Monday, July 2, 2012

LVH and New ST-segment elevation: False Positive or True Positive STEMI?

A 72 year old man fell from standing and had head trauma.  He was initially disoriented, but cleared.  BP was 80/50 prehospital.  On arrival, it was 90/70.  There was a scalp laceration.  Head CT was negative.  Patient stated he had had experienced some chest pain prior, but had no active chest pain.  He has a past history of hypertension, chronic renal insufficiency, prior anterior MI with proximal LAD stent, and cardiomyopathy with EF of 35%.

Here is his ED ECG:

There is sinus rhythm at rate of about 85 bpm.  There is profound LVH, with a V2 S-wave of 55 mm.  There is typical ST elevation of LVH ("secondary repolarization abnormalities) in V2 and V3.  There are Q-waves of his previous MI in V4 and V5, with ST elevation in V4 (discordant) and also V5 (concordant).

V4 and V5 make this ECG worrisome for STEMI, but by no means diagnostic.  Whenever there is this much voltage, it can greatly distort repolarization and result in a false positive cath lab activation.  The fact that the patient has no ongoing chest pain is very important.

A previous ECG from 11 days prior was obtained:

Here there is bradycardia at a rate of 42, with a PVC.  The LVH is present, but voltage is not as profound.  The ST segments are not nearly as abnormal here as they are on the presentation ECG.

Now there is much more worry for STEMI.  However, the difference in heart rate and voltage, and the hypotension and/or syncope, can entirely account for the change in ST segments.

He went to the cath lab and had no change in his coronary arteries from the previous angiogram.  Troponin I peaked at 0.50 ng/ml (baseline values were about 0.15 ng/ml from chronic renal failure).  Echocardiogram showed no wall motion abnormality, with normal biventricular function, LVEF of greater than 55%, and severe concentric LVH.

Here is his ECG then next AM.
No great change from presentation.
His presentation was explained by an excess of antihypertensive medications.

Now, you might think reading this as negative for STEMI can only be done by the retrospectoscope.  But this case was sent to me as an unknown (by an undergraduate student who will start med school in the fall, and who is a whiz with EKGs!).   This was my response (again, without knowing anything about the outcome):

"It looks like ischemia superimposed on LVH, but not necessarily due to ACS.  Could be demand ischemia from a number of causes.  I would not be surprised with either a positive or negative troponin, but I would be surprised if the trop was very high (> 10 for troponin I).  What was the troponin?  Was there  ultimately a cath?  What was the outcome?  It’s a good one for posting if we get all the details."

I only add this in order to show that a careful informed reading of even the most scary ECGs is possible.

What would I do in this case?

1. I would have obtained an emergent echocardiogram to look for new wall motion abnormality.
2. Had the patient had active chest pain, or not had the change in voltage or heart rate, I would have activated the cath lab.


 

2 comments:

  1. The morphology of the ST-segments in V4/V5 bothered me the most on this ECG. Could they be explained by the two leads lying along the zone of transition?

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  2. Yes, but then we still have a concordant ST segment in V5, so nothing entirely follows the rules, right?

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