Friday, July 13, 2018

A man in his 40s with chest pain


Case submitted and written by Alex Bracey, with edits by Pendell Meyers and Steve Smith


This ECG was tossed onto my desk on my first day of a new rotation at a community site. The technician was nowhere to be found by the time I turned to ask what the story is or where the patient is located.
Initial ECG at 1350 - are you concerned?




















- There is 0.5 mm STE in aVL, no clear STE in lead I.

- There is ST depression in II, III, and aVF.

- Nicely demonstrated here, leads III and aVL are reciprocal: STD in III is reciprocal ST depression to STE in aVL. This is diagnostic of occlusion (OMI).

- There is also some slight STD in V4-V6. Out of context, STD in V4-V6 as well as II, III, and aVF, with slight STE in aVR may make you think of diffuse supply demand mismatch ischemia as can happen with any pathology involving diminished blood flow to the majority of the heart, such as left main stenosis or severe three vessel disease. However, the morphology and STE in aVL with the morphology of the reciprocal STD inferiorly sets this case apart and identifies OMI rather than just global supply/demand mismatch.
- STEMI criteria are not met.


No prior ECGs were available.


My co-resident and I went to find the patient in the main ED. He was a man in a his late 40s who was alert but looked as though he was trying to maintain a smile through some discomfort. He told me that he had been having chest pain for ~6 hours, described as a heaviness in his chest, that started just after signing his divorce papers. He was an active smoker with hypertension and had a closely related family member that had an MI at the age of 49.


We gave him aspirin and asked for a repeat ECG.


While awaiting the repeat ECG, it was suggested that cardiology be consulted emergently for intervention. A senior team member, while concerned about the ECG wanted to wait for the troponin to result before involving cardiology. At 14:35, ~45 minutes after in the initial ECG the patient, the troponin I resulted as 0.701 ng/mL (normal range 0.000 - 0.045 ng/mL).

At this point, even if the ECG is confusing to you, the diagnosis is made: chest pain with an elevated troponin in this context is acute myocardial infarction. No matter what the ECG shows, with continued chest pain the patient must go emergently to the cath lab. In this case, you have BOTH a diagnostic ECG and a diagnostic troponin.

A repeat ECG was obtained shortly after:
Repeat ECG @ 1447

Similar to prior. The artery is still occluded.





At this point, cardiology was consulted and I described the findings and relayed concern for acute coronary occlusion in the absence of a STEMI. The cath lab was not immediately activated, but cardiology staff was sent to evaluate the patient. The patient was admitted to cardiology and underwent cardiac catheterization ~2.5 hours after presentation and initial ECG.


Prior to the publishing of the cath note, we received a phone call from the interventional cardiology who commended us and informed us, with some surprise, that he had found thrombus in the LCx second obtuse marginal, which had successfully undergone PCI with one drug eluting stent.



On the actual cath report, no initial stenosis percentage or TIMI flow were reported; rather, only the post procedure TIMI III and residual stenosis of 0% are documented.


This is the subsequent ECG taken just after PCI:
ST changes are resolving.



One day later, the troponin I peaked at 48.2 ng/mL. He was discharged home the subsequent day with a diagnosis of "NSTEMI."


TEACHING POINTS:

STEMI criteria will miss a significant number of acute coronary occlusions. While this criteria exists and is still recognized as the standard for diagnosing acute coronary occlusion, patients will continue to have delay to definitive management (e.g., PCI). As in this case, the diagnosis was made at hospital presentation, but he patient waited for 2 hours until intervention. Even then, the cardiologist was surprised to find an acute lesion. As we've said before, we must change the language to include those that will benefit from emergent intervention even though they do not manifest STEMI criteria (see this post: OMI Manifesto).

We were fortunate to have a fairly receptive interventionalist on this case; however, that will not always be the case. In such instances, serial ECGs become invaluable, as the patient may manifest worsening STE or even simply dynamic ECG changes which may be enough to convince an interventionist to emergently activate the cath lab. But notice that in this case there was no serial change; you cannot depend upon it!

Do not wait for the troponin to result before getting cardiology involved with a concerning ECG and story; the troponin plays a supporting and complimentary role in the diagnosis of OMI. Keep in mind that contemporary troponin assays will only start to manifest at the 4-6 hours mark, and many people with ACO will present well before that point. Had this patient’s troponin been undetectable, it would not have changed where this patient needed to go: the cath lab. Had it been negative, it may have delayed his time to PCI. Time is myocardium.



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Comment by KEN GRAUER, MD (7/13/2018):
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It is cases like this one that emphasize the tremendous importance and educational impact of Dr. Smith’s ECG Blog. This case should not have been delayed for several hours before being recognized for the OMI that it is. I’ll add the following points:
  • As per Drs. Bracey, Smith and Meyers  — dependence on strict STEMI criteria will miss a significant number of acute coronary occlusions. This is especially so in cases like this one, in which only lead aVL manifests ST elevation. It is important to appreciate that lead aVL is the “highest” lateral lead — and with acute occlusion of the 1st or 2nd obtuse marginal branch of the LCx — lead aVL may occasionally be the only lead to show ST elevation.
  • There is ample evidence on the rest of the initial ECG (done at 13:50) to support the conclusion that changes in lead aVL must be assumed acute until proven otherwise. As per Dr. Bracey, Smith and Meyers — this evidence includes reciprocal ST depression in each of the inferior leads, with an exact “mirror-image opposite picture” of the ST elevation in aVL seen by the shape of the ST-T depression in lead III. In addition, there is ST segment flattening with 0.5-1mm of ST depression in leads V4, V5 and V6.
  • The appearance of anterior leads V1, V2 and V3 is also worthy of mention. On initial inspection of the 1st ECG (done at 13:50) — there appears to be a QS complex in each of these 3 anterior leads. This raises suspicion of anteroseptal infarction at some point in time. The disproportionately tall (and fatter-than-expected-at-its-peak) T wave in lead V3 might raise suspicion of an acute event in the LAD distribution, if not for 2 points: ithe even more convincing ECG picture in the limb leads that suggests acute LCx Obtuse Marginal occlusion; andiithe likelihood of some chest electrode lead misplacement, given the prominent negative P wave component in V1, V2 — and, the unexpected decrease in S wave amplitude from V1-to-V2, that then unexpectedly increases again by lead V3. Sure enough, a definite initial positive deflection (r waveis seen in lead V3 of the 2nd ECG (done at 14:47) — which makes prior anteroseptal infarction less likely.
COMMENT: The presentation of this case reminds me of my experience as the provider charged with interpreting all ECGs done by the 35 practitioners at our ambulatory Family Medicine Center over the 30 years that I served in the Residency Program as full-time core faculty. In that role, I was often presented a series of tracings without any history. The challenge was determining which tracing(s) showed findings that mandated dropping whatever I was doing to immediately find out the history, because of concern for a potential acute condition. Credit to Dr. Alex Bracey for doing just that in this case! Had he not directly hunted down the patient in the ED — there is a very good chance that this patient’s OMI would not have been recognized in time.
  • MORALIt’s impossible to appropriately interpret ECGs without clinical correlation! The initial (13:50) ECG in this case might not necessarily be cause for alarm in the absence of symptoms — especially if a prior ECG was found showing similar changes. But on learning that the patient in this case had new-onset chest discomfort just a few hours earlier — acute OMI has to be assumed until proven otherwise, regardless of what serum troponin shows — and regardless of whether the 2nd ECG shows serial changes.


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