What do you think of these 2 ECGs in patients with chest pain? How to approach these?

What do you think of these 2 ECGs in patients with chest pain?  How to approach these?

ECG 1 (sent to my by Sam Ghali @EM_resus)

ECG 2

ECG 1 

This was sent to me with no clinical information and the question "what do you think?"  

My answer was: "sinus rhythm with right atrial enlargement, probable right ventricular hypertrophy, and old inferior MI with inferior LV aneurysm."  The T-wave inversion in I and aVL is reciprocal to the Old inferior aneurysm.

After I sent my answer, I received this history:

66 yo man presented with chest pain

History of CAD [unclear details out of state, stent(s)?]

STEMI alerted pre-hospital

Found to have very elevated lactate

Significant AKI

Aortic thrombus (chronic) on CT

hS Trop T:   1609->2471->1929 ng/L

Cards was planning on  cath when metabolic situation settled

Angiogram: no culprit and all open arteries.

Final diagnosis: type II MI due to illness

The Queen of Hearts said "OMI with mid confidence."  Version 1 of the Queen does not do a good job of recognizing LV aneurysm morphology, whether it is anterior (which for an expert is not too difficult because they almost always have QS-waves) or inferior (which is even very difficult much of the time for me, because inferior aneurysm frequently has QR-waves)

How to approach?  --when the diagnosis could be "ST Elevation due to Old MI" or "LV Aneurysm Morphology", it is essential to look into the old charts and old ECGs, if available.  It is also essential to assess for other etiologies of the symptoms, and in this case the patient had physiological derangement, with elevated lactate and AKI.  This points to another inciting etiology rather than ACS as the primary mover.  

These physiological derangements do not rule out ACS, but make it much more likely that the patients illness was incited by another factor.

ECG 2

I was reading ECGs on the system and came across ECG 2 and said out loud: "This is a fake."  A colleague sitting next to me asked "why?", and I answered that there is a "saddleback" in lead III and well-formed Q-wave.  Saddleback ST elevation is rarely due to OMI. 

However, on very few occasions Saddleback STE actually is due to OMI.

The Queen of Hearts had stated "Not OMI with low confidence"

There was a previous ECG available:

This confirmed my opinion.

I found out later that the patient had gone to the cath lab.  And I found out that the cath lab activation was a result of this follow up ECG:

I find this to be a negative ECG, except that there is now new ST Depression in V4-V6.

However, there is new tachycardia, and that new ST depression could be a result of supply-demand ischemia from tachycardia.

This time, the Queen of Hearts diagnosed this as "OMI with High Confidence."

This Queen interpretation led to a false positive cath lab activation.

Alternative Management: Always look into the patient's chart!! (including the old ECG above, which was not seen)

In fact, I found that I had blogged this patient before (!!!) due to the ECG that looked like inferior aneurysm.  There were many previous similar ECGs.  Here is that post: 

A Patient with Vertigo

Angiogram 3 months ago:

Severe three vessel native CAD with occlusion of the mid-Cx, mid-LAD, and mid-RCA including several areas of in-stent stenosis or occlusion.  4/4 patent bypass grafts (RIMA > dLAD, LIMA > OM, SVG > rPDA, and free radial > rPLA1) with severe native vessel stenosis just beyond the anastomosis in the dLAD, OM, and rPDA

Previous coronary disease and h/o CABG tells you that there probably is an old infarct and that the baseline ECG is likely to be abnormal and that you should read the present ECG in that context.

Previous Echo:

Normal left ventricular cavity size, mildly increased wall thickness and moderate LV systolic dysfunction.

The estimated left ventricular ejection fraction is 35-40 %.

Regional wall motion abnormality- basal inferior akinetic.

Regional wall motion abnormality- basal inferolateral, akinetic.

Regional wall motion abnormality-apex small .

An Akinetic wall can have the same "LV aneurysm" Morphology as a Dyskinetic wall ("diastolic dyskinesis" is the echo definition of aneurysm.)

The cath lab was activated and there was no acute OMI.  False Positive.

Discussion:

These are very complex cases in which there could be OMI or there could be old MI.  These are the kind of cases in which you want to consult your friendly cardiologist and have a discussion.  But that is only if your cardiologists accept the idea of OMI (Acute Coronary Occlusion in the Absence of ST Elevation criteria).  To make such a consultation,  there must be mutual trust that the consultant will not dismiss your concerns or say "Nah, couldn't be."

It can take years to build such trust.

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MY Comment, by KEN GRAUER, MD (7/30/2024):

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The "theme" of My Comment in today's case is — Shape is KEY!

• For clarity and ease of comparison in Figure-1 — I've labeled and put together the initial 2 ECGs in today's case.

MY Thoughts on ECG #1:

This is a complex tracing. I saw the following:

• There is significant baseline artifact. This is relevant to our interpretation given the difficulty it poses for assessment of ST-T wave changes in multiple leads.
• That said — the rhythm is clearly sinus with a normal PR interval.
• QRS morphology is not normal. That said — the QRS is really not wide (ie, not more than 0.10 second). Given the all upright QRS complex in lead V1, with narrow but definite terminal S waves in lateral leads I and V6 — this QRS morphology is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• The QTc is prolonged (I measure the QT at ~0.44 second — which corrected for the rate of ~80/minute, comes out to a QTc ~0.49 second).
• There is marked LAD (Left Axis Deviation) — with entirely negative QRS complexes in each of the inferior leads. This is consistent with LAHB (Left Anterior HemiBlock).
• There is RAA (Right Atrial Abnormality) — as determined by the presence of tall, peaked and pointed P waves in the inferior leads (ie, P waves ≥2.5 mm in amplitude).
• There may be RVH (Right Ventricular Hypertrophy) — which always needs to be considered if there is true right atrial enlargement. Because of the artifiact — we can not tell if QRS morphology in lead V1 is triphasic (rsR') or represents a qR pattern, which could be consistent with pulmonary hypertension (for more on RAA, RVH — See My Comment in the February 12, 2023 post).
• There may be LVH by Peguero criteria (See My Comment in the June 20, 2020 post) — as suggested by the very deep S waves in leads V3 and V4 (with the PURPLE arrow in lead V3 showing that S wave amplitude is cut off in this lead).

Regarding Q-R-S-T Changes:

• More than inferior Q waves — there is marked fragmentation on each downslope of the S wave in the inferior leads (RED arrows in these leads). It is because of this marked fragmentation that the “attempt” to form a positive deflection in each inferior lead never makes it back to the baseline before being overtaken by resumption of S wave negativity. In my experience — this fragmented QRS shape in any one (let alone all 3) of the inferior leads strongly suggests inferior infarction at some point in time.
• Regarding R wave progression — I interpreted the seemingly multi-phasic upright complex in lead V1 as the result of IRBBB rather than RVH because: i) There is marked LAD with no more than modest depth of the S wave in lead I; and, ii) I thought the overall ECG picture more suggestive of coronary disease rather than RVH. Yet predominant positivity never occurs in the lateral chest leads — and I could not rule out the possibility of RVH on this ECG alone.
• The shape of the S-T segments in the inferior leads is coved, of relatively long duration, and shows slight ST elevation. This shape forms a “picture to remember” — that does not look acute. That this inferior lead ST-T wave appearance is unlikely to be acute — is further supported by a lack of reciprocal ST depression in high-lateral leads I and aVL. Instead (as per Dr. Smith) — this “picture” strongly suggests inferior wall aneurysm, especially given the inferior lead S wave fragmentation marker of prior inferior MI described above.
• Finally — there is ST segment straightening and depression beginning in lead V3 beyond that expected for simple IRBBB (BLUE arrows in the chest leads).

BOTTOM Line: Like Dr. Smith — as a single ECG that I interpreted knowing only that the patient had "chest pain" — I thought ECG #1 did not look acute. But there are multiple complexities that beg further explanation.

• I suspected prior inferior MI with IRBBB/LAHB — and now with inferior wall aneurysm. There is ST depression in leads V3-thru-V5 that I thought likely to reflect multi-vessel disease — but with need to explain the reason for RAA, probable LVH, and possible RVH. But – not an OMI.
• As per Dr. Smith — this patient turned out to have Troponin elevation due to Type-2 MI (clean coronaries on cath). Instead — his clinical presentation was dominated by acute renal failure with severe acidosis. We are left with more questions than answers (ie, How severe is his underlying coronary disease? Any RVH or pulmonary hypertension?) — but this is not the ECG of acute coronary conclusion.
• Personal NOTE: I have been fooled more than once by chest pain in the setting of severe underlying disease (ie, acidosis, sepsis). The KEY is to recognize that ECG #1 is unlikely to represent an acute OMI — with clinical priority to treat underlying conditions, and to then reassess symptoms and repeat ECGs as needed.

Figure-1: I've labeled the initial 2 ECGs in today's case.

MY Thoughts on ECG #2:

I found today’s 2nd tracing easier to interpret — in that there were far fewer complicating findings.

• The rhythm is sinus — with normal intervals (PR-QRS-QTc). There is LAD (negative QRS in lead aVF) — but an axis not leftward enough to qualify as LAHB (predominant positivity in lead II).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are very large and wide Q waves in leads III and aVF — with a small-but-present Q wave in lead II (RED arrows in these leads). This patient has had inferior infarction at some point in time.
• R wave progression shows slight delay in transition (the R wave only becomes taller than the S wave is deep between lead V4-to-V5).
• S-T elevation is seen in each of the inferior leads, followed by a prominent upright T wave. That said — the shape of the elevated inferior lead ST segments manifests an upward concavity (ie, "smiley" configuration). As per Dr. Smith — this shape is less likely to represent an acute cardiac event.
• Although both high-lateral leads ( = leads I and aVL) manifest ST depression — the precise mirror-image opposite ST-T wave picture from lead III — is seen in lead aVL (within the BLUE rectangle, in which I merely inverted one QRST complex from lead III). This to me suggested a similar acuity (or lack thereof) for both lead aVL and the inferior leads.
• There is slight, nonspecific ST-T wave flattening in leads V1,V2 and V6.

BOTTOM Line: Once again, as a single ECG that I interpreted knowing only that the patient had “chest pain” — I thought ECG #2 did not look acute. 

• The deep, wide Q waves in leads III and aVF (with small-but-present Q in lead II) — strongly suggest prior infarction. This patient almost certainly does have underlying coronary disease. Clinically, if I was managing this patient — more information would clearly be needed (ie, specifics of the history; repeat ECG; troponins; comparison with prior tracings, etc.). But as a single ECG without the benefit of more information — the shape of these inferior lead ST segments — and the lack in the chest leads of any suggestion of associated acute posterior involvement — suggest this is not the result of acute coronary conclusion.
• As per Dr. Smith — review of this patient's chart told the story. Not surprisingly — the patient had very severe underlying coronary disease — but no acute OMI.