ECG Blog #519 — LV "Strain" or Acute MI?

The ECG in Figure-1 was obtained from a patient who presented to the ED (Emergency Department) with typical CP (Chest Pain).

QUESTIONS:

• Given this brief history — How would you interpret this ECG?
• What is in your differential diagnosis?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on this CASE:

The history in this patient who presented to the ED with typical CP is clearly worrisome — and immediately places this patient in a higher-risk group for having an acute cardiac event. This places the "burden of proof" on us as providers to rule out an acute event — rather than the other way around (ie, We need to assume the abnormal findings on this ECG represent an acute MI until we can prove otherwise!).

Looking at today’s initial ECG in Figure-1:

• The rhythm in ECG #1 is sinus at ~80/minute. All intervals (PR,QRS,QTc) and the axis are normal.
• There are deep S waves in anterior leads V2 and V3. This may represent LVH (Left Ventricular Hypertrophy).
• The principal concern in this patient with new CP are the tall T waves with ST elevation in leads V2 and V3.
• 
  
• PEARL #1: When LVH is manifest on ECG by the presence of deep anterior S waves — then LV "strain" from LVH (and not from acute infarction) may manifest as anterior ST segment elevation!

Consider the ECG in Figure-2 — which I’ve taken from ECG Blog #461:

• The BLUE arrows in Figure-2 clearly highlight significant ST elevation. However, this ST elevation is not the result of acute infarction. Instead — this patient turned out to have marked LVH without any evidence for acute ischemia or infarction (Note the very deep S waves in leads V2,V3).
• Note within the RED insert in Figure-2 how the mirror-image of the ST-T elevation in these anterior leads — looks exactly like the typical ECG picture that we are used to seeing when LV “strain” is present in the lateral chest leads.

Figure-2: Tracing from my ECG Blog #461 — in which anterior ST elevation was not because of acute MI, but instead was solely the result of LV "strain" in a patient with marked LVH!

Take another LOOK at today’s initial ECG — that I’ve reproduced in Figure-3. Keep in mind that this patient presented to the ED for new CP.

• As noted earlier — there are deep S waves in leads V2,V3. 

QUESTIONS:

• Is the ST elevation and the tall T waves that we see in these anterior leads the result of LV “strain” — or — Does it seem like these ST-T wave changes may be more than what we might expect from simple LVH?
• 
  
• In view of this patient’s CP — Is there anything we can do? (ie, to help distinguish if the anterior lead ST-T wave changes in Figure-1 are the result of LV “strain? — or acute ischemia? — or, of both LV “strain” + acute ischemia?).

Figure-3: Today’s initial ECG — that I’ve reproduced from Figure-1.

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Confession: When I first saw today’s case — I was not at all certain regarding my impression for distinguishing between LV “strain” vs acute ischemia with infarction.

• Instead — I saw features consistent with LVH (ie, the deep S waves in leads V2,V3) — and — features consistent with acute ischemic ST elevation.

For clarity in Figure-4 — I’ve labeled ECG findings prompting my concern:

• PEARL #2: The concept of “proportionality” is KEY. While fully aware from clinical examples such as the case I illustrate above in Figure-2 — T wave amplitude in leads V2,V3 in Figure-3 "looks" disproportionately increased (both of these T waves rising ~10 mm above the baseline). The base of these T waves also “looks” wider-than-I-would-expect from simple LVH.
• To Emphasize: I have no numerical numbers for telling me the “accepted size” of T waves that would be consistent with LV “strain” from LVH. Instead — I rely on “pattern recognition” that my “eye” instantly recognizes from the experience of seeing countless cases. Even then — I was still not certain of my suspicion from pattern recognition alone. 
• That said — In support of my suspicion that the T waves in leads V2,V3 are hyperacute (and potentially indicative of acute ongoing infarction) — was the following: i) The clinical setting (Today’s patient presented with new CP); — ii) Neighboring leads V1 and V4 show subtle-but-real ST segment straighteing (slanted RED lines in these leads in Figure-4); — and, iii) Subtle ST segment flattening (if not slight ST depression) is seen in lateral lead V6 (BLUE arrow in this lead) — potentially consistent with an early Precordial "Swirl" pattern (See ECG Blog #380 — for review of Precordial Swirl).
• 
  
• P.S.: Limb lead findings in ECG #1 did show some ST segment flattening — but I interpreted this as nondiagnostic. However, the above noted chest lead findings were enough to significantly increase my index of suspicion.

Figure-4: I've labeled the initial ECG.

PEARL #3: The clinical reality is that we will not always be able to confirm our clinical suspicion as to whether or not a patient's symptoms are indicative of acute ongoing infarction from a single initial ECG. Fortunately — there are some simple, routine actions that will often very quickly provide a definitive answer. Among these actions are the following:

• i) Check Troponin. In 2026 — Patients presenting to an emergency facility for new CP will almost automatically have a serum Troponin assay immediately drawn. Initial results are often forthcoming within 1 hour in an active ED. Any degree of Troponin elevation in a patient with new worrisome symptoms is significant (and may of itself be indication for prompt cath — even with a nondiagnostic ECG). 
• KEY Point: Although any elevation of Troponin is significant in a patient with new worrisome CP — Keep in mind that an initial normal hs-Troponin does not rule out acute infarction! (See Pearls #3,4,5 in ECG Blog #392 — for more on the fine points regarding use of serum Troponin levels).
• 
  
• ii) Look for a prior ECG on your patient. Perhaps the fastest and easiest way to determine if seemingly nondiagnostic ECG findings are "new" (therefore indicative of a new acute change until proven otherwise) — is to compare the initial ECG with a baseline tracing on the patient.
• iii) Do bedside Echo — looking for a localized wall motion abnormality. Interpreting bedside Echo for a wall motion abnormality can be tricky — and requires a skilled operator. But if your patient with new CP manifests a localized wall motion abnormality — this is highly suggestive of acute ongoing infarction. (NOTE: If the Echo is normal — but your patient was not have CP at the time the Echo was done — then this does not rule out acute infarction).
• 
  
• iv) Repeat the ECG within a short period of time (I favor repeating the ECG in a patient like the one in today's case within 10-to-20 minutes!). It is often surprising how quickly (and dramaticallly) a non-diagnostic initial ECG may change within a very few minutes!

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The Repeat ECG ...

Providers on the case "read my mind". They were suspicious of an ongoing acute event from the history and initial ECG — but could not at that point convince the interventionist.

• A prior tracing was not readily available for comparison.
• Providers repeated the ECG within 15 minutes.

To facilitate comparison in Figure-5 — I've put the initial ECG next to the repeat ECG done just 15 minutes later.

• To no one's surprise — Cardiac catheterization was immediately arranged on seeing the repeat ECG.

 

Figure-5: Comparison between today's 2 ECGs.

PEARL #4: Clinicians sometimes wait much longer than is needed to repeat an initial non-diagnostic ECG. Especially when CP is ongoing — the dynamic ST-T wave changes that are obvious in Figure-5 occurred within 15 minutes!

• There is no need to wait longer than this to repeat the initial ECG.
• And if you are still concerned by the history — but the 1st repeat ECG remains non-diagnostic — Have a low threshold to continue repeating frequent ECGs until such time that you can feel comfortable with a definitive diagnosis. 

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CASE Conclusion:

• Unfortunately — I do not have further follow-up on this case.
• That said — the cause of the serial ECGs in Figure-5 is virtually certain to be acute proximal LAD occlusion.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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