Sunday, May 3, 2015

Severe LVH and PseudoSTEMI

An elderly male with end stage renal disease had hypotension (50's systolic) and syncope (LOC, and loss of radial pulses) during dialysis. He quickly regained consciousness.  There was no chest pain or SOB.  The patient has an implanted cardioverter defibrillator (ICD) due to previous cardiac arrest; it did not shock. His BP was 106/59 in the ED, with a pulse of 90.

He had a history of out of hospital cardiac arrest due to ventricular fibrillation and also recurrent ventricular fibrillation/polymorphic ventricular tachycardia, for which he received the Implantable defibrillator.

Previous echo had shown severe concentric LVH.

He also had a h/o CAD with PCI to mid LAD 2011.

Here is his ED ECG:
There is sinus rhythm with a wide QRS at 138 ms.  It is very similar to LBBB, but because of Q-waves in aVL, it does not meet formal criteria.  However, it is surely an intraventricular conduction delay, and all of the rules of appropriate discordance apply.   Applying these rules, there is no concordant ST elevation.  There is discordant ST elevation in V1-V3, and this was very concerning to the clinicians.  It is not, however, out of proportion (ST/S ratio not greater than 0.25).  The highest ST/S ratio is no more than 0.12, within normal limits.  There is also high voltage.

Here is the most recent ECG from 6 months prior:
Sinus rhythm. QRS is 107 ms (much shorter).  There is high voltage.   There was much less ST elevation at this time, and the increased ST elevation concerned the clinicians.  But the QRS is now wider too (new conduction delay) and the heart rate is also much slower and both of these can greatly affect the ST elevation.  A faster heart rate generally exaggerates ST elevation in LVH, LBBB, and paced rhythm.  Finally, the T-wave inversion in V4-V6 is deeper than typical for LVH.  There is a very long QT.

Anterior STEMI is very unlikely here, even though the patient has a history of LAD CAD:

1) there is no chest pain or SOB
2) there is history of severe concentric LVH
3) there is appropriate and proportional discordance
4) the increase in ST elevation compared to the previous ECG can be explained by heart rate.

Nevertheless, there was still concern for anterior STEMI, so a bedside echo was appropriately done:

Here is the parasternal long axis:

This shows severe LV hypertrophy and good wall motion

A short axis echo was done:

This shows severe concentric hypertrophy and no wall motion abnormality.

This allayed fear of possible STEMI and a formal echo was done which also showed no wall motion abnormality.  It confirmed severe concentric hypertrophy with a diastolic septum measurement of 1.76 cm (normal up to 11 mm)

The first troponin returned at 0.50 ng/mL (normal, less than 0.030).  This patient frequently has troponins in the 0.12 - 0.16  range.

This ECG was recorded 8 hours later.
ST elevation persists, now with more upright T-waves

The next troponin was 0.41 ng/mL.

The syncope and hypotension was thought to be due to volume depletion from over-dialysis.  The patient did well.

Learning Point

1. Severe concentric hypertrophy can result in many ECG abnormalities that mimic STEMI and NonSTEMI.
2. LVH may evolve into conduction delay (IVCD).  The rule of appropriate discordance may come into play in IVCD and also in LVH.
3. Heart rate can affect ST segments, particularly in LVH, LBBB, and paced rhythm
4. Bedside echo can help in differentiating ischemic ST elevation from STE secondary to LVH or other etiologies.


  1. the final diagnosis was hypovolemia; do you think that this might have been suggested by parasternal view showing the free and lateral ventricular walls touching each other? or was this just attributed to the LVH?

    1. Eric,
      Yes. Very good point!
      Steve Smith

    2. it's cardiac amyloidosis

    3. it's cardiac amyloidosis

    4. It could have been, it's a good thought, but it was not.

  2. Steve,
    Any explanation for the changes seen in leads V4-V6 on the repeat ECG 8 hrs later?

    1. I'm attributing it to both heart rate and sequelae of transient, non-ACS, ischemia.

    2. There was a small infarct, remember, with elevated troponin due to supply/demand ischemia (not ACS)


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