- For clarity in Figure-1 — I've reproduced the initial tracing in today's case, together with mirror-image blow-ups of the QRST in leads V3 and V4.
- As per our most recent referral to this phenomenon (See My Comment in the April 2, 2023 post in Dr. Smith's ECG Blog) — ST-T wave changes of LV “strain” most often manifest in one or more of the lateral leads. But instead of seeing ST-T wave changes of LV “strain” in lateral leads — some patients manifest a “mirror-image” of strain in anterior leads. The especially peaked shape of the elevated ST-T waves in leads V2,V3 in Figure-1 could reflect LV “strain” in this patient with extremely deep S waves in these 2 anterior leads. Doesn’t the mirror-image of the ST-T waves in the RED insert for lead V3 in Figure-1 look consistent with how LV “strain” might look in the lateral leads of a patient with marked hypertension?
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| Figure-1: The initial ECG in today's case (See text). |
- As noted above — The ST-T wave appearance of in leads V2,V3 in Figure-1 could be completely consistent with the appearance of LV "strain" in anterior leads.
- In contrast — the ST-T wave in lead V4 looks disproportionately tall (as well as hypervoluminous) compared to the modest QRS amplitude in this lead. Similarly, the mirror-image of the ST-T wave in lead V4 (RED insert) — looks disproportionately more negative-than-would-be-expected for LVH strain.
- Support that the ST-T wave appearance in lead V4 is potentially concerning (beyond simply reflecting a "transition lead" between the predominantly negative QRS in V3 and the all-positive QRS in V5) — is forthcoming from the ST-T appearance in lead V5. In view of how marked LVH in this patient is likely to be (given the S wave = 26 mm in lead V3) — I would have at least expected a "blunted" ST-T wave pattern of "strain" in lateral lead V5 if all ECG changes were the result of LVH, instead of an unexpected upright T wave in this lead (ie, Note that lead aVL does show a "blunted" ST-T wave pattern of "strain" with even less R wave amplitude than we see in lead V5).
- To Again Emphasize: Without the benefit of any history — the initial ECG in today's case is not diagnostic. But awareness of the difficulty in trying to identify acute OMI superimposed on preexisting LVH — should focus our concern on potentially disproportionate ST-T wave findings that might signal early hyperacute changes. Repeating the ECG within 15-30 minutes will usually resolve the question of acuity.
- The importance of correlating ECGs to the clinical history cannot be understated. As soon as I learned the history in today's case (ie, that today's patient had a history of documented coronary disease — and he presented with severe, new-onset chest pain) — the likelihood that the ECG findings described above in leads V4,V5 were indicative of an acute ongoing event dramatically increased!
- As per Dr. Meyers — Confirmation of an acute ongoing event was immediately forthcoming as soon as baseline ECGs on this patient were obtained.
- Confirmation of an acute ongoing event until proven otherwise was also immediately forthcoming the moment the slightly elevated initial troponin came back (ie, at a level = 25 ng/L — vs the upper normal value of 20 ng/L). As per Dr. Meyers — "an elderly patient with known CAD and ongoing ACS-sounding CP despite medical management, with positive troponin is indication for emergent cath regardless of the ECG!".
- Retrospective review of challenging cases such as today's provide invaluable insight. Seeing the distribution of subsequent ST elevation on serial tracings — and comparing this to the subtle initial findings teaches us as it shines a new light on the initial tracing.
- Finally — As truly impressive as the PM Cardio Queen of Hearts AI app is in recognizing acute OMI — it is not perfect. No computerized application should substitute for clinician oversight and judgment. Instead — Queen of Hearts is an invaluable aid to the thinking clinician — and I strongly suspect that a repeat ECG done 15-30 minutes after the initial tracing would have been interpreted as acute by both clinician and Queen of Hearts.
- The rhythm in Figure-1 is sinus at ~60/minute (ie, There are small-but-present upright P waves in front of each QRS in the long lead II rhythm strip — all manifesting a constant normal PR interval). The QRS is narrow. The QTc is not prolonged given the slow rate. The frontal plane axis is normal (about +30 degrees).
- Voltage criteria for LVH are satisfied, assuming the patient is not a young adult (ie, Peguero Criteria — given the very deep S wave = 28 mm in lead V3 — See My Comment in the June 20, 2020 post in Dr. Smith's ECG Blog for "My Take" re ECG diagnosis of LVH).
- In high-lateral leads I and aVL — there are wide Q waves (considering the small QRS amplitude) — and slight ST elevation with hyperacute-appearing T waves.
- In the inferior leads — there are mirror-image reciprocal ST-T wave changes to the slight ST elevation and peaked T wave in lead aVL.
- In leads V4 and V5 — the ST segments are completely flat, with disproportionately peaked T waves.
- In lead V6 — there is unexpected ST depression with terminal T wave positivity (unexpected given the contrast in appearance from the ST-T waves seen in neighboring leads V4,V5).
- In anterior leads V1,V2,V3 — R wave progression is delayed but an initial r wave is present in each of these 3 anterior leads. The remarkable finding is the overly peaked T waves, especially in leads V2,V3. Even with the extremely deep S wave in lead V3 — I thought the T waves in leads V2,V3 were disproportionately tall.
- "Young" adults often manifest increased QRS amplitude without true chamber enlargement. While no strict "cut-off" point for what constitutes a "younger adult" has been established — I've found voltage criteria for LVH to be a less reliable indicator of true LV chamber enlargement in adults under 35.
- Assuming today's patient is ≥35 years old — Peguero Criteria for LVH voltage would be easily exceeded (ie, Sum of deepest S in any chest lead + S in V4 ≥23mm [female] or ≥28mm [male]).
- ST-T wave changes of LV “strain” most often manifest in one or more of the lateral leads. But instead of seeing ST-T wave changes of LV “strain” in lateral leads — some patients manifest a “mirror-image” of strain in anterior leads. The unusual (unexpectedly peaked) shape of the elevated ST-T waves in leads V2,V3 in Figure-1 could reflect LV “strain” in this patient with significantly increased voltage. Doesn’t the mirror-image of these ST-T waves in the RED inserts for leads V2,V3 in Figure-1 look consistent with how LV “strain” might look in the lateral leads of a patient with marked hypertension?
- BOTTOM Line: If today's patient presented to the ED for new-onset cardiac-sounding chest pain — I would not be able to rule out an acute cardiac event from this single tracing.
- As per the follow-up provided by Dr. Smith — Negative troponins and the lack of any significant change in today's ECG from the appearance of prior tracings ruled out an acute coronary event.
- That said — I remain intellectually curious as to WHY in ECG #1 there appears to be significant LVH — and WHY there are 11/12 leads that manifest abnormal ST-T wave changes potentially consistent with some form of underlying heart disease?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
Sent by Anonymous, written by Pendell Meyers
A man in his 60s with history of CAD and 2 prior stents presented to the ED complaining of acute heavy substernal chest pain that began while eating breakfast about an hour ago, and had been persistent since then, despite EMS administering aspirin and nitroglycerin. There was associated diaphoresis, but no dyspnea, nausea, or vomiting. He reported having covid 2 weeks ago, but had seemingly fully recovered.
Triage 1104:
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| What do you think? |
The triage ECG was sent to me with no history (I did not have access to baseline ECGs), and I said that I thought this was just LVH causing the anterior STE and T waves. I told the sender that I did not see OMI. I sent this ECG (with no history, no baseline ECG) to Dr. Smith twice, months apart, and he also said LVH without clear OMI.
PM Cardio Queen of Hearts interpretation of the triage ECG: "Not OMI high confidence"
However, there were several prior / baseline ECGs on file:
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| What do you think now? (both of these ECGs are "Not OMI High Confidence" by PM Cardio Queen of Hearts AI). |
Compared to baseline, there is more STE in anterior leads, and significantly increased area under the curve of the T wave in V3 and V4. By seeing the comparison, the diagnosis is LAD OMI until proven otherwise.
The triage ECG was interpreted correctly as "No STEMI." Due to the state of the ED at the time, the patient was placed in a waiting area.
The first high sensitivity troponin I returned elevated at 25 ng/L (upper limit of normal for men in this assay is 20 ng/L). Unfortunately, the only action that was taken at this time was to repeat the troponin (still waiting in waiting area due to miserable boarding and overcrowding problems).
It is easy to say this in retrospect, especially not being the one in charge of this overcrowded waiting room full of unseen patients, but an elderly patient with known CAD and ongoing ACS-sounding chest pain despite medical management with positive troponin is already an indication for emergent cath, regardless of the ECG!
The second troponin returned higher at 45 ng/L. This finally prompted a repeat ECG at 1341:
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| Obviously STEMI(+) OMI. As expected PM Cardio Queen of Hearts AI says OMI for these. |
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| Pre-intervention. |
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| Arrows at site of occlusion. |
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| Outline of occluded portion of LAD without flow. |
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| After lesion was crossed. |
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| After intervention. |
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| STE/T waves slightly deflating compared to pre-cath ECG. |
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| Very beginning of terminal T wave inversion in V4 and V5, continued T wave deflation. |
Formal echo showed EF 20% (previous EF on file 34% 5 months ago), severe global hypokinesis, akinesis of the mid-apical myocardium, akinesis of inferolateral, inferior, and inferoseptal myocardium.
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He survived to discharge and 2 month follow up. Long term follow up not available.
Learning Points:
OMI is a clinical diagnosis, for which the ECG is a surrogate test. Sometimes the provider can see the OMI on the ECG, sometimes not even with expert training. Sometimes OMI can be recognized only comparison to the prior ECG, as it was for me in this case. In retrospect, V4 on the triage ECG seems out of normal proportions to me now. Perhaps this will help me see the next similar case sooner, to prevent the 2.5 hour delay in this case.
If you're lucky, serial ECGs can help make a difficult diagnosis into an easy diagnosis.
Comparison to baseline ECG is vital. Do not assume that a prior ECG is a baseline ECG.
Obvious ACS history with ongoing pain despite medical management and upgoing troponin is an indication for emergent cath regardless of ECG findings.
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