Friday, June 22, 2018

A 60-something year old man with chest pain and a wide QRS

Written by Pendell Meyers, with edits by Steve Smith


A man in his 60s with history of CAD s/p PCI, HTN, presented with chest pain which started while doing construction on his house several hours prior to arrival.

Here is his ECG on arrival at 2052:
What do you think? Should you activate the cath lab?














Yes, because there is an acute coronary occlusion causing OMI of the inferior wall. This is evident based on the LBBB with excessively discordant STE in leads II, III, and aVF, with reciprocal findings in I and aVL.

But the current guidelines do not use the modified Sgarbossa criteria, but rather the original Sgarbossa criteria. Because the STE in the inferior leads does not meet the 5mm threshold, it is negative by the original Sgarbossa criteria, as there is no concordant STE or STD.


The patient was given ASA and NTG drip with improvement but not full resolution of pain.

Initial troponin T was undetectable.

Troponin T at 2200 was 0.10 ng/dL (elevated).

Here is his repeat ECG several hours later at 0022:
There has been interval marked improvement of OMI findings, implying the artery has reperfused.


 Another repeat at 0248:
Still no signs of reocclusion.

Troponin T at 0306 was 0.80 ng/dL.

Troponin T at 0649 was 1.60 ng/dL.

The patient was admitted to cardiology for urgent cath.

1629: Cath shows an acute thrombotic ostial RCA in-stent restenosis culprit, 95% stenosed at the time of cath with TIMI 3 flow. Stent placed with good angiographic result. He also had a 70% chronic mid LAD stenosis, as well as 30% LCX.
Left main, LCX, and LAD, no large vessel occlusions.
LAD lesion described above.

RCA showing 95% ostial stenosis immediately after the tip of the catheter.

Another view showing the ostial RCA stenosis.

Intervention on ostial RCA lesion underway.

Post intervention with good angiographic result.



Troponin T peaked at 3.75 ng/mL the next morning (large MI). The characteristics of this lesion and the highly elevated troponin meet our definition of acute coronary occlusion surrogate criteria (when the angiogram is not performed at the time of the occlusion) used in the derivation and validation of the modified Sgarbossa criteria studies.


I looked back in the chart and found an almost identical presentation 4 years prior. He presented at that time with chest pain.


Presentation ECG at 2317:
Even more obviously positive for the modified Sgarbossa criteria with very excessive discordant STE in II, III, and aVF, with reciprocal findings in aVL and I. Notice how the original Sgarbossa criteria are falsely negative in this case both times.

0124
Cath showed a 90% in stent thrombosis in the proximal RCA, described as "severely thrombotic." TIMI flow was increased from 2 to 3 after intervention.

0253
Findings resolving.

0937
Ongoing resolution with a hint of terminal T wave inversion in the inferior leads.


Serial Troponin T rose from undetectable to 3.63 ng/dL over the course of about 16 hours.



Learning Points: 

Use the modified Sgarbossa criteria to look for OMI in LBBB. The modified criteria are more sensitive than the original criteria as evidenced by cases like this.

Just because there is not complete occlusion at the time of cath does not mean there wasn't complete occlusion at the time of the ECG prior to cath. This is why we have criteria for OMI when the angiogram is not performed at the same time as the ECG evidence of occlusion. Finally, complete transmural ischemia (what happens when there is OMI without collateral circulation) does not even require complete occlusion. A near-occlusion with TIMI 1 flow without collateral circulation may result in similar amount and speed of myocardial loss, and therefore similar benefit of immediate reperfusion therapy until proven otherwise.

Unlike most diagnostic tests, the modified Sgarbossa criteria are also more specific than the unweighted Sgarbossa criteria.  It is unusual to find a test that is both more sensitive and specific than the original test, but this is one.  

Here is the table from the validation cohort:
Compare lines 1 and 4
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Comment by KEN GRAUER, MD (6/23/2018):
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Highly insightful case by Drs. Meyers & Smith regarding the clinical utility of Modified Smith-Sgarbossa Criteria for diagnosis acute OMI in the setting of LBBB. Details in the paper by Dr. Smith et al on use of these modified criteria is found under the Rules + Equations Tab on this blog. I will play “Devil’s Advocate", and offer the following points:
  • As emphasized by Dr. Meyers — Use of the Modified Smith-Sgarbossa Criteria are clearly diagnostic in this case!
  • Another way to arrive at the same conclusion that the 1st ECG (@ 20:52) is diagnostic of acute OMI is qualitative — by recognizing the presence of ST segment elevation in leads in which it just should not be there. This is seen in all 3 inferior leads in ECG #1 (Figure-1). Support that this ST elevation is acute is provided by the presence of “mirror-image” reciprocal ST-T wave changes in lead aVL.
  • IF any doubt existed about the acuity of the initial ECG — lead-to-lead comparison with the 2nd ECG that was done (@ 00:22) should have clarified the picture. While slight-but-definite differences in QRS morphology make interpretation of ST-T wave changes challenging for the chest leads in the 2 tracings shown in Figure-1 — there is unmistakable reduction in inferior lead ST elevation, and in high lateral lead (ie, leads I, aVL) reduction in reciprocal changes. Given associated reduction in chest pain — the clinical picture of OMI with spontaneous reperfusion is irrefutable with this 2nd ECG done at 00:22.
Figure-1: Simultaneous view of the 1st 2 ECGs in this case to facilitate lead-to-lead comparison and appreciation of qualitative ST-T wave changes.
My purpose in posting the first 2 ECGs recorded together in Figure-1, is that this combination tells a story. For those clinicians not yet as comfortable with qualitative ST-T wave assessment — a picture is worth 1,000 words.
  • Although correctly classified as LBBB — ECG #1 is an atypical form of LBBB because: i) there is excessive fragmenting; ii) there is no predominant upright R wave in any of the lateral leads; and iii) the initial Q waves seen in the inferior leads are not “normal” for LBBB in view of the positive, then negative deflections that follow (ie, a qrS is not a “normal” inferior lead morphology with simple LBBB). In this context — there is inferior ST elevation that should not be there in each of the 3 inferior leads in ECG #1.
  • Perhaps the most markedly abnormal-appearing ST-T wave in ECG #1 is seen in lead I. Despite the artifact and tiny overall QRS complex in this lead — the depressed and straightened ST segment “shelf”, that then rises to a disproportionately tall and peaked terminal T wave has to be assumed acute until you prove otherwise.
We often learn the most from challenging cases that do not go the way we might optimally want them to go. Soul-searching is tough work. Armchair quarterbacking the next day is far easier. Our THANKS to Drs. Meyers and Smith for this highly insightful and instructive case, in which the cath lab should have been activated after ECG #1 (@ 20:52) — and if for any reason not then — then after ECG #2. In the “retrospectoscope” — a 2nd tracing would have been ordered before 00:22. Finally, appreciation of qualitative ST-T wave changes can facilitate optimal application of modified Smith-Sgarbossa Criteria.


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