 clearly fits the description of deWinter T waves. As per Dr. Smith — this entity is now formally endorsed as a "STEMI-equivalent" pattern in the 2022 ACC Guidelines.
  • In discussing deWinter T waves — I find it helpful to return to the original commentary by deWinter and colleagues (N Engl J Med 359:2071-2073, 2008) — in which they described a “new ECG pattern" without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.
  • To quote the authors’ original description of the new ECG pattern they reported on: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”
  • The authors went on to say: i) That the QRS complex was usually not widened (or no more than minimally widened); — andii) That most patients in their experience also manifested 1-2 mm of ST elevation in lead aVR.

  • To illustrate the spectrum of ECG findings — the authors included in their 2008 NEJM manuscript a composite picture taken from 8 representative tracings of patients in their study who manifested deWinter T waves. PEARL — I often refer to this composite picture (that I put in Figure-2) — as it serves to remind us of variations on the "theme" of deWinter T waves.

Figure-2: The deWinter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms.

MY OBSERVATIONS regarding De Winter T Waves: Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

  • Many (most) of these cases do not fit strict definition of “deWinter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, the number of leads that manifest giant T waves is limited.
  • I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. I suspect that to a large extent — what is seen on ECG depends greatly on when during the process the ECG is obtained. That said, for the practical purpose of promptly recognizing acute OMI — I feel ( = my opinion) that it matters less whether STEMI-criteria are satisfied or whether a "true" deWinter T wave pattern is present — vs the presence of simply "hyperacute" T waves (that are deWinter-like — and which indicate acute coronary occlusion all the same)


The Need for Prompt Cath: — Way #2 —
Giant T waves were not seen in each of the chest leads of the initial tracing in Figure-1. But regardless of whether you wanted to accept ECG #1 as consistent with a deWinter T wave pattern (or a "deWinter-like" pattern) — in a patient with new cardiac chest pain, this initial ECG is clearly indication for prompt cath:
  • There is J-point ST depression in 6 leads ( = leads I,II,III; aVF; V4,V5,V6). This ST depression is marked in most of these leads — in association with marked ST elevation in lead aVR, suggesting at the least diffuse ischemia.
  • ST coving and elevation is seen in leads V1 and V2. While the amount of ST elevation in these leads is not marked — its presence is clearly abnormal in lead V1, and the ST segment straightening in lead V2 in a patient with new chest pain suggests an ongoing acute process.
  • Hyperacute T waves (ie, much fatter-at-their-peak and wider-at-their-base than they should be) — are especially prominent in leads V3 and V4, and to a lesser extent in leads I,II; and V5,V6.
  • Although the QRST complex in lead aVL is tiny — the ST segment is elevated in this lead, and the T wave is hyperacute.
  • Reciprocal ST depression is seen in each of the inferior leads.

  • BOTTOM Line: In a patient with new chest pain — the findings in ECG #1 have to be interpreted as suggestive of acute proximal LAD occlusion until proven otherwise. Without a prior tracing for comparison — it's impossible to know if the QS complexes in leads V1-thru-V3 represent new anteroseptal infarction? — an old infarction? — or, a new infarction superimposed on a prior infarction. But even if this patient had a prior anterior infarction — the abnormal ST-T waves in literally all 12 leads is clear indication for prompt cath!


The Need for Prompt Cath: — Way #3 —
For ease of comparison in Figure-3 — I've put the first 2 tracings from today's case together.
  • Has there been any change during the 15 minutes that passed in the time between the recording of ECG #1 and ECG #2?

    Figure-3: Comparison between the first 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

    Comparison Between ECG #1 and ECG #2:
    Only 15 minutes passed between the recording of ECG #1 and ECG #2. But — Isn't there a significant difference between these 2 tracings?
    • I see no significant difference between these 2 tracings in the limb leads.
    • But in the Chest Leads — Lead-to-lead comparison suggests to me that there has been progression of ST-T wave abnormalities in each of these 6 chest leads! While the increase in ST elevation in leads V1 and V2 is subtle — there is clearly more J-point ST depression in leads V3 and V4 of ECG #2 — and — there is increased hyperacuity of the T waves in leads V3-thru-V6 that is most easily appreciated by comparing relative height of T waves in these leads, with amplitude of the QRS complex.

    • BOTTOM Line: The fact that ST-T wave changes have increased during the 15 minutes between the recording of these 2 ECGs qualifies as dynamic ST-T wave change — which in a patient with new chest pain, by itself is indication for prompt cath. 

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