Written by Jesse McLaren
A 65 year old with diabetes presented with a syncopal episode while sitting, associated with weakness but no chest pain or shortness of breath. Vital signs were normal and first ECG was labeled as normal by the computer and confirmed by the treating emergency physician and cardiology over-read. What do you think?
There’s normal sinus rhythm, normal conduction, normal axis,
normal R wave progression, and normal voltages with J waves from early repolarization. There's inferior down-up ST segments and hyperacute T waves, with reciprocal up-down T wave in aVL.
I sent this "normal" ECG without any information to a number of ECG enthusiasts, who were all concerned about possible OMI - whether subtle high lateral OMI with inferior reciprocal change, or subtle inferior OMI with high lateral reciprocal change.
First troponin I came back at 2,800 ng/L (normal <16 in females and <26 in males), and a repeat ECG was done:
There’s wandering baseline that makes it difficult to interpret, but there's no longer inferior ST depression and T waves are smaller. There is residual minimal ST elevation from early repolarization.
Because of the syncope and troponin elevation the patient was referred to cardiology as cardiac syncope. Repeat troponin declined to 2,500 and repeat ECG ECG was done after another 2 hours, also interpreted as normal. Repeat trop declined to 2,500, and another ECG was done:
(Marqette 12SL algorithm)
Similar to prior. The cardiologists were concerned the second ECG might have shows subtle inferior ST elevation indicative, which could be associated with RCA occlusion that could have produced heart block leading to syncope. So they took the patient urgently to cath: 100% occlusion of inferior obtuse marginal branch of the circumflex, with collateral circulation. Had the cardiologists followed NSTEMI or transient STEMI guidelines, which recommend non-urgent cath, the patient could have redeveloped an OMI and had a worse outcome.
But this foresight will not be recorded, because the patient was diagnosed as "transient STEMI", even though no ECG ever met STEMI criteria. In fact the only ST elevation was baseline elevation from early repolarization, and relative to that the patient only had ST depression and hyperacute T waves. So this was transient STEMI(-)OMI, not transient STEMI.
Discharge ECG had small inferior T waves and subtle reperfusion TWI in V5-6
Here's a comparison of initial and discharge ECGs:
This confirms the initial ECG had inferior ST depression followed by hyperacute T waves (deWinter), and also lateral hyperacute T waves V4-6. On discharge the inferior deWinter waves resolved and the lateral T waves deflated and inverted.
Take home
1. Syncope is an uncommon presentation of ACS, but anginal equivalents are more likely in older patients with diabetes
2. Circumflex occlusions can have subtle to no ECG changes
3. You can’t trust ECG's labeled "normal"
4. Hyperacute T waves and reciprocal change can help identify STEMI(-)OMI
5. Arteries can be totally occluded with flow intermittently maintained by collaterals
6. deWinter waves can happen in any coronary artery: see this case and this case
- Infarction was diagnosed in today's case by the findings of i) Significantly elevated Troponin; ii) 100% occlusion of the inferior obtuse marginal branch of the LCx, albeit with collateral circulation; and, iii) Subtle ECG changes on serial tracings, including suggestion of reperfusion T waves.
PEARL #1: Not all patients with acute MI report chest pain. The Framingham studies from many years ago taught us that the incidence of “Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).
- The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
- In the other half of this 30% (ie, in ~15% of all patients with MI) — patients found on follow-up ECG to have had infarction did not have chest pain — but they did have “something else” thought to be associated with their MI.
- The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
- BOTTOM Line: Be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is sometimes appreciated. Not all patients with acute (or recent) MI have chest pain.
- Cardiac syncope was found in ~9% of patients in the Framingham studies. That said — the actual percentage of patients with cardiac syncope was clearly higher than this in Framingham, as up to 1/3 of patients had syncope of unknown cause. This data highlights the point made above by Dr. McLaren — that diagnostic cath of today's patient (despite the lack of STEMI criteria) may have been lifesaving!
- Syncope is not a common cause of acute MI. That said — syncope more often is encountered as a consequence of an acute MI. Potential mechanisms that may cause syncope in association with acute MI include: i) A cardioinhibitory and vasodepressor reflex response resulting from vagal stimulation (most commonly seen with acute inferior MI); ii) Development of high-grade AV block (also more common with acute inferior MI); and/or, iii) Sustained VT (which is fortunately much less common in the acute reperfusion era).
- As per Dr. McLaren — the initial ECG in today's case is cause for concern: i) There are hyperacute T waves in each of the inferior leads — as determined by being "fatter"-at-their-peak and wider-at-their-base than expected (especially in lead III — in which the T wave dwarfs the QRS in this lead); and, ii) The tiny QRS complex in lead aVL is associated with a decidedly coved ST segment with T wave inversion in a shape that is clearly not normal.
- Chest lead findings in ECG #1 are nonspecific and not diagnostic.
- Impression of ECG #1: While it may clearly be challenging to know what to do with this initial ECG in the absence of chest pain — the likelihood of recent or ongoing acute OMI as the cause of this older patient's syncope increased dramatically the moment the 1st troponin came back elevated!
- Putting It All Together: Syncope (as the presenting symptom) + hyperacute changes on ECG #1 + a 1st Troponin = 2,800 ng/L — should be enough to indicate the need for prompt cardiac catheterization.
- Fortunately in today's case — the cardiology team became concerned enough about subtle inferior lead ST elevation 2 hours after ECG #2 was done, that they performed cardiac cath which made the diagnosis.
- MY Point: ECG #2 does not provide clear indication of how to proceed! Although true that it looks as if there now is some inferior lead ST elevation that was not present in ECG #1 — Bad data in means bad data out! — In my opinion, ECG #2 is not interpretable in this patient in whom you are very concerned may be in the midst of an acutely evolving infarction. This is because there is so much artifact in the 5 beats shown in the limb leads as to leave me with no idea about what is "real" vs artifact. This 2nd ECG should have been immediately repeated.
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| Figure-1: The first 2 ECGs in today's case. |
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