Tuesday, October 18, 2016

LAD occlusion or Early Repolarization?

This male in his 20's presented with chest pain:
There is sinus rhythm with a PVC.
There is 2.5 mm ST elevation at the J-point, relative to the PQ junction, in both of leads V2, V3.
This meets the ACC/AHA criteria (for age less than 40) for anterior STEMI.
The ST segments in V2 and V3 are not upwardly concave (they are straight).

Is it STEMI?  Is it Early Repolarization (Normal Variant ST Elevation)?

We have derived a formula to help with this:

Go here for the formula: http://hqmeded-ecg.blogspot.com/p/rules-equations.html

Here is the study, a derivation and validation: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. Thus, there must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the LAD occlusion group as obvious anterior STEMI.


--Bazett-corrected QTc is the computer measurement.
--RAV4 = R-wave amplitude, in mm, in lead V4.
--ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters.

Formula that was derived and validated:
(1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).
A value greater than 23.4 is quite sensitive and specific for LAD occlusion.

A value less than 23.4 might still be LAD occlusion, but it is unlikely.  A value less than 22.0 is extremely unlikely to be LAD occlusion.

I and at least hundreds of other with whom I have been in contact have used this with a high degree of accuracy.

How to use it?  It does not rule in or rule out LAD occlusion.  Rather, it serves as a warning to evaluate intensively with use of clinical skills, serial ECGs, stat echo and, if needed, angiography.

For this ECG: Strictly speaking, the formula may not apply, as there is a straight ST segment in V2 and V3.  Thus, if we had seen such an ECG in the LAD occlusion group, it would have been excluded as "obvious" STEMI, as early repolarization should have upwardly concave ST segments.  

Unfortunately, there are exceptions to this rule.

Therefore, let's try to apply the rule.  But be very careful with the result.

If we do apply the formula, the numbers are:
--QTc = 410
--STE60V3 = 4.0
--RAV4 = 18
Score = 23.1, which is less than 23.4 and therefore most compatible with early repolarization.

It would be appropriate to do serial ECGs, troponin, and emergent echocardiogram to look for anterior, septal, and apical WMA.


The patient ruled out for myocardial infarction.  This ECG manifests an unusual early repolarization variant.


  1. Dr Smith, instead of using the formula, would you be comfortable saying this is non-STEMI based on non-symmetrical T waves in every lead, no reciprocal changes, good R wave progression and no QRS distortion in V2-V4?
    Also, if it were a STEMI, wouldn't the PVC shows signs of concordant ST or T changes?

    1. Without the formula, I would be fairly confident from Gestalt (overall appearance) that this is not STEMI. But none of the features you suggest are reliable enough by themselves to say this. Also, we don't know from the EKG whether it is a "non-STEMI" or not. That is diagnosed by troponin. We know that the EKG does not show STEMI. There is a difference between "no STEMI" and "non-STEMI." Make sense?

  2. Interesting case! Nice illustration of how Dr. Smith applies his formula — though I think the clinical point he adds ( = it would be appropriate to do serial ECGs, troponin and stat Echo at the time of chest pain) is extremely important to optimal management (in ruling out acute stemi) of this patient. To me, the straight-take-off ST elevation that begins in V1, and is lacking in V6 is especially unusual — so insightful to know that this patient ruled out. Of interest, the 1 PVC that we see is "interpolated" (ie, occurs between to narrow beats without compensatory pause) — and presumably associated with "concealed conduction" (ie, I don't see the next on-time P wave, which means it is probably hidden within the ST-T wave of the PVC — which means this PR interval that follows the PVC is prolonged due to retrograde conduction from the PVC — which is called "concealed" because we have to imply this without actually seeing it on the ECG). Also of interest is QRS morphology of this PVC ( = RBBB/LAHB) — which means this is probably a "fascicular PVC" (from the left posterior hemifascicle). Finally of interest — is that the ST-T wave of this PVC in lead aVL looks highly unusual — which was another reason why optimal management entails serial ECGs, troponin and stat Echo. On occasion, ST-T wave changes of acute ischemia/infarction are only seen in PVCS — so that is one of the considerations to contemplate here. GREAT case!

  3. Thanks steve n ken for a nice explanation


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