Monday, February 20, 2017

Chest Pain, LBBB, and a ratio that does not quite meet the Modified Sgarbossa Criteria


A 55 year old male heavy smoker presented with agonising chest pain and this ECG:
There is sinus rhythm.
There is left bundle branch block (LBBB)
There is no concordant ST elevation.
The highest ST/S ratio is in V3, at approximately 4.5/24 = 0.19
This is not a high ratio, but it is also not normal.

See this post:

A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia

The mean maximal ST/S ratio in non-ischemic LBBB is about 0.11.  So 0.19 (19%) is abnormal.

In our validation study of the Modified Sgarbossa Criteria for diagnosis of acute coronary occlusion, we found that it performed similarly well using a cutoff of 20% or 25%:

Sensitivity and Spec at 20%: 84% and 94%
Sensitivity and Spec at 25%L 80% and 99%

So at a ratio of 0.19, there is still a high probability of occlusion.

I was sent this ECG by Facebook messenger, and asked my interpretation.  Here is my response:

"V3 is suspicious for excessive discordance. I would say it does not look like an acute STEMI, but I could be wrong."

The patient received thrombolytic therapy.

An angiogram was done after thrombolysis:

It showed moderate diffuse coronary disease and no thrombus.
LAD: mid segment moderate disease
OM: mid segment moderate lesion.
OM2: ostial moderate lesion
Ramus: moderate mid segment lesion
RCA: diffuse disease mid to distal, moderate lesion

The angiogram was considered to be "negative" for a culprit.

An ECG was repeated:
LBBB is resolved.
There is T-wave inversion in V2 and V3 highly suggestive of Wellens' waves
This represents LAD reperfusion

An echo was done:

There were septal, apical, and anterior wall motion abnormalities.

     --(high sensitivity troponin I BiomerieuxVIDAS TNHS):
99% reference = 19 ng/L (%CV = 7% at this level)
LoD = 2 ng/L

Initial: 13 ng/L (detectable, but still below the 99%)
Followup: 38 ng/L  (above the 99% and with a significant rise)

Here is the manufacturer's chart for interpretation:
You can see that a rise in high sensitivity troponin of greater than 10 ng/L is a "rule in."

Even with a "negative" angiogram, the weight of evidence heavily favors LAD occlusion at the time of the ECG:

1. There was excessive discordance, even if it did not meet the 20% or 25% cutoff
2. There was coronary disease, even if no thrombus; thrombus would likely be lysed by tPA
3. The followup ECG (most important) was consistent with reperfusion of the LAD
4. There were corresponding wall motion abnormalities.
5. The high sensitivity troponin had a diagnostic delta, even though the absolute level was minimally elevated

Learning points

1.  The cutpoints of 20% and 25% for the Modified Sgarbossa criteria maximize specificity, but are not fully sensitive for acute coronary occlusion.  Every case must be evaluated carefully.

2.  Not all ACS has a clearly visible culprit.

3.  The best way to assess whether ST elevation represents ischemia is to look at followup ECGs.  If the ST elevation resolves or evolves, then it is ischemic, even with all negative troponins!

See my last case:

Chest pain, ST elevation, and negative serial trops: normal variant ("early repol"). Right?


  1. Thank you doctor for this case.

    could the Chapman's sign here be the clue to go with the diagnosis of ACS?

    1. Great question. It is actually Cabrera's sign. I had intended to mention that. "Cabrera's sign" is a notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5. "Chapman's sign" is a notch on the ascending limb of the R-wave in I, aVL, or V6).

    2. However, Chapman's and Cabrera's signs are signs of old, not acute, MI.

  2. sir .
    i am getting confused ! once before you said modified scarbossa validated. but now you decrease the cut of to 19 . what is wrong ?

    1. The cutoff of 25% is very specific, but only about 80% sensitive. Nothing is perfect!

  3. Doesn't the first ECG also show Cabrera's sign? Not very sensitive but in context may have been useful?

    1. Ian,
      I had intended to mention that. However, Chapman's and Cabrera's signs are signs of old, not acute, MI.

  4. My interpretation (prior to reading what happened) — was nothing definitive BUT — that there were 3 leads that caught my eye regarding not-quite-normal ECG findings. In addition to the borderline J-point ST elevation in lead V3 that Dr. Smith discusses in detail — I thought neighboring lead V4 suggested disproportionate ST-T wave upright morphology (given modest S wave depth) — and, neighboring lead V5 manifests slight coving in the J-point area that for the last 2 (of the 3) complexes in this lead, seems to be slightly above the baseline. Although the QRS in lead V5 is small in size and fragmented, it nevertheless is primarily upright — and the ST-T wave with typical LBBB should in general be oppositely directed to the positive QRS in V5 as it is in V6. This makes for 3 leads in-a-row ( = V3,V4,V5) that while non-definitive, do show questionable findings … Finally, lead II has a horizontal “shelf” to its ST segment that is just not “normal” — and which could reflect a reciprocal change … None of these findings appeared definitive to me — but with a high-likelihood presentation (ie, a 55-year old smoker with “agonizing chest pain” and LBBB) without possibility of prompt catheterization — the decision to use thrombolytic therapy seems reasonable (and perhaps preferable to waiting for serial changes). Fascinating follow-up tracing and deductions by Dr. Smith on this case! In addition, my bet would be that IF an earlier tracing on this patient showing LBBB had been available — that it would have been revealing and different from what we see in this LBBB tracing. THANKS again to Dr. Smith for presenting this case, and adding insight to astute clinical use of modified Smith-Sgarbossa criteria when the patient presents with LBBB


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