Sunday, July 14, 2024

Which of these, if either, is OMI? Which of these underwent emergent angiography and PCI? Which should have?

 Sent by anonymous, written by Pendell Meyers


Case 1:

A man in his 50s presented with acute chest pain. Normal vital signs.

Here is his ECG at triage:

What do you think?












Here's what Version 1 QOH thinks:





It is diagnostic of acute LAD OMI, with the precordial swirl pattern. See this post if you dont know that pattern yet:




Here was a repeat ECG done within 20 minutes (still with ongoing pain):

It still looks like active OMI to me, but perhaps slightly improved from the first one.



The cath lab was activated, and then not cancelled, and the angiogram showed 99% TIMI 2 flow proximal LAD culprit lesion, stented in less than 90 minutes of arrival. 


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Case 2:

A woman in her 60s presented with acute chest pain. Normal vitals.

Here is her triage ECG below:

"Initial EKG read as mild ST depression."
What do you think?









This one, too, is a swirl pattern and diagnostic of LAD occlusion.


QOH Version 1:






The physician wrote:

"Troponin was mildly elevated"

Repeat ECG (below) read as "No changes."



Outcome of case 2?

"Admitted for NSTEMI. Cath days later showed complete occlusion of the LAD, stented. Stopped measuring troponins on the day of presentation around 5,000 ng/L as it was still rising."



Another missed OMI by the False STEMI-NonSTEMI Dichotomy

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MY Comment, by KEN GRAUER, MD (7/14/2024):

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The utility of today's excellent post by Dr. Meyers — is that it highlights the difference in outcome in 2 patients with similar presentation (ie, New-onset CP from precordial "Swirl" LAD OMI— depending on whether or not the initial ECG was correctly interpreted
  • I focus my comments on some additional fine points regarding subtleties in the interpretation of today's tracings.

CASE #1: A Man in his 50s with acute CP ...
For clarity in Figure-1 — I've corrected the angulation and digitized the initial ECG in Case #1. As per Dr. Meyers — this initial tracing is diagnostic of acute LAD OMI with the precordial "Swirl" pattern (I summarize "My Take" on recognizing Precordial "Swirl" at the bottom of the page in the October 15, 2022 post).
  • Patients with precordial "Swirl— have evidence of acute LAD OMI. In addition — there is transmural ischemia of the septum, most often resulting from occlusion proximal to the 1st septal perforator branch of the LAD.

  • The most striking abnormality to my "eyes" in Figure-1 — is in lead V2 (within the RED rectangle). In a patient with new CP — there simply is no way that the ST-T wave appearance in lead V2 is normal. Although slight upsloping ST elevation is commonly seen in leads V2,V3 as a normal finding — the amount of J-point ST elevation seen in Figure-1 is much greater than what can be accepted as "normal". The ST-T waves in this lead are clearly hyperacute — in that they are disproportionately hypervoluminous (much taller-than-they-should-be given small S wave amplitude in lead V2 — much wider-at-their-base than these ST-T waves should be — and with a straighter ST segment takeoff compared to the gentle upsloping typically seen in a normal tracing).
  • In the presence of acute LAD OMI — "Swirl" is recognized by a characteristic ST-T wave abnormality in leads V1 and V6. The obviously abnormal ST-T wave appearance in lead V2 confirms that the ST-T wave in neighboring lead V1 is also abnormal. That is, there is a subtle-but-significant amount of ST elevation in lead V1, as well as abnormal coving of the ST segment in this lead.
  • As opposed to DSI (Diffuse Subendocardial Ischemia) — in which ST elevation in lead aVR is generally more than any ST elevation that might be seen in lead V1 — the opposite is seen with precordial Swirl. So despite the marked limb lead artifact in Figure-1 — the coved and elevated ST segment in lead V1 is more prominent than the slight ST elevation in lead aVR, with a morphology in lead V1 that is characteristic of "Swirl".
  • Recognition of septal transmural ischemia with "Swirl" is confirmed in Case #1 by the reciprocal ST-T wave changes seen in lead V6, which shows a relatively straightened and depressed ST segment (BLUE arrows in lead V6).
  • Supportive evidence of proximal LAD OMI — is forthcoming from reciprocal ST depression in at least 2 of the inferior leads (BLUE arrows in leads II and aVF).

PEARL #1:
 Note that we see 3 QRS complexes in simultaneously-recorded leads V4,V5,V6. Isn't the ST-T wave of the middle QRS complex very different in morphology than the ST-T wave of the 1st QRS complex in these leads? The pattern of precordial "Swirl" could not be diagnosed if the ST-T wave morphology of the middle QRS complex was real — because there is no flattened ST depression in lead V6.
  • The KEY is to appreciate that the long lead II rhythm strip is also simultaneously recorded. Note the bizarre dip and distortion of the ST-T wave of beat #12 in the long lead II. This is obvious artifact — and it tells us to ignore the ST-T wave of the middle beat in simultaneously-recorded leads V4,V5,V6.

BOTTOM Line for CASE #1: 
Prompt recognition of the precordial "Swirl" pattern of acute LAD OMI resulted in stent reperfusion in less than 90 minutes from the time of arrival in the ED.
  • Prompt, accurate ECG interpretation saves myocardium!

Figure-1: The initial ECG in CASE #1. (To improve visualization — I've straightened the angulation and I've digitized the original ECG using PMcardio).


=======================================

CASE #2: A Woman in her 60s with acute CP ...
For ease of comparison — I've labeled both tracings in Case #2, and have put them together in Figure-2.
  • ECG #1 in Case #2 was interpreted by providers as, "mild ST depression".

  • ECG #2 in Case #2 — was compared to ECG #1, and interpreted by providers as showing, No changes".

BOTTOM Line for CASE #2:
As per Dr. Meyers (and as per QOH) — the ECGs in Case #2 once again are diagnostic of acute LAD OMI with the pecordial "Swirl" pattern. This determination was confirmed by marked troponin elevation and by ultimate cardiac catheterization (performed days later) showing complete LAD occlusion.
  • Inaccurate ECG interpretation in patients with new CP — leads to loss of myocardium that could have been saved.
  • Failure to appreciate one's shortcomings in ECG interpretation ability + failure to consider QOH assistance — delays diagnosis and increases the amount of lost myocardium. Ultimately, cardiac cath was done in Case #2, with stenting of the "culprit" LAD lesion. Unfortunately — this occurred far too late for optimal benefit.

What Can be Learned from CASE #2?
The rhythm in both tracings in Case #2 shows AFib with a controlled ventricular response (with a PVC in the 2nd tracing).
  • We are not told IF this AFib is new (as a result of the acute LAD OMI) — or, if this AFib is this patient's longstanding rhythm (nor are we told if the patient is on anticoagulation or is taking rate-slowing medication). Presumably the AFib is not a new rhythm — since new-onset AFib is usually associated with a rapid ventricular response.
  • NOTE: It's important to determine if the AFib is new or old — since prognosis of acute LAD OMI that causes new AFib is associated with a more severe course and poorer outcome. Whereas new AFib that occurs as a result of acute LAD OMI may need immediate cardioversion — longstanding AFib with a controlled ventricular response is much more likely not to need any specific treatment.

ECG #1 in CASE #2:
  • The most striking abnormality to my "eyes" in Figure-2 — is seen in lead V1 (within the RED rectangle). In a patient with new CP — there simply is no way that the ST-T wave appearance in lead V1 is normal. Although the amount of ST elevation in this lead is minimal — the coved shape of the ST segment in lead V1 is clearly abnormal (and characteristic of the "Swirl" shape in lead V1 — seen here with subtle terminal T wave inversion).
  • I found it interesting that the shape of the ST-T wave in neighboring lead V2 (within the BLUE rectangleis quite different than the ST-T wave shape in lead V1. Given that we know that the ST-T wave in lead V1 is abnormal — the ST-T wave in lead V2 is "bulkier"-than-it-should-be (hyperacute!), especially in view of the very modest amplitude of the S wave in this lead V2.
  • In support of these V1,V2 ECG findings indicating proximal LAD OMI — is the reciprocal ST-T wave depression in each of the inferior leads (BLUE arrows in leads II,III,aVF).
  • In this context — the ST depression in leads V5 and V6 fulfills criteria for precordial "Swirl" (with the flat ST depression in V5 — and the scooped ST depression in V6 showing the 2 ST-T wave shapes characteristic of Swirl).

The Most Glaring Error in CASE #2:
In a patient with new CP — the combined findings in the leads highlighted above are diagnostic of acute LAD OMI with precordial "Swirl". That said — there is a subtlety to the findings in ECG #1, such that providers might be less than certain of the diagnosis from this initial tracing.
  • IF at all uncertain — the next step is EASY. Simply repeat the ECG in no more than ~10-20 minutes. We are not told how much time passed between the recording of these 2 ECGs in Case #2 — but given the interpretation of ECG #1 by the provider ( = "mild" ST depression) — it is likely that much longer than 10-20 minutes passed between tracings.

PEARL #2:
 The BEST and most time-efficient way to compare serial ECGs — is to put both tracings side-by-side (as shown in Figure-2— and then to compare the 2 ECGs going lead-by-lead.
  • This side-by-side comparison of ECG #1 and ECG #2 was obviously not done in today's case — since if it had been done, there is no way that providers could not have noticed: i) Loss of R wave in leads V2 and V3 — compared to R wave amplitudes seen in these leads in the initial ECG; andii) Change in the shape of the ST segment takeoff in lead V2 compared to the upsloping shape of the ST segment in V2 of the initial ECG (RED arrows highlighting the definite straightening of the ST segment takeoff in lead V2 of ECG #2 — and the much more obviously disproportionate ST-T wave in this repeat tracing).
  • PEARL #3: Note the timing of the lead switch between leads aVR,L,F and V1,2,3 in ECG #2 — such that the ST segment (1st RED arrowis from lead V2. Seeing ST segment straightening in all 3 ST-T waves in this lead V2 — confirms that this is a "real" finding. The PEARL — is to appreciate that sometimes important clues are "tucked away" in a lead switch that may split complexes into the QRS complex for the first 3 leads (just before the lead switch) — and the ST segment for the next 3 leads (just after the lead switch).

  • NOTE: It might be easy to think there is "no difference" in the ST-T waves in lead V3 of ECG #1 and ECG #2 if each tracing was looked at separately. This is precisely why serial ECG comparison needs to be accomplished by looking lead-by-lead. The BLUE arrows in lead V3 of ECG #2 highlight that the ST segment takeoff has become straighter and the T wave more disproportionate in this repeat tracing!
  • Finally — BLUE arrows in lead aVL of ECG #2 now unmistakeably show ST coving and slight elevation that was not evident in ECG #1. This is a significant change — since ST elevation in lead aVL is a hallmark of proximal LAD OMI.

  • CONCLUSION: In a patient with new CP — Any doubt that might have been present after assessing ECG #1 — should have been eliminated after lead-by-lead comparison with ECG #2.


Figure-2: Comparison of the 2 ECGs in CASE #2. (To improve visualization — the original ECGs have been digitized using PMcardio)










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