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

Don't miss them!!!

Use the Queen of Hearts and save myocardium and lives!


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

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

===================================
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)










Thursday, July 11, 2024

See how bad the outcome can be if you don't know OMI findings on the ECG, and don't use the Queen of Hearts

This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech.  

How is it possible that a kid who has not even started medical school can know so much about EKGs and cardiology?  Because:

1) He has been reading this blog for a long time.  

2) He is curious

This is how Pendell got started.

Case

A 43 year old male with a history of DM II, hyperlipidemia, and a family history of myocardial infarction presented to a family clinic with two days of epigastric pain that started after consuming a meal. He described the pain as a “crushing and discomforting” feeling with no radiation. He reported that the pain was worse with exertion and nothing relieved it. His BP was 138/88 and his HR was 77 BPM. He had an EKG taken at the clinic:

What do you think?









There was no old EKG for comparison, however, this EKG alone is diagnostic of LAD occlusion. 


The T waves in V1-V4 are hyperacute. There is positively sloped ST-segment straightening in V2 and V3. There is a fragmented QS complex in V2. Lead aVL has a very subtly convex T wave with terminal T wave inversion. There is very slight horizontal ST segment straightening in leads III and aVF. These inferior leads could be normal, however, in combination with the hyperacute anterior T waves, they should be interpreted as showing reciprocal changes. V6 also has very slight ST depression. This EKG shows precordial swirl pattern (STE in V1-2 with STD in V5-6).


Smith: there is also a Q-wave in V2 and a small amount of STE.  STE is almost never normal in the context of a Q-wave.  Also, there is STD in V5-6. STE in V1-V4 is never normal if there is also STD anywhere except aVR.  There are many reasons that this ECG is diagnostic of LAD OMI.


Thus, this is yet another case of "Precordial Swirl".



An argument can be made that the reciprocal changes here are not prominent enough to call, but it is important to remember that many LAD occlusions do not show reciprocal changes at all. 


The computer diagnostic algorithm diagnosed “Sinus rhythm. Normal EKG”. The attending provider wrote “Agree with electrocardiogram interpretation”.  The cardiologist overread was: Sinus Rhythm. Normal ECG.


Smith: All physicians, including cardiologists, have a hard time with subtle OMI ECG findings.  This result is common and not surprising. 


In general, family medicine physicians may not have the same amount of exposure to EKGs as an emergency medicine specialist or a cardiologist, but they shouldn’t have to rely on the traditional diagnostic computer algorithm. 


Had the physician instead used the Queen of Hearts, who diagnoses OMI with high confidence, the outcome may have been different:

OMI with High Confidence


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Case continued


Unfortunately, this EKG went unnoticed, and the atypical symptoms with which the patient presented did not prompt any further cardiac workup. A CBC and a metabolic panel were ordered, and both were unremarkable, save for hyperglycemia. The patient was sent home with a prescription for omeprazole to treat presumed peptic disease. He spent the following weeks with continued episodic heartburn and worsening dyspnea on exertion.


No patient with chest pain should be sent home without troponin testing.  Even if you miss the ECG, at least you'll be able to diagnose an MI with troponins, though if it is OMI, you may lose a lot of myocardium before making the diagnosis.  


He re-presented to the family clinic for a follow-up visit a month after his original appointment. His BP was now 82/68, and his HR was 112. On this visit, he expressed worsening exercise tolerance, new orthopnea, and he told his provider that the omeprazole did not relieve any symptoms. An EKG was taken again:

This EKG shows a completed anterior wall infarction! There are hardly any R waves in any of the precordial leads!


The provider recognized the dramatic changes between this tracing and the tracing taken a month prior. He sent the patient to the ED for further evaluation. A chest x-ray in the ED found bilateral pleural effusions. The patient’s BNP was 738, and his D-dimer was elevated, prompting a CT scan to rule out PE. The scan did not find PE, but showed evidence of coronary plaque:

There are areas of dense white in the LAD (red and blue circles) and in the first diagonal (green circle).


An echocardiogram showed severely reduced global systolic function with an EF of 20-25% and an LV apical thrombus. Troponin I values trended from 0.262 to 0.746 ng/mL in 6 hours (URL for this assay is 0.034 ng/mL). The patient was admitted from the ED and finally had an angiogram the next morning:


Angiogram:


Image 1:

This is the LAO caudal, or spider projection. The red arrow shows a roughly 80% stenosis of the proximal LAD. The blue arrow shows another stenosis of the LAD distal to the first diagonal branch of about 99%. The green arrow shows a 95% stenosis of the ostium of the first diagonal branch. 


Image 2:

This is the LAO cranial projection. Here, the mid LAD (blue arrow) and the ostial first diagonal (green arrow) stenoses are better visualized. All three lesions had TIMI 2 flow prior to stenting.





This is an RAO cranial projection of the left coronary vessels after thrombectomy and stenting. The blue arrow indicates the LAD, and the green arrow indicates the first diagonal. There is now TIMI 3 flow through all lesions, but there is widespread vasoconstriction.





This is the RAO caudal projection. The LAD (blue) and first diagonal (green) are noticeably narrower than the other vessels.




Here is the post-cath EKG:

There is no change. The LV aneurysm morphology persists. There was hardly much viable myocardium left to be saved by PCI after a month of occlusion.


On day three of his hospital admission, he had a cardiac MRI taken:

The MRI showed:

  • Increased LV volume

  • Severe segmental LV dysfunction with a calculated EF of 26%

  • Thinning and akinesis of the entire anterior wall, apical segments, entire anterior septum, and the mid inferior wall.

  • Large multiloculated apical thrombus (black mass at the apex)

  • Transmural infarction showing nonviable myocardium throughout the entire anterior distribution and all apical segments


The patient was eventually discharged from the hospital. Three months later, he had a follow up appointment for a reassessment of his LV function. An echocardiogram showed an EF of 20-25%. At this point, there was no improvement in LV function and he was out of the convalescent phase of his MI, so the decision was made to install an ICD for arrhythmia prophylaxis.


One month after ICD implantation, an EKG was taken:


Notably, the T wave inversions are now resolved. The R waves have not recovered, however.


He now has regular appointments with the heart failure team.


Learning Points


All of this could have been avoided by:


1.  Expert ECG interpretation -- this is too much to ask of any clinician

2.  Queen of Hearts --  makes the diagnosis easy

3.  The patient should have had serial troponins.  These would have made the diagnosis of MI earlier, but it might still be labeled "NSTEMI" and not get intervention until all that myocardium is lost.






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

MY Comment, by KEN GRAUER, MD (7/11/2024):

===================================
I reviewed today's case from the perspective of a family physician educator with prior experience teaching ECG interpretation nationally to primary care clinicians over a period of 3+ decades.
  • In our primary care residency program, despite our faculty's competency in the basics of reading primary care X-rays — all of our X-rays were overread by a radiologist.
  • I overread all ECGs for our 35 providers.

  • BOTTOM Line: Unless primary care clinicians attain a level of excellence in the interpretation of outpatient X-rays and ECGs — these tests should be routinely overread by physicians with recognized expertise in this interpretation.


Editorial Comment: I begin my thoughts on today's Blog post with the above reflections to provide perspective for my concerns about this case.
  • This patient should not have been sent home from the primary clinic with the history he gave and today's initial ECG (that I've reproduced and labeled in Figure-1).
  • A 2-day history of a "crushing and discomforting feeling" that is worse with exertion and not relieved by any home measures that are tried — even if primarily "epigastric" in location — is a potential presentation for ACS (Acute Coronary Syndrome) that needs to be recognized.
  • Primary care clinicians are trained in the basics of ECG interpretation. While not expected to be experts if such clinicians limit their practice to an ambulatory setting in which they rarely order outpatient ECGs — these primary care clinicians are expected to recognize that in a patient with new symptoms (as in today's case) — the ECG in Figure-1 is not "normal".
  • If the training of primary care clinicians is such that they are unable to recognize that today's initial ECG is not normal — then before the patient is sent home, there should be some form of backup overread. As per Dr. Smith — Queen of Hearts offers one form of immediate backup overread with impressive accuracy for identifying OMI on ECG.
  • Alternatively (and ideally, in addition to QOH) — in 2024, ready access to on-line consultation with either a local or remote expert in ECG interpretation should be available to any primary care clinician within minutes.
  • The above said — of even more concern in today's case, is that the cardiologist overread of today's initial ECG completely missed the diagnosisThis oversight by cardiology is hard to justify.

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


Today's Initial ECG: 
As per Dr. Smith — the ECG in Figure-1 is diagnostic of acute LAD OMI.
  • I've enclosed the reason today's initial ECG should not be overlooked within the RED rectangle. There is simply no way that the QRS complex and ST-T wave in lead V2 can be interpreted as "normal". The hyperacute ST-T wave in this lead completely dwarfs the tiny QRS complex. A repolarization variant will never do this. In addition to its height — this ST-T wave manifests an extremely wide base and straightening of the ST segment takeoff (RED arrow).
  • As a more subtle point — the QRS complex in lead V2 is abnormal. Although there is variation in QRS morphology for each of the complexes in this lead — the "theme" is fragmentation of the QRS, with no more than a tiny vestige for an r wave that I interpret as a Q wave "equivalent" in this patient who has had symptoms already for 2 days.

  • In the context of this marked abnormality in lead V2 — the 2 neighboring leads within the RED rectangle are also clearly abnormal. Lead V1 never normally manifests this much ST elevation, nor this tall of a T wave. And, given these abnormalities in leads V1,V2 — the ST-T wave in lead V3 is also hyperacute (taller and wider-at-its-base than expected, given modest amplitude of the QRS in this lead).
  • In support of this ECG representing acute proximal LAD OMI — is the clearly abnormal complex in lead aVL (within the BLUE rectangle) — which shows a surprisingly wide and deep Q wave (given tiny size of the QRS in this lead) — as well as slight-but-real ST elevation of coved morphology with terminal T wave inversion. Acute ECG findings of this nature in lead aVL is a common accompaniment of proximal LAD OMI. The Q in aVL and the Q-wave "equivalent" fragmentation in lead V2 suggest in this patient with a 2-day history of symptoms — that infarction has already taken place.
  • Finally, as per Dr. Smith — the subtle-but-real ST segment flattening in each of the inferior leads (BLUE arrowsis consistent with representing reciprocal ST depression. To Emphasize — As an isolated finding, I would be uncertain about the clinical significance of the ST-T waves in the inferior leads. But in the context of leads V1,V2,V3 and aVL being diagnostic of acute LAD OMI — the subtle degree of ST flattening in leads II,III,aVF is clearly consistent with reciprocal ST-T wave changes.

In Conclusion: Today's case is concerning because of unfortunate oversights that should not have occurred. The consequence of these oversights is the need for lifelong commitment of this patient to the heart failure clinic.






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