Unusual: Troponin Trajectory to Help Determine Ongoing/Recurrent Infarction vs. Completed Infarction.

A 40-something male with no PMH of any kind presented  to urgent care on a weekend (cath team is at home) with cough starting 2 weeks prior and SOB one week prior.

He underwent a chest x-ray:

As this was consistent with "pulmonary edema vs. viral infection," and he was transferred to the ED

The faculty physician did an immediate cardiac and lung ultrasound:

Many B lines (probable pulmonary edema)

Parasternal short axis cardiac ultrasound:

The anterior wall is closest to the transducer and shows an obvious wall motion abnormality

Further history:

The patient denied chest pain but stated that he had had about 3 episodes of chest pressure, lasting 5 minutes each, in the past week.

The physician was alarmed by these findings and ordered an ECG:

This is diagnostic of Anterior MI, but:

Is this an "old" MI, a completed transmural anterior MI, or is there ongoing myocyte necrosis?

The QS-waves suggest that there is no myocardium left.

  

The T-waves are taller than one would expect in a completed MI, but the highest T/QRS ratio of V1-V4 is still only about 0.33, close to diagnosing acute STEMI, but not quite (see discussion of ratio below).
A ratio less than 0.36 is still consistent with a subacute STEMI.

Is it old, or is it subacute and ongoing?  We usually determine this from ongoing chest pain, but this patient NEVER had chest pain.

The ECG in a true "old anterior MI with persistent ST Elevation," usually associated with an aneurysm, looks like this proven LV aneurysm:

Notice that there is anterior ST Elevation and QS-waves.  This could easily be mistaken for a STEMI.  The difference is that STEMI has a taller T-wave, at least when it is less than 6 hours after occlusion.

I derived and validated a formula to differentiate anterior LV aneurysm from acute anterior STEMI.

This formula depends on the fact that an acute MI has a tall T-wave and that the T-wave is proportional to the QRS.  If any lead from V1-V4 has a T/QRS ratio greater than 0.36, then acute STEMI is most likely, unless the duration of symptoms is greater than 6 hours (as the infarct progresses, the T-wave gets smaller).

So in this case, it is difficult to ascertain symptom duration because the patient never had any pain.  However, he has been SOB for a week, so it is likely that the infarct started 1-2 weeks ago.

However, was it:
1) a completed infarct that is now complicated by pulmonary edema? or
2) a small infarct with a lot of viable, but ischemic and stunned (wall motion abnormality) myocardium, or
3) did he have a small infarct and now a recurrent occlusion with impending transmural infarction?

The distinction is critical, as if there is new, recurrent occlusion, then he needs the artery opened NOW in order to save that myocardium.  If the myocardium is all dead, then there is no great urgency.

The QS-waves suggest that it is completed, but QS-waves are not definitive.

Usually you can tell by the presence or absence of chest pain whether there is ongoing ischemia or not.  But this patient never had and does not have chest pain.  His SOB is due to pulmonary edema, which will be there whether there is active ischemia or not, as his ejection fraction is poor either way.

So how can we get some indication of the trajectory?

We decided to check the troponin trajectory.  This is not usually an accurate way to assess the current state of the artery, and if the troponin is rising, you will not know whether there is ongoing infarction (rising troponin can be from ongoing necrosis or from release of troponin from already infarcted myocardium).

However, if the troponin is falling, then it is likely that there is no more ongoing infarction.

This is NOT the way to approach a case of acute symptoms, as in these cases, the troponin lags far behind the ECG, and waiting for the initial troponin, or especially for a 2nd troponin, takes too long and will result in unnecessary infarction.  For example, the initial troponin is negative in approximately 50% of STEMI cases.  While the 2nd is almost always positive, by that time all the damage is done.


The first troponin I returned at 2.53 ng/mL.

Here is the one hour ECG:

Not much changed

The second trop I returned at 2.417 ng/mL.  So we decided that angiogram could wait for the next day.

He was treated with IV Nitroglycerin and furosemide.

There might even be some advantage to waiting, other than doing it in work hours:  

Occlusions that have organized over days may be difficult to open, difficult to pass the wire.

Some think that heparin therapy for 12-24 hours before angiogram helps in softening the thrombus and thus helps to open the artery (This was conveyed to me by one of our cardiologists. I had never heard it and cannot find any literature on it.  If anyone knows, please forward!)

Here is the 5.5 hour EKG:

T-waves are not as tall.
Does this mean that the artery is opening?  Possibly, but it is more likely due to improving hemodynamics with nitro and furosemide. 

Here is the ECG the next AM:

T-wave are smaller still.
This really looks like an LV aneurysm, though it is really too early to tell whether an aneurysm will form or not.

Troponin profile

Angiogram:

There was indeed a 100% LAD occlusion, and it was very difficult to pass the wire.  The interventionalist estimate from the characteristics of the lesion was of a 2 week old thrombus.

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Comment by KEN GRAUER, MD (9/17/2019):

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Interesting case of a 40-ish year old male with the unexpected finding of recent large anterior MI — despite the absence of chest pain. From an ECG interpretation perspective — I thought the initial ECG offers a number of interesting teaching points that are worthy of mention.

• I’ve reproduced this initial ED ECG in Figure-1. My sequential impressions were as follows:

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

DESCRIPTIVE ANALYSIS of ECG #1: The patient was a previously healthy 40-ish year old male with 1-2 weeks of coughing and dyspnea, but no chest pain.

• Rate & Rhythm — Sinus rhythm at a fairly fast rate of ~95/minute.
• Intervals (PR-QRS-QT ) — To my measurement — the longest PR interval is seen in lead I = 0.22 second, which is consistent with 1st-degree AV block. Assessing QRS width is challenging. This is because the QRS complex in leads V2, V3 and V4 clearly looks wider-than-normal. That said, the QRS complex is not more than half a large box in duration in any lead (ie, not more than 0.10 second) — which means that the QRS is narrow. The QTc looks normal (clearly less than half the R-R interval).
• Axis — The mean frontal plane axis is indeterminate! That’s because, other than lead aVF (which is predominantly negative) — the QRS complex in the 5 other limb leads is virtually isoelectric.
• Chamber Enlargement — None! This is also tricky — because overly deep anterior S waves often signal LVH. That said — the reason anterior S waves are so deep on this tracing is most likely not due to LVH, but rather to the loss of anterior R waves from recent infarction. PEARL: It becomes difficult to diagnose LVH on ECG in the presence of anterior infarction — because these 2 conditions produce opposing forces. That is, marked LVH (with increased lateral lead R wave amplitude, and increased depth of anterior S waves) may result in reduction (or even loss) of anterior r waves on ECG. By the same token — loss of anterior forces (ie, loss of anterior r waves) due to anterior MI may result in deeper anterior S waves that simulate LVH.

Q-R-S-T Changes:

• Q Waves in the Inferior Leads? — I stared for a long time at the inferior leads, in my attempt to determine IF there were any inferior Q waves. I believe there are not. There appears to be an initial small positive deflection in lead II (which I’d describe as an rR’S complex). There appear to be small-but-real initial r waves (positive deflections) in both leads III and aVF. I’d describe QRS complex morphology in leads III and aVF as consistent with an rSR’ (or rSr’) pattern. Technically — lack of any clear-cut inferior lead Q waves means we cannot diagnose prior inferior MI with any certainty. PEARL: Given the clinical context of this case — the unusual rR’ pattern in lead II + no more than very tiny initial r waves in leads III and aVF + notching (fragmentation) of the downslope of the S wave in lead aVF in this patient with a large, recent anterior MI may serve as an “ECG infarct equivalent” pattern in the inferior leads. I suspect this patient with total LAD occlusion most likely had a “wraparound” LAD that resulted in inferior wall involvement at the time of his infarction.
• Q Waves in the Anterior Leads? — YES! There is a Qr pattern in lead V1 (perhaps reflecting incomplete RBBB in association with anterior MI?). As noted by Dr. Smith above — there are deep QS complexes in leads V2-thru-V4. R waves finally develop in leads V5 and V6 — but these r waves are TINY (with a fragmented initial r wave in lead V6). PEARL: The finding of deep QS complexes in several anterior leads is not indicative of prior MI if there is complete LBBB. On the contrary — we expect to find small, if not absent r waves in anterior leads in the presence of this conduction defect. But despite “looking wide” — QRS complexes in leads V2-thru-V4 are not more than half a large box in duration — which means that the QRS complex in this tracing is not wide, and there is no bundle branch block. Given that there is no bundle branch block here — precordial lead QRS appearance is therefore diagnostic of extensive anterior (anterolateral) infarction at some point in time.
• ST-T Wave Changes — As per Dr. Smith, ST-T waves in leads V1-thru-V4 look taller-than-expected. Qualitatively — I thought the SHAPE of these ST-T waves did not look acute (ie, rather than coved — there was a clear upward concavity to these ST-T waves). In addition — true reciprocal ST depression was absent from this tracing (I thought the isolated shallow T inversion in aVL was probably not acute). PEARL: Despite my “gut” feeling that ST-T wave changes on this initial ED ECG did not look acute — it's important to appreciate that there was enough unexpected ST elevation to mandate additional information before drawing any conclusions. Considerations included: i) Emphasis on the history (ie, NO chest pain — but increasing dyspnea that could be consistent with anterior MI occurring 1-2 weeks earlier); ii) Search for a prior ECG (I don’t believe any was available); iii) Checking the “troponin trajectory” (discussed in detail by Dr. Smith above); and, iv) Clarifying the anatomy with cardiac catheterization.

Our THANKS to Dr. Smith for presenting this instructive case!