Submitted by anonymous, edited by Jesse McLaren
The first person "I" and "me" is this anonymous sender.
A 50 year old presented to the emergency department of a remote rural community (where the nearest cath lab is a plane ride away) with one hour of mild chest pain radiating to the back and jaw, and an ECG labeled ‘normal’ by the computer interpretation. What do you think, and how would you manage the patient?
There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s clear T wave inversion in III/aVF, which is reciprocal to subtle ST elevation and hyperacute T waves in I/aVL (broad, symmetric, and larger than the entire QRS in aVL). This is diagnostic of Occlusion MI of the high lateral wall, either from circumflex or first diagonal.
But the first ECG was labeled normal by the computer, and the first high sensitivity troponin after only one hour of symptoms was 5 ng/L, also normal (<12 ng/L). Neither of which are unusual for Occlusion MI, but both of which can result in delayed diagnosis and treatment.
The ECG was signed off by a colleague and the patient handed over to me to follow serial troponins. As an avid reader of Dr. Smith’s ECG Blog, I immediately recognized the first ECG as diagnostic of OMI, called the cath lab and texted a photo of the ECG to the interventional cardiologist.
But they did not notice the high lateral OMI, and advised against reperfusion based on lack of STEMI criteria. They noted “J-point
elevation in the anterior precordial leads, with slight concave-up ST segment
elevations, particularly in leads V2 and V3. There was also flattening of the
ST segments in the inferior limb leads. It was clear that [patient] was
suffering an acute coronary event, however there were no clear
electrocardiographic criteria for thrombolysis or primary coronary angioplasty.
I asked that another troponin be drawn, frequent electrocardiograms be taken.” While there were no STEMI criteria, the ECG did show OMI in need of reperfusion.
Repeat troponin increased mildly from 5 to 16, and repeat ECG is below:
Similar, except straightening of the ST segments in I/aVL, and some ST depression in V3. Even more diagnostic of OMI, not of the LAD but a high lateral vessel.
Because there was no clear STEMI and troponin was low, the interventional cardiologist advised me to treat the patient as Non-STEMI rather than thrombolytics, and repeat trop in the morning and call them back, sooner if anything changed.
They said that as the trop had only gone from 5 to 16 in an hour, and ECG elevation had not developed, that it wasn’t a STEMI and could do enoxaparin and repeat trop/ECG in the morning. Didn’t require TNK or urgent transfer. With a “normal” ECG and a senior colleague that signed off on it, I didn’t feel confident giving TNK without cardiologist recommendation, and he said not to.
The pain resolved. Three hours later the patient had an episode of bradycardia, but remained painfree, and the ECG was repeated:
Resolution of ST/T changes suggesting reperfusion
In the morning the patient remained pain free. A repeat troponin rose to 1785 and the ECG was repeated:
Nearly normal ECG, so artery is still open but at risk for reocclusion.
The patient was prepared for transfer but due to bad weather there was further delay of the flight. Troponin rose to 8495. Three days after the episode of chest pain, the angiogram found 80% mid LAD stenosis with TIMI 3 flow, and a 2mm first diagonal artery with 95% stenosis and no TIMI flow listed. Circumflex artery was normal. Echo showed normal LV function. Follow up ECGs are not available, but would likely show reperfusion T wave inversion in the high lateral leads.
The interventional cardiologist attributed the MI to a the mid LAD not the first diagonal, writing that “[patient] had recanalized but was likely a totally occluded LAD prior to the first electrocardiogram…If the LAD had been totally occluded mid-vessel at the time of the first electrocardiogram I could expert 3 to 4mm or greater of ST elevations across the entire precordial leads. The subtle anterior ST segment elevations suggest only a transient occlusion.”
But the first ECG did not show reperfusion of the mid LAD, it showed occlusion of the first diagonal.
The patient was very lucky they did not lose more myocardium. First, the patient could have been sent home after two ‘normal’ ECGs and a normal-minimal troponin, but was fortunate to have a physician who looked for and identified OMI and was not dissuaded by the automated interpretation, or the early troponin levels, or a senior colleague signing off they were normal. Secondly, the patient spontaneously reperfused and was lucky to not reocclude during the prolonged delay to cath. But myocardial salvage should not depend on good luck.
If the patient had not spontaneously reperfused they could have had a cardiac arrest without ever receiving reperfusion therapy despite their first ECG being diagnostic of an occluded artery. On the other hand, if the interventionalist had been convinced of OMI the patient could have received thrombolytics and early transfer after the first ECG, without waiting for a troponin rise, and could have reduced the size of the infarct.
Here’s the Queen of Hearts interpretation of the first ECG:
I think the real advantage of shift to OMI - and AI - is to identify patients that will benefit from early intervention. This has huge implications for rural and remote communities, which involve major resource decisions like booking urgent flights, and high risk decisions like giving thrombolytics. Our STEMIs would get flown out as soon as a plane is available (typically 3-4h, may be up to 8h), whereas Non-STEMIs can wait days, like this patient.
McLaren comment: This case illustrates both quality gaps under the STEMI paradigm, and opportunities for improvement through the OMI paradigm shift:
1. STEMI criteria routinely miss OMI
2. Computer intepretations not only miss OMI but can label them ‘normal’
3. Initial troponin(s) after acute symptoms are falsely reassuring
4. >25% ‘NonSTEMI’ have totally occluded arteries and higher mortality
5. OMI can be learned by individuals, and AI based on OMI can make advances widely available. In the context of remote rural communities, this can help emergency physicians advocate for their patients, and reduce reperfusion delays by days for STEMI(-)OMI
MY Comment, by KEN GRAUER, MD (9/8/2023):
===================================
- At what point in today's case can the diagnosis of acute OMI (Occlusion-based MI) be made with confidence (at least with the diagnosis of OMI until proven otherwise)?
- Once the diagnosis of acute OMI is made in today’s case — Does this merit immediate plane transport to a 24/7 cath-capable facility? If so — WHY?
- What are the Lessons to Learn from today's case?
- As you comtemplate the above issues to address — Take another LOOK at these first 2 ECGs in today's case. Keep in mind the presenting History (ie, a 50yo presenting to a rural ED with a 1-hour history of CP radiating to the back and jaw — and an initial ECG labeled as "normal" by the computer interpretation).
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| Figure-1: The first 2 tracings in today's case. |
- The ST-T wave in lead aVL of ECG #1 is hyperacute. Perhaps the reason the consulting cardiologist did not appreciate the ST-T wave abnormality in this lead — is that the size of the T wave in lead aVL is not large. But we can not expect this T wave to be "large" — because overall QRS amplitude in lead aVL is so tiny. What counts is not "how tall" the T wave in lead aVL is, but rather how disproportionate the ST-T wave is (ie, with the T wave in lead aVL being nearly twice the height of the tiny r wave in this lead — in association with a proportionately very much widened T wave base in lead aVL).
- The ST elevation in the other high-lateral lead ( = lead I) is also abnormal. In the context of the abnormal ST-T wave appearance in lead aVL — the upward sloping, but clearly elevated ST segment in lead I should not be interpreted as a repolarization variant.
- Any doubt about potential "acuity" of these high-lateral lead ST-T wave findings in leads I and aVL — should be instantly removed on seeing the ST segment straightening and mirror-image opposite (reciprocal) ST depression in leads III and aVF. Once again, it is the disproportionality of the ST-T wave change that tells us the hypervoluminous depression (especially in lead III) — can not be normal given, the tiny size of the R wave in this lead.
- The Lesson: T wave height is much less important than the shape and proportionality of the ST-T wave, relative to QRS amplitude in the lead being looked at. In a patient with new CP — the above described ST-T wave changes showing marked disproportionality in leads I, III, aVL and aVF of ECG #1 — have to be recognized as hyperacute changes that are diagnostic of acute OMI until proven otherwise.
- The Need for Immediate Transport? As per Dr. McLaren — today's patient was lucky in that the acute coronary occlusion spontaneously reperfused — and the patient remained pain-free. As we've emphasized on numerous occasions in Dr. Smith's ECG Blog — the problem is that spontaneous reclosure of the "culprit" artery could have occurred at any point in time, potentially with lethal consequence. As a result — Optimal management should have been for the interventional cardiologist to recognize the OMI on the basis of the new CP history in association with the above described initial ECG changes. Prompt transfer to a cath-capable center should have been arranged right after the initial ECG was recorded.
- The ST-T wave appearance in ECG #1 brings to mind the possibility of the South African Flag pattern — in which there is ST elevation (or hyperacute T waves) in lateral limb leads I and aVL — reciprocal ST-T wave depression in lead III — and ST elevation in lead V2, but not in any of the other chest leads (Note how these 4 leads follow the GREEN marking of the South African Flag in the visual that appears above ECG #1 in Figure-1).
- As we have reported on in a number of posts in Dr. Smith's ECG Blog (Please see My Comment at the bottom of the page in the April 4, 2022 post and in the January 12, 2023 post) — the South African Flag pattern suggests that there may be acute OMI of either the 1st or 2nd Diagonal Branch of the LAD.
- Returning to the chest leads in the initial ECG in Figure-1 — there is slight ST elevation in lead V2 — but none in lead V3. Although baseline artifact makes assessment of the ST-T wave in leads V4 and V6 difficult — there does not appear to be ST elevation in lateral chest leads V4,V5,V6.
- Limb lead findings in ECG #2 look more hyperacute than they did in ECG #1 — because of subtle-but-real increased ST segment straightening in leads I, III and aVL.
- Chest lead findings in ECG #2 are are more pronounced than they were in ECG #1 — with now definite straightening of the ST segment in lead V2 — as well as ST flattening and depression now clearly seen in lead V3.
- IMPRESSION: I thought ST-T wave findings in ECG #2 were now highly suggestive of the South African Flag Sign — given hyperacute ST elevation in leads I and aVL — with reciprocal ST depression in lead III (also in aVF) — and with definite straightening of the ST segment takeoff in lead V2, which clearly looks different than the lack of ST elevation in any other chest lead (and with ST flattening and depression in lead V3). These ECG findings are consistent with results of cardiac catheterization showing 95% narrowing of the 1st Diagonal, with no indication of TIMI flow.
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