A 50-something with sudden severe epigastric and chest pain presented looking extremely ill.
Here is her ECG:
There is ST Elevation in V2-V6, worrisome for ischemia.
Or is it?
Notice the very large R-waves and the very prominent J-point notching, with small S-waves.
This is typical of Benign T-wave Inversion, which is commonly seen in black patients of African heritage.
This case was sent from Australia and the patient was aboriginal. I have never heard of or seen benign T-wave inversion in Australian aboriginal blacks.
The cath lab was activated and the patient was taken for angiogram, which was normal.
The lipase returned at 16,000. The patient had pancreatitis.
One other tip: Pancreatitis often causes chest pain, but usually has severe epigastric tenderness; acute MI, though it may cause epigastric pain, usually does not have severe epigastric tenderness.
If the patient did have severe tenderness, and you recognize this benign pattern on the ECG, then you would be dissuaded from activating the cath lab.
If there was no other etiology of pain found, and you are not certain about the ECG, it is of course not wrong to activate the cath lab.
In either pathology, the patient may appear very ill.
The link above has 11 cases, one of which is this one (if you only want to read one):
15 yo AAM with ST Elevation and T-wave Inversion. Hypertrophic Cardiomyopathy or Normal ("Variant")?
Here is her ECG:
What do you think? |
There is ST Elevation in V2-V6, worrisome for ischemia.
Or is it?
Notice the very large R-waves and the very prominent J-point notching, with small S-waves.
This is typical of Benign T-wave Inversion, which is commonly seen in black patients of African heritage.
This case was sent from Australia and the patient was aboriginal. I have never heard of or seen benign T-wave inversion in Australian aboriginal blacks.
The cath lab was activated and the patient was taken for angiogram, which was normal.
The lipase returned at 16,000. The patient had pancreatitis.
One other tip: Pancreatitis often causes chest pain, but usually has severe epigastric tenderness; acute MI, though it may cause epigastric pain, usually does not have severe epigastric tenderness.
If the patient did have severe tenderness, and you recognize this benign pattern on the ECG, then you would be dissuaded from activating the cath lab.
If there was no other etiology of pain found, and you are not certain about the ECG, it is of course not wrong to activate the cath lab.
In either pathology, the patient may appear very ill.
The link above has 11 cases, one of which is this one (if you only want to read one):
15 yo AAM with ST Elevation and T-wave Inversion. Hypertrophic Cardiomyopathy or Normal ("Variant")?
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MY Comment by KEN GRAUER, MD (11/28/2019):
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Interesting case, that at least in part reflects a repolarization variant — since acute cardiac catheterization was done, and was found to be normal. That said — I’ll offer a somewhat different perspective on this case, in that I’m not entirely convinced ( = my opinion) that all ECG findings are solely the result of a repolarization pattern.
- For clarity — I’ve reproduced and labeled the ECG in Figure-1.
Figure-1: The ECG in this case (See text). |
The patient in this case was a 50-something black aboriginal woman, who presented with sudden severe epigastric and chest pain. She looked extremely ill, and was found to have a markedly increased serum lipase consistent with acute pancreatitis.
As per Dr. Smith — ECG findings of concern in Figure-1 for a possible acute cardiac event include:
- ST segment coving with slight elevation in the chest leads.
- Fairly deep and symmetric T wave inversion in multiple leads.
On the other hand — ECG findings suggestive of a repolarization variant include:
- Prominent J-point notching — which is especially marked in lead V3, and also well seen in lead V2 (PURPLE arrows in Figure-1).
- A typical upsloping shape to the ST segments in leads V2 and V3, leading to T wave inversion — in a pattern similar to a number of the repolarization variants shown in the link provided by Dr. Smith at the end of his comment.
Additional ECG findings against this being acute OMI include:
- Voltage for LVH in lead aVL (that clearly surpasses the R wave amplitude criterion in this lead, which is 12 mm). Generous R wave amplitude in other chest leads. There is also T wave inversion in high lateral leads I and aVL (as well as in the lateral chest leads) — although the slowly downsloping ST depression typical of LV “strain” is lacking ...
- The unusual finding of small-but-definite q waves in 5 of the 6 chest leads (BLUE arrows). Most of the time when small q waves of similar size are seen across multiple chest leads (as in Figure-1) — it is not the result of infarction.
- PEARL: Awareness of the fact that diffuse ST-T wave abnormalities are surprisingly common with cases of severe acute pancreatitis (See HERE).
MY THOUGHTS: This is clearly a difficult case — and I completely agree with Dr. Smith that the providers cannot be faulted for activating the cath lab. I thought the ECG findings in Figure-1 were most likely the result of a combination of factors:
- I suspect this patient has J-point notching and a component of ST-T wave abnormalities consistent with benign T wave inversion in black patients of African heritage.
- In Addition — this ECG suggests LVH (marked increase in QRS amplitude in lead aVL in a 50-something black patient). At least some of the lateral T wave inversion we see may be the result of LV “strain”.
- To me — the ST segments (before they transition to T wave inversion) — just look “different” from most repolarization variants I’m used to seeing, in that the ST segment is not as coved, and not as upsloping.
- MY THEORY — I think this patient has LVH + a component of non-ischemic T wave inversion as a result of her severe acute case of pancreatitis (which is known to cause ST-T wave abnormalities) — both of which are superimposed on top of a baseline repolarization variant.
- The Way to Find Out — Without additional information — I don’t believe we can fully attribute the ECG findings in Figure-1 to a benign repolarization variant. We Need: i) more history (Is this patient hypertensive?); ii) an Echo (Is there significant LVH?); and, iii) either a baseline ECG for comparison and/or a follow-up ECG on this patient after her acute illness has resolved. Until then — the most I’d be comfortable saying is that this ECG most probably does not reflect acute OMI.
Our THANKS to Dr. Smith for presenting this interesting case!
The rhythm is sinus with a rate of 65 bpm, but the voltage of the QRS is suggestive of LVH, because R in I + S in III is more than 25 mm as well as RaVL is more than 11 mm. The QRS axis is -30° and R wave progression is abnormal too, since the transition occurs in V2.. The T wave could be abnormal by this?
ReplyDelete@ Unknown — Your question came in BEFORE I had an opportunity to write out my comment. I agree entirely with the point you raise (Please See My Comment above — :)
DeleteHow would you comment on small q waves in V2-3?
ReplyDeleteAstute observation Maks! Your question was asked BEFORE I wrote my comment (There is always a slight lag between the time Drs. Smith/Meyers publish their cases — that I only then get to see and review). BLUE arrows in my Figure-1 (above) highlight small q waves in actually 5 of the 6 chest leads. While the lateral chest lead q waves that are small and narrow are almost certainly “normal septal q waves” — one clearly does not see “septal q waves” as anteriorly as V2,V3. I see this finding on occasion. I’ve seen literature suggesting that in older patients it may be due to a “tortuous aorta”. In younger or middle-aged patients, this is highly unlikely. Small anterior q waves could reflect scar as in prior infarction or cardiomyopathy — but most of the time in my experience, it doesn’t. When I see this finding — I simply note in the Descriptive Analysis portion of my interpretation that, “there are small and narrow q waves in leads V2-V6”. Then I “Suggest clinical correlation”. That said, as I note above — in the vast majority of cases when I see similar-looking q waves as we have here — it is not the result of infarction (especially if ST-T waves do not suggest acute OMI). THANKS again for your question!
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