Case 1.
A middle aged male presented with chest pain.
Here is his ECG (Figure 1):
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| What do you think? |
Interpretation: All repolarization abnormalities, dramatic as they may seem, are consistent with the huge QRS voltage present and thus with "secondary" repolarization abnormalities (abnormal repolarization sedondary to, or as a result of, depolarization abnormalities of LVH). There may be ischemia present, but it is not evident on the ECG. Importantly, all ST-T abnormalities are discordant to (in the opposite direction of) the majority of the QRS)
Indeed, this was the patient's baseline ECG. All troponins were negative. Echo showed massive concentric LVH.
In this paper, Dr. Birnbaum writes: "In patients with ACS without LVH, ST depression with negative T waves in the lateral leads is a sign of sub-endocardial ischemia and is an independent predictor of adverse outcome [11–13] . Some experts advocate that in ischemic ST depression, the negative T waves are symmetrical, whereas in cases secondary to LVH, the T waves are asymmetrical. However, no study has evaluated the accuracy of this sign."
But by far the biggest clue that it is not ischemic is the voltage, not the symmetry.
So the above ECG has slightly assymetrical inverted T-waves. Here are a couple examples of Wellens' Pattern B (deep, symmetric) waves (Figure 1b):
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| From Wellens' first paper: see the right panel. The T-waves really are more symmetric than the ones above. |
Case 2.
In LVH, T-wave inversions are usually much more assymetric, like these (Figure 2):
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| Acute Chest pain, but baseline ECG. No MI. |
Case 3.
And sometimes the lateral T-wave is biphasic, with the terminal portion more upright (Figure 3):
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| Acute chest pain. Baseline EKG, no MI. |
Case 4.
And sometimes the LVH is most prominent in limb leads, with high voltage in aVL. This one mimics inferior STEMI (Figure 4):
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| Concentric LVH, NO wall motion abnormality |
Case 5.
Figure 5. Contrast the above with this one, which has both LVH and inferior STEMI:
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| There is limb lead LVH with superimposed inferior STEMI. For details, read this post. |
How about diagnosing anterior STEMI in the setting of LVH?
Notice the right precordial (V1-V3) ST elevation in Figures 3 and 4 above.
Case 6.
Figure 6. Worrisome ST elevation in LVH usually happens in the precordial leads, mimicking Anterior STEMI, like this one (Figure 6):
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| Acute Chest Pain. When I saw this, I knew immediately that this is the patient's baseline ECG, with no MI. Notice the S-wave in V2 is 45 mm. There is no ST elevation beyond V2. ST elevation in V2 is about 3.5 mm, and not more than 4 mm. |
Armstrong EJ et al. Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy. October 1, 2012; Volume 110, Issue 7, Pages 977–983.
In this paper, the authors study LVH vs. MI and conclude that an ST/S ratio of 0.25 or greater (similar to the modified Sgarbossa criteria for LBBB) should be used to determine if there is STEMI in the presence of LVH. This paper did not use the correct methodology, in my opinion, and came up with a result that is too insensitive for STEMI.
The appropriate methodology for such a study would be to find cases of LVH with secondary ST elevation and compare them with cases of LVH and "primary" (ischemic) ST elevation. I have tried this twice and failed because I could not find enough cases of LVH with anterior STEMI. They are quite rare. I believe the reason for this rarity is that, when patients with LVH have an LAD occlusion, it greatly diminishes the QRS voltage and the LVH on the ECG disappears!
In Figure 6, they would require 12 mm of ST elevation in lead V2 to diagnose STEMI. I believe that if this patient suffered an LAD occlusion, the S-wave amplitude would dramatically fall, probably so much that it would no longer look like LVH, and it would not be difficult to diagnose STEMI.
The bottom line is this: when there is LVH in precordial leads, there will often be discordant ST elevation in right precordial leads. It will be proportional to the QRS amplitude, probably about 10:1 or less.
Case 7.
Figure 7. This patient with LVH had chest pain (Figure 7)
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| LVH with ST-T abnormalities with superimposed ischemia. The computer algorithm erroneously read this as "LVH with secondary repol abnormalities" This patient had an acutely occluded bypass graft to the first diagonal, but with good collateral circulation so that there is only subendocardial ischemia. Notice there is concordant ST depression in V3 and V4. Tropoinin I peaked at 22 and there was a pre-existing posterolateral WMA |
Case 8.
Here is another patient with severe LVH who presented with chest pain and ruled out for MI.
Figure 8a. Presentation ECG:
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| Believe it or not, this is not the same patient as the at the top of this post. I double-checked! These are baseline ST-T abnormalities |
Figure 8b. Here is the same patient's previous ECG:
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| There are slight differences, including the PACs, but there was no acute MI. |
Very educational post. I learned so much. Is there RBBB in ECG of the figure 8b?
ReplyDeleteThank you for the kind words. YES — there is RBBB in Figure 8b. The QRS is wide — there is an rSR’ in lead V1 — and there are wide terminal S waves in lateral leads I and V6 — so this satisfies criteria for RBBB — :)
DeleteSo sorry for disturbing but if a patient comes in with chest pain, the ecg shows a left strain pattern, but trop I is negative. Would you still treat it as ACS?
ReplyDeleteNot if they looked like those above and did not have any dynamic changes. I might to an echo to rule out wall motion abnormality. I would give aspirin, and if the clinical situation was very suspicious, I would treat for ACS up to and including angiogram, but not because of the EKG -- because of any other worrisome factors.
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