Acute chest pain in a patient with LVH and known coronary disease. What does the ECG show?

A 40-something with severe diabetes on dialysis and with known coronary disease presented with acute crushing chest pain.

Here is his ED ECG:

What do you think?

There is a flat and downsloping ST segment in V2 and V3.  This could be due to posterior OMI.  

Is there an old ECG for comparison?

Here is the most recent previous ECG:

Indeed, there was some normal ST elevation in V2 and V3, discordant to a relatively deep S-wave which could be due to some LVH.

Here is another previous ECG:

So it looks like a posterior OMI. 2 years prior he had an angiogram which showed 90% proximal stenosis of the circumflex.  It seems that this was probably the infarct vessel.

At this point, I was quite certain that this was a posterior OMI. We initiated "Pathway B", (pathway A is cath lab activation; pathway B is to consult cardiology about possible cath lab activation).  

Appropriately, they recommended IV NTG and cath lab if that was not successful.

Here is the Queen's interpretation as submitted to the telegram bot; she does not have the benefit of comparing with an old one:

But when I put it through the PM Cardio app, which is now available in Europe, she says OMI with low confidence.

The pain did not resolve with NTG, and so he went to emergent angiography:

1. Left main: no obvious stenosis.

2. LAD: severe in-stent restenosis in the mid (80%) and distal (90%)

segment and diffuse disease distally.

3. D1: severe (90%) de-novo stenosis in the mid to distal segment.

4. Ramus intermedius: large, severe in-stent restenosis at the distal

stent edge (90%) and severe de-novo stenosis at the ostial segment (90%).

5. LCX: non-dominant. Occluded (it was small and did not supply much prior

angiography).

6. RCA: Dominant: severe (80%) de-novo proximal stenosis. It supplies a

large RPDA and RPLA.

This angiogra is consistent with acute posterior OMI

Cath showed multiple vessel disease and following discussion with CV surgery, patient was deemed poor surgical candidate for CABG given his multiple comorbidities and poor rehab potential, thus, MPI was done for further evaluation which showed no significant reversible ischemia, so decision was made for medical management as patient has been symptom free for almost two days and has been clinically stable.

- Dual Anti Platelet Therapy: continue ASA 81 mg and Plavix 75 mg daily

- Continue atorvastatin 40 mg daily

YOU TOO CAN HAVE THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

See these related posts:

--A dialysis patient with nonspecific symptoms and pseudonormalization of ST segments (patient has LVH and baseline ECG has non-ischemic STE in V2, V3)

--OMI Can be Diagnosed by "Pseudonormalization of ST Segments" 

(The patient has LVH and baseline LVH ECG has non-ischemic STE in V2, V3)

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MY Comment, by KEN GRAUER, MD (1/25/2023):

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Today’s interesting case by Dr. Smith offers the unique perspective of assessing the initial ECG of a patient who has had prior events — and, who now presents with new symptoms.

• As per Dr. Smith — today's patient is a 40-something year old patient with severe diabetes, renal failure and known coronary disease — who presents with “acute crushing CP”.
• For clarity and ease of comparison in Figure-1 — I’ve reproduced today’s initial ECG, together with the patient’s most recent prior ECG.
• In his discussion — Dr. Smith highlights the flat and downsloping ST segment in leads V2,V3. As a result, his concern is great about acute posterior OMI.

Take Another LOOK at ECG #1 — before you take another look at the most recent prior tracing. 

QUESTION:

• In view of today’s presenting history — What ELSE do you see in ECG #1?

To facilitate comparison in Figure-1 between today’s initial ECG and the most recent prior ECG — I’ve enclosed the KEY leads within RED and BLUE rectangles, respectively. 

• As you now Take Another LOOK at ECG #1 in comparison to ECG #2 — How do these 2 tracings differ?
• 
  
• If told only that ECG #2 is the "most recent previous ECG" — What might this mean clinically?

Figure-1: I've reproduced and have labeled today's initial ECG — with the most recent prior ECG placed below it to facilitate comparison.

A “Deep Dive” Dissecting the First 2 ECGs in Today’s CASE:

Dr. Smith correctly concluded that for today’s patient, who presents with "crushing new CP" — the initial ECG, interpreted in context with the 2 prior ECGs that were found — essentially confirms acute posterior OMI. I nevertheless thought it may be insightful to “retrace” my sequential thoughts as I viewed this case:

• I initially only saw only ECG #1 in Figure-1 — without knowing specifics about the history (beyond that this patient presented to the ED, presumably for chest pain).

Looking Closer at the Initial ECG: 

The rhythm in ECG #1 is sinus at ~70/minute. All intervals are normal (PR, QRS, QTc). 

• The frontal plane axis is leftward enough to qualify as LAHB (ie, the QRS being predominantly negative in lead II — therefore defining a leftward axis clearly more negative than -30 degrees). 
• LVH is present — with voltage satisfied in lead aVL (R in aVL ≥12 mm) — and especially by the very deep S wave in lead V2 (which measures more than 25 mm).
• A fairly large Q wave is seen in lead aVL.
• R wave progression is poor — in that transition (where the R wave becomes taller than the S wave is deep) never occurs! Although LAHB may delay transition (because of loss of some anterior forces) — it usually does not result in such tiny R waves as we see in ECG #1, in which the R wave in leads V5,V6 does not exceed 2 mm in amplitude.
• There is also marked fragmentation of the terminal ascending S wave in lateral chest leads V4,V5,V6, which display marked notching (within the YELLOW ovals in these lateral chest leads).
• 
  
• Regarding ST-T waves — There is ST segment flattening in multiple leads (RED lines in leads II,III,aVF; and in V2,V3,V4,V5).
• The ST segment is coved but isoelectric in lead aVL — with fairly deep, symmetric T wave inversion in this lead (BLUE arrow in aVL). The T wave is also inverted in leads I and V6 (BLUE arrow in V6).
• Finally — There is ST elevation in lead aVR (RED arrow in this lead).
• 
  
• Putting It All Together: Before learning about the history — I suspected from ECG #1 that this patient had significant multivessel disease because: i) Abnormal ST segment flattening is present in 7/12 leads (Leads II,III,aVF; and in V2,V3,V4,V5) — with abnormal T wave inversion in 3 of the remaining leads (leads I,aVL,V6); ii) There is ST segment elevation in lead aVR; and, iii) There is marked fragmentation — which is a common indicator of "scar" (within the YELLOW ovals in leads V4,V5,V6).
• KEY Point: In addition to the above findings suggesting underlying multivessel disease — the ST segment straightening, with abrupt angulation at the junction of the ST segment with ensuing upright T waves in leads V2 and V3 (within the RED rectangle in ECG #1) — is clearly abnormal, because there typically should be slight ST elevation with gentle upsloping of the ST segment in these leads. As per Dr. Smith, in a patient with new chest pain — these flattened ST segments in leads V2,V3 suggest acute posterior OMI until proven otherwise.
• I thought the lateral lead T wave inversion, in association with more-peaked-than-expected T waves in the inferior leads and in leads V2,V3 — might reflect infero-postero-lateral reperfusion T waves.

YOUR Thoughts on Comparing ECG #1 with ECG #2?

To emphasize — Comparison between ECG #1 and ECG #2 is made difficult by the fact that we are only told that ECG #2 is the "most recent previous ECG" on today's patient.

• ECG #2 is clearly abnormal. There is ST segment flattening in multiple leads — in association with abnormal ST segment coving, with deeper T wave inversion in high-lateral leads I and aVL than is seen in ECG #1. It would be important to know the clinical circumstances at the time ECG #2 was obtained (ie, Was ECG #2 associated with recent infarction? — OR — Is this tracing reflective of this patient's true "baseline" ECG?).
• That said — Note the appearance of the ST-T wave in leads V2,V3 (ie, within the light BLUE rectangle in ECG #2). This is how a "normal" ST-T wave should look in these leads — being slightly elevated, with gentle upsloping of the ascending ST segment.
• 
  
• BOTTOM Line: Although we do not know the clinical circumstances at time ECG #2 was obtained (and many of the same leads show similar ST segment flattening as is seen in ECG #1) — there is no doubt that the ST-T wave appearance in leads V2 and V3 becomes clearly abnormal in association with "acute crushing CP" at the time ECG #1 is obtained. As per Dr. Smith, in this patient with underlying multivessel disease — today's initial ECG is diagnostic of new acute posterior OMI until proven otherwise.