Saturday, August 22, 2020

Dynamic ST Change in a mid-50s Man with Chest Pain

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MY Comment by KEN GRAUER, MD (8/21/2020):
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The patient is a mid-50s man who presented to the ED for new-onset chest pain of ~1 hour duration. His symptoms awakened him from sleep. He was still having chest pain in the ED at the time ECG #1 was done (Figure-1).

QUESTION:
  • HOW would YOU interpret his initial ECG that is shown in Figure-1?

Figure-1: The initial ECG in this case (See text).



MY THOUGHTS on ECG #1: Although significant baseline artifact is seen (especially in the limb leads) — the tracing is clearly interpretable. The rhythm is sinus at ~80-85/minute — the PR, QRS and QTc intervals are normal — and the frontal plane axis is normal (about +50 degrees).
  • There is lots of voltage in the chest leads (ie, The R wave in lead V5 =25mm satisfies voltage criteria for LVH).
  • Transition occurs normally between leads V2-to-V3 — albeit transition from a negative-to-a-positive complex is abrupt, with dramatically increased R wave amplitude (~30 mm) already seen in lead V3.
  • There are small and narrow Q waves beginning in lead V3 — and continuing through to lead V6 (with small q waves also seen in leads I and aVL).
  • The most concerning finding in ECG #1 relates to T wave morphology — especially for the T wave in lead V2 that clearly appears to be disproportionately tall with respect to the small-amplitude QRS complex in this lead.
  • T waves in other chest leads are of far less concern. There is no more than minimal (not necessarily abnormal) ST elevation in leads V2, V3 and V4 — with an upward concavity (ie, “smiley”-configurationshape to the ST segment with J-point notching in lead V3 (and possibly also in lead V4).
  • I thought assessment of the ST-T wave in lead V1 was not helpful. Whereas the 1st and 3rd complexes in this lead seem to show a more-than-usual amount of ST elevation — there is no ST elevation in the 2nd complex, and artifact is distorting, producing a somewhat different ST segment shape for each of the 3 complexes in this lead.
  • Finally — there are some subtle findings in 3 of the limb leads that I was uncertain about. These were: iSuggestion of ST segment flattening in leads III and aVF (compared to a normal appearance of gently upsloping ST segments that we see in leads I and II)andii) Suggestion of ST segment coving and ever-so-slight elevation (with shallow T wave inversion) in lead aVL. The task of determining IF these subtle findings are real and significant is made all-the-more difficult by the baseline artifact that we see.

BOTTOM Line Regarding ECG #1: In the setting of new-onset, ischemic-sounding chest pain in this 50-something man — I was concerned  that in lead V2, the slightly elevated ST segment, with disproportionately tall T wave might represent a hyperacute change — and, in that context — that the subtle findings I note above in leads III, aVF and aVL might be real.
  • Other findings on this tracing were potentially consistent with a repolarization variant. These included: i) A normal QTc interval; ii) Marked increase in QRS amplitude in anterior leads; iii) Each of the Q waves in this tracing (ie, in leads I, aVL; and V3-thru-V6) are small and narrow in size; andiv) Other than in lead V2 — the amount of ST elevation; the J-point notching; the “shape” of the ST segment and T wave amplitude with respect to R wave amplitude in each of the chest leads seems proportional and consistent with a repolarization variant.


The Case Continues: Initial troponin was normal. The cath lab was not activated at this time. The patient was treated with aspirin, nitroglycerin and IV morphine. His symptoms improved — but he was still having chest pain 45 minutes later when ECG #2 was obtained (Figure-2).

QUESTION:
  • After seeing ECG #2 — What are YOUR thoughts on this case?

Figure-2: The 2nd ECG that was done 45 minutes later in this case (See text).



MY THOUGHTS on ECG #2: My initial impression after seeing ECG #2 — was that overall QRS amplitude and the shape of ST-T waves was similar to ST-T wave appearance in ECG #1.
  • QUESTION: Did YOU Note any significant difference(s) between these 2 tracings?


MY Confession: In my haste to assess the follow-up ECG ( = ECG #2) — I failed to put the 2 tracings next to each other. Instead — I simply flipped from looking at the 12 leads in ECG #1 in one glance — and then looking at all 12-leads in ECG #2 in the next glance ...
  • PEARL #1: The most time-efficient way to compare 2 serial tracings is after you have completely interpreted the 1st tracing (as I do above) — Then, to put both ECGs right next to each other — And then, to proceed with a lead-by-lead comparison of the 2 tracings. See how much EASIER this becomes by looking at Figure-3.

Figure-3: I’ve put the 2 tracings in this case together. See how much EASIER it now is to do a lead-by-lead comparison between the 2 tracings (See text).



Lead-by-Lead Comparison in Figure-3: There is less baseline artifact in ECG #2 compared to ECG #1. Of note, the frontal plane axis is the same — and there is no significant change in either QRS amplitude or QRS morphology in any of the 12 leads between the 2 tracings. As a result — any change in ST-T wave morphology will be real — and not the result of a change in axis or lead placement.
  • The rhythm is sinus in both tracings — but the heart rate is slower in ECG #2 (ie, about 65/minute — compared to ~85/minute in ECG #1).
  • I see no change in ST-T wave appearance in any of the limb leads.
  • But there is a definite change in the amount of ST elevation between the 2 tracings! In Figure-3 — the horizontal, dotted RED lines drawn in leads V2-thru-V5 clearly show a notable increase in ST elevation in ECG #2.
  • It now is valid to assess ST-T wave appearance in lead V1 of ECG #2 — since the artifact in this lead is now minimal. Unlike what we saw in ECG #1 — both QRS complexes in lead V1 of ECG #2 now look the same. I thought the T wave to be taller and there to be more J-point ST elevation in lead V1 of ECG #2 than is usually seen in this lead.

BOTTOM Line Regarding Figure-3: I still was not convinced that the overall appearance of ECG #2 was not the result of a repolarization variant — especially given the similar peaked shape of T waves in 10 of the 12 leads and the lack of reciprocal ST depression (despite ST elevation beginning as early as in lead V1).
  • PEARL #2 — As emphasized by Dr. Smith in the July 24, 2013 post in Dr. Smith’s ECG Blog — the ST-T wave appearance in repolarization variants may be dynamic! On occasion — ST-T wave appearance with repolarization variants may change from one-hour-to-the-next — or, ST-T wave appearance may change due to a difference in heart rate, performance of exercise, or variation in vagal tone — and, sometimes even without any obvious explanation.
  • This Pearl #2 notwithstanding — the change that we see in Figure-3 regarding the increased amount of ST elevation in multiple leads of ECG #2 qualifies as a dynamic ST-T wave change in this patient with ongoing chest pain. As a result — I thought cardiac cath was clearly indicated to clarify the clinical picture.


Follow-up in this Case: Based on ECG #2 — cardiac cath was performed. The angiogram showed completely normal vessels (No evidence of coronary disease!). Serial troponins were normal. LV function was normal on cath and Echo. The patient was discharged from the hospital.


Dr. Smith's Comments: I shared this case with Dr. SmithHis Thoughts: “ECG #1 does not look like OMI at all. It is a repolarization variant with J-waves in leads V2 and V3 (this is not terminal QRS distortion). But in ECG #2 — the amount of ST elevation increases from 1mm to 3mm in leads V2 and V3. However, the heart rate is very different between the 2 tracings — and I think this difference accounts for the change in ST elevation. Moreover, formula values are 15.97 for ECG #1 and 16.68 for ECG #2 — both values being very low (normal)."  

Additional comment by Smith: you might be very reluctant to call this change negative, and it might very well be considered risky to NOT activate the cath lab.  But there is an alternative, if availalble, for these difficult situations: emergent high quality echo with contrast, or Strain Speckle Tracking Echocardiography (if you have it and know how to use it). Absence of a wall motion abnormality in the anterior wall, septum, and apex would rule out OMI.

Learning Points:
  • The BEST way to compare serial ECGs — is to completely interpret one of the tracings first — and then to put both tracings together (as was done in Figure-3) as you go about lead-to-lead comparison. This makes it EASIER to appreciate differences between the 2 ECGs.
  • On occasion — repolarization variants may show dynamic ST-T wave changes on serial tracings. This is especially true if there has been a change in heart rate.
  • The finding of dynamic ST-T wave changes on serial ECGs, in association with ongoing chest pain is an indication for cardiac cath.
  • Final PEARL: Considering that the completely normal cardiac cath and serial troponins confirmed that the ECGs in this case represented a repolarization variant — it is helpful to appreciate that the abrupt transition that we see in lead V2 in both tracings (from a predominantly negative QRS in lead V1 — to a dramatic increase in positive R wave amplitude in lead V3) is the likely reason why the T wave in lead V2 of both tracings initially looked so disproportionately tall! We now know this T wave in lead V2 was not hyperacute — but simply a reflection of abrupt transition causing slight lag in development of the tall R wave until lead V3.

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NOTE: My sincere THANKS to Dr. Tharindu Uyanage (of Australia) for sharing the tracings and this case with us!
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4 comments:

  1. What about the appearance of the inferior leads with perhaps some depression and a suggestion of some elevation in Avl with that appearance of the fattened t wave in v2? That would concern you for Omi, no?

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    1. @ PM — Your question IS valid — and we acknowledge this in comments above both by Dr. Smith and myself. After seeing ECG #2, I wrote above — “I thought cardiac cath was clearly indicated to clarify the clinical picture”. I was not yet convinced that we were not seeing a repolarization variant — but given the differences in the 2 ECGs and the symptoms, I would have wanted to be certain — so I thought activation of the cath lab at this time (as was done) was completely appropriate.

      Dr. Smith was more certain than I for the reasons he cites, that despite the ECG findings you mention — this was not ACS. I’ve learned to totally respect his “eye” and experience in recognizing these cases. That said, Dr. Smith does acknowledge that it wouldn’t be wrong to activate the cath lab (to be completely sure) — but he suggests an alternative (if available in your institution) = Strain Speckle Tracking Echo — which in the hands of experts could have allowed you to rule out ACS without need for cath.

      THANKS again for your excellent question! — :)

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  2. This is a very humbling post. I too, thought that the second ECG was very worrying.
    This blog always reminds me that I can NEVER be ALWAYS sure of anything.

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    Replies
    1. THANKS for your comment Ken! Yes — being a clinician on the "front lines" is always a humbling experience! We ALL are learning every day. One of the KEY lessons from this case is that even if you suspect these 2 ECGs reflect a normal repolarization variant which changes from one tracing to the next — it is 100% appropriate to err on the side of caution and proceed to cardiac cath! Alternatively — Dr. Smith presented some other tools (above) that could be used to increase your degree of certainty. But if in doubt — best to be prudent in cases like this in which there IS a change in ST-T wave morphology on serial tracings.

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