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".

Precordial Swirl -- 20 cases of Swirl or Look-Alikes

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

Click here to sign up for Queen of Hearts Access

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.

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

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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 diagnosis. This 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 arrows) is 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.