LBBB: Using the (Smith) Modified Sgarbossa Criteria would have saved this man's life

Case submitted and written by Dr. Jesse McLaren (@ECGcases), of Emergency Medicine Cases

Reviewed by Pendell Meyers and Steve Smith

An 85yo with a history of hypertension developed chest pain and collapsed, and had bystander CPR. The paramedics found the patient with ROSC and a GCS 7, and an ECG showing LBBB with possible lateral ST elevation. The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. On arrival, GCS was 13 and the patient complained of ongoing chest pain. Vitals were HR 58 BP 167/70 R20 sat 96%. Below is the first ED ECG, labeled LBBB by the machine. Are there any indications to activate the cath lab?

There is sinus rhythm, LBBB and disproportionately discordant STE in V4 (ST/S = 2/6 = 0.33) that meets the Modified Sgarbossa Criteria. There is also a hint of concordant STE in V5 but it might be less than 1mm. There is also a hint of concordant STE in III.

In III, there is slightly less than 1 mm STE in the context of an isoelectric QRS. In LBBB, when the QRS is isoelectric (neither positive nor negative), the ST segment should also be isoelectric. 1 mm of STE here is highly suggestive of OMI.

Lead aVL has at least 1 mm of reciprocal STD in the context of a QRS which is under 4 mm. Thus, there is nearly 30% discordant STD, which is very specific for OMI (see both the derivation and the validation of Smith Modified Sgarbossa criteria - see validation results below).  

According to the validation of the Modified Sgarbossa Criteria, the traditional weighted Sgarbossa criteria only has a negative likelihood ratio of 0.51, which is insufficient to rule out Occlusion MI in a patient with a high pre-test probability. The Modified Sgarbossa Criteria has a better negative likelihood ratio (though still insufficient in a high risk patient), and a very high positive likelihood ratio.

Accordingly, in the algorithm by Cai et al for patients with LBBB and ischemic symptoms (See below) — the first indication for PCI is clinical: patients with hemodynamic instability or acute heart failure. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. If the patient is stable, the next consideration is ECG criteria: Sgarbossa criteria of 3 or more (concordant STE or concordant STD in anterior leads), or Modified Sgarbossa Criteria (disproportionate STE). If none of these are present then proceed with serial ECGs, troponins, and bedside echo.

In this case, cardiology noted “old LBBB, negative Sgarbossa”, so they kept the patient in the ED for repeat ECGs and troponin levels. But the lack of traditional Sgarbossa criteria is not reassuring enough for such high pretest probability (elderly patient with chest pain, out of hospital cardiac arrest and LBBB), and the Modified Sgarbossa Criteria confirms Occlusion MI in this case.

 

The patient still had chest pain and the ECG was repeated one hour later, labeled LBBB by the machine. Are there any indications for cath lab activation?

Disproportionately discordant STE remains in V4 and has now progressed to V3 (ST/S = 3/11 = 0.27), while V5 is back to isoelectric. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes. But it didn’t meet traditional Sgarbossa criteria so the cath lab was not activated.

 

Thirty minutes later the first Troponin I came back elevated at 650 ng/L (normal <26), and bedside ultrasound found anteroseptal akinesia. The patient still had chest pain and a third ECG was performed. Any indications for cath lab activation?

An initial level of 650 ng/L represents a too rapid rise to be attributable only to Type II MI from brief cardiac arrest.  This ALONE is very strong evidence of acute coronary occlusion.

There is still disproportionate STE in V3-4, and there is also inferior concordant STE in III/aVF (or if you think the QRS in III is isoelectric, not technically concordant but still diagnostic), with reciprocal STD in aVL. So now there is high-pretest probability + refractory ischemia (with biochemical and echo confirmation) + Modified Sgarbossa + original Sgarbossa + dynamic changes. (Using Barcelona criteria V4 had discordant change of 1mm in a lead of 6mm or less, and the reciprocal STD in aVL had excessive discordant STD, but neither of these would have added anything to the modified Sgarbossa criteria in this case).

 

The cath lab was activated three hours after arrival in the ED, and found a 100% mid LAD occlusion and 90-95% RCA occlusion. Which was the culprit lesion?

 

Occlusion MI with both anterior and inferior injury can be from 1) occlusion of the LAD which wraps around the apex to supply the inferior wall (our colleague Emre Aslanger has shown us that the LAD does not have to literally be a type III "wraparound" LAD to supply the anterior and inferior leads' territories), 2) occlusion of a large RCA which supplies the inferior and lateral walls, or 3) occlusion in one of these arteries that interrupts collateral circulation to the other. 

Because only the inferior leads met Sgarbossa criteria on the third ECG, the RCA was felt to be the culprit lesion and the LAD was assumed to be chronic. So the RCA was stented. This is faulty reasoning because the anterior leads meet the better disproportional discordant STE criteria of the Modified criteria.

But the first two ECGs met Modified Sgarbossa Criteria in leads V3-4, and bedside echo found anteroseptal wall motion abnormalities corresponding with the LAD occlusion. The patient continued to have chest pain after the RCA was reperfused, so the LAD was then stented. But by this time the patient went into cardiogenic shock and passed away. As the discharge note acknowledged in hindsight, the inferior ECG changes resulted from LAD occlusion that compromised collateral circulation to a previously diseased RCA.

Meyers note: As Dr. McLaren points out, skilled ECG interpretation helps us see prospectively that the LAD was the clear culprit in this case. RCA occlusion typically should not produce OMI in V3, for example, unless there is chronic LAD occlusion with RCA-to-LAD collaterals. It is clear to me that the LAD is at least one culprit. The anterior leads are more diagnostic in this case than the inferior leads. It seems to me that the angiographers' lack of knowledge of the modified Sgarbossa criteria may have been a critical missing piece of information for this patient's care.

Learning points

1.      Refractory ischemia or electrical/hemodynamic instability are indications for the PCI. VF arrest is of course "electrical instability"!

2.      Relying on traditional Sgarbossa criteria can lead to reperfusion delays

3.      Modified Sgarbossa Criteria can help identify Occlusion MI and the culprit vessel, complemented with bedside echo

4.      Anterior and inferior STE can result from wraparound LAD occlusion, RCA occlusion, or occlusion of one compromising collateral circulation to the other