Tuesday, November 24, 2015

Very young man with chest pain, then cardiac arrest

A very young man, approximately 30 year old, called 911 because of 1 hour of severe chest pain.

The medics got him into the truck and recorded the following ECG:
It starts as sinus rhythm with probable inferior STEMI, but becomes ventricular fibrillation (or polymorphic ventricular tachycardia) halfway through!

He was defibrillated immediately and awoke.

He arrived awake and alert in the ED and had a bedside echo prior to arrival of the ECG tech:

This is a subcostal view and clearly shows the base of the heart with good function, but the apex with poor function.

This made me suspect not only inferior STEMI, but anterior as well, due to an LAD lesion with a wraparound to the inferior wall.

He then had this ECG:
De Winter's T-waves in precordial leads and ST elevation in inferior leads.  There are already QS-waves in V2 and V3. 
This suggests a partly open proximal LAD to a wraparound distal LAD supplying the inferior wall in addition to the anterior wall.

The cath lab was activated and angiography revealed a subtotal occlusion of the LAD (but not 100% - it was probably 100% at the time of the arrest).  There was a large clot burden with some thrombus embolized to the apex (accounting for the inferior STEMI).

He underwent thrombectomy of the proximal LAD and stenting of a residual atherosclerotic lesion.  The distal thrombus could not be removed.

Door to balloon time was less than 60 minutes; symptom onset to balloon time was less than 120 minutes (fast!!).

Here is the ECG after PCI:
Residual ST depression precordial, continued ST elevation inferior, loss of R-waves anterior.

Peak troponin I was over 100 ng/mL, a large STEMI.

Here is the ECG the next morning:
Minimal ischemia, but total loss of anterior depolarization forces (QS-waves).

There was never any ST elevation recorded, though it may have been there on the prehospital ECG if the ventricular fibrillation had not interceded.  And yet the entire anterior wall appears to be infarcted.

When de Winter reported his de Winter's waves, he reported that they were "persistent" and always associated with "occlusion."  However, "persistent" was not defined as having this on multiple serial ECGs; rather, it was reported that patients who had them had them for up to 2.5 hours of chest pain.    "Occlusion" was not defined, so it is unlikely that it was always 100%.

My belief, based on multiple cases with serial ECGs is that de Winter's T-waves represent a subtotal occlusion of the LAD such that it looks like a synthesis of subendocardial ischemia with ST depression AND hyperacute T-waves.  Thrombus is dynamic and is always forming and lysing, so that the angiogram may not exactly represent the state of the artery at the time of the ECG.

See this case.

And see also this case.

Formal echo is consistent with all of this:
Decreased left ventricular systolic performance -- moderately severe.
The estimated left ventricular ejection fraction is 30%.
Regional wall motion abnormality-distal septum, anterior and apex, large.
Regional wall motion abnormality-anterolateral.
Regional wall motion abnormality-distal inferior wall.
No contrast perfusion uptake of septum and apical walls (i.e., continued ischemia in spite of an open artery) 

This would seem to indicate "No reflow" (see this case)]: downstream platelet-fibrin aggregates have occluded small vessels, such that reperfusion is very limited in spite of an open epicardial artery.  "No Reflow" usually implies less than TIMI 3 flow in spite of an open artery.  In this case, the flow in the LAD after PCI was not commented upon.

This was repeated a few days later:
Regional wall motion abnormality-distal septum anterior and apex large.
Regional wall motion abnormality-anterolateral .
Regional wall motion abnormality-distal inferior wall .
Decreased left ventricular systolic performance moderately severe .
Left ventricular hypertrophy concentric .

This ECG is from day 5:
QS-waves are persistent, consistent with the large anterior wall motion abnormality

Learning Points:

1. The LAD can occlude and re-open, and can shower downstream thrombi that occlude more distally, in this case resulting in inferior STEMI also (due to wraparound LAD)

2.  de Winter's T-waves were the only sign of LAD occlusion.  One can miss the ST elevation.

3.  The angiogram may not exactly represent the state of the artery at the time of the ECG.  de Winter's T-waves probably represent a state of subtotal occlusion of the LAD.

4.  The thrombus in ACS is dynamic.

5.  Downstream platelet fibrin aggregates can result in profound infarction, even with rapid reperfusion of the epicardial infarct-related artery.  If it results in less than TIMI-3 flow, it is called the "No Reflow" phenomenon.


  1. first ECG after defibrillation:

    - PRD inferior + minimal PRE in aVL = concomitant atrial injury ?

    thanks Dr Smith


  2. Was this patient 'visually healthy'? What was his height/weight?

    1. A very healthy, thin, athletic young man. Don't fall into the old trap that the only young people who get STEMI are diabetics, smokers, cocaine users etc. People always look for an explanation like that when a young person, especially a woman, has an MI. But young people do get STEMI even when otherwise healthy!

  3. hi
    What are the other occlusions that may result in both Anterior and Inferior STE ?

    1. Proximal RCA with RV involvement and "pseudoanteroseptal MI" I have some cases on this blog


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