A 60-something male presented stating that he had had chest pain that morning which awoke him from sleep but then resolved after several minutes. He has had similar pain in the past which he attributed to acid reflux. He has a history of untreated hypertension.
He is pain free now.
His systolic BP was 200.
The patient is pain free at the time of this ECG:
There are well-formed Q-waves in precordial leads. The T-waves are inverted. Thus, this is either:
1) a subacute MI with a significant (large amount) of completed infarction, or
2) old MI with persistent ST Elevation (LV aneurysm).
The patient is pain free now, so it is either a reperfused subacute MI or a Non-OMI superimposed on an old MI (aneurysm).
If this is subacute MI, then the first troponin should be VERY high, unless the infarct occurred many days or weeks ago.
The first troponin returned at 541 ng/L.
This is not high enough to be subacute MI unless the infarct happened at least a week ago.
What did the Queen of Hearts say?
Recorded at 45 minutes after arrival
Time 6 hours
21 hours
Here is the troponin profile:
This confirms that the patient has an acute MI. The fact that the patient is pain free tells us that this is either a NOMI or a reperfused OMI. But the ECG tells us that that there is also old or subacute MI.
Therefore, this is a NOMI or reperfused OMI SUPERIMPOSED on an old (LV aneurysm) or subacute MI.
How could we tell the difference between subacute MI that is many days old and LV aneurysm?
A high quality echo should show dyskinesis and wall thinning if this is aneurysm. If it is subacute MI, then it will show akinesis and no wall thinning.
High Quality Contrast Echo
--Normal left ventricular cavity size, mildly increased wall thickness and mild LV systolic dysfunction.
--The estimated left ventricular ejection fraction is 45-50 %.
--Regional wall motion abnormality-distal mid and apical anterior, apical inferior, apical lateral, apical septum and apex, aneurysmal.
ADDITIONAL REMARKS
Prior infarct with aneurysm in the distal LAD vascular territory. No convincing evidence for LV thrombus.
The patient refused angiogram.
He was supposed to get a stress test and/or angiogram later but never showed up
- I offer a few additional thoughts on today's initial ECG — which I've reproduced in Figure-1.
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| Figure-1: The initial ECG in today's case. |
- As per Dr. Smith — the principal concerns regarding this initial ECG relate to distinction as to what is "new" (or at least recent) — vs "old" — vs "new or recent superimposed on old". Finding a prior baseline ECG on this patient could be extremely helpful for distinguishing between these entities (although prior tracings are not always available at the time we'd like to have them ... ).
- What can be said about ECG #1 — is that anterior MI has definitely occurred at some point in the past. There is loss of r wave from lead V1 (which manifests a small-but-definitely-present initial r wave) — to lead V2 (which manifests an entirely negative QS complex).
- This is followed by an exceeding wide Q wave in lead V3 — in association with ST segment straightening and fairly deep terminal T wave inversion in this lead. (I like to look for fragmentation with such wide Q waves as a sign in support of previous "scar" — but baseline artifact rendered my search for fragmentation useless).
- Narrow q waves continue in leads V4,V5,V6. That said — the finding of a q wave that is deeper in lead V4 than in lead V6 is consistent with definite anterior MI having occurred at some point in time (whereas isolated narrow q waves of similar size to that seen in leads V5,V6 of ECG #1 — might simply reflect normal septal q waves and not prior infarction).
- Finally — I see nothing acute in the limb leads of ECG #1. Reciprocal ST depression in inferior leads would be helpful in support of a recent event if present — but given that many acute anterior OMIs do not manifest reciprocal limb lead changes, their absence does not rule out a recent event.
- My impression on seeing today's initial ECG — was that extensive anterior infarction had occurred at some point in time.
- Looking at leads V1,V2 — the ST segment coving with minimal ST elevation and no more than a hint of terminal T wave inversion is clearly consistent with LV aneurysm.
- Lead V3 confirmed the likelihood of prior infarction (given how large and wide the Q wave in this lead is) — but the shape of the elevated ST segment in lead V3 potentially looks recent (ie, ST straightening with steep descent into terminal T wave inversion). Persistent T wave inversion in leads V4 and V5 — which only by lead V6 are resolving (the T wave still being positive-negative biphasic in this most lateral chest lead) — could clearly be consistent with reperfusion T waves from recent anterior infarction, perhaps superimposed on chronic LV aneurysm.
- BOTTOM Line: I thought it impossible to know for certain from this single ECG what was "old" vs "new" (or recent) — vs "new or recent superimposed on old".
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