Sent by Anonymous, written by Pendell Meyers and Steve Smith
An elderly man with good neurologic baseline but history of CABG presented to the ED with acute lightheadedness, shortness of breath, and chest pressure radiating to both arms. He had just recently been admitted for similar symptoms which had been diagnosed as an NSTEMI, and he received a stent to the ostial LCX one week ago. At that time his EF was 30%.
He returned to the same hospital where he had just received his LCX stent.
Here is his first ECG at triage, with chest pain temporarily resolved:
What do you think?
The first ECG has an intra-ventricular conduction delay (IVCD) which is of the LBBB type (for textbook LBBB most would list a monophasic R wave in lateral leads V6 which is not present in this case). For such a QRS complex, the modified Sgarbossa criteria should be used. With the exception of lead V2, there is appropriate ST segment discordance. However, in V2 there is no discordance (i.e., it is isoelectric, which suggests that there is relative ST depression). Moreover, the ST segment is downsloping, which should never happen in LBBB. This is nearly diagnostic of posterior OMI, to the point where serial ECGs and close investigation is mandated. Additionally, there may be evidence of inferior involvement, with slightly too much STE and large volume T waves.
The 2nd ECG does indeed evolve to the point where the modified Sgarbossa rule is positive, with concordant STD in V2 and V3 (and also in V4,5)
Bottom line: the 2nd ECG clearly meets original and modified Sgarbossa criteria with concordant STD maximal in V1-V4. It is diagnostic of acute posterior OMI until proven otherwise, in the setting of this patient with clear ACS symptoms.
Here was his most recent ECG on file (not a baseline, recorded at the end of his stay for his NSTEMI)
Looks like posterior reperfusion T waves, which would make sense for a LCX STEMI(-) OMI. Notice the QRS is narrower at this time, without LBBB, but you could call it LAFB. |
The EM provider diagnosed positive Sgarbossa criteria given the concordant STD in leads V2 and V3, and activated the cath lab.
The cardiologist cancelled the activation.
The first troponin (high sensitivity trop T) returned at 1600 ng/L. Again they tried to get the patient considered for emergent cath, with ongoing pain despite aspirin and heparin. But the cardiologist refused.
Side note: high sensitivity troponin T cannot directly be translated to compare to the older assays with which we have studied OMI, but we can make a rough guess: 2,000 ng/L roughly equals 2.00 ng/mL, well above our cutoffs used in our OMI studies (1.00 ng/mL for contemporary troponin T assays). This is a large MI. (This level of troponin T is roughly equivalent to high sensitivity troponin I of over 20,000.)
See this study of hs trop T in OMI: Baro R, Haseeb S, OrdoƱez S, Costabel JP. High-sensitivity cardiac troponin T as a predictor of acute Total occlusion in patients with non-ST-segment elevation acute coronary syndrome. Clin Cardiol [Internet] 2019;42(2):222–6. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1002/clc.23128
Troponin peaked at 2000 ng/L in the middle of the night.
Early the next morning the patient developed progressively worsening hypoxemia and hypotension.
He coded and died about 12 hours after ED arrival.
No angiogram was ever done during that visit, and no autopsy was requested.
It is clear that this patient died of untreated posterior OMI, leading to cardiogenic shock, with the thrombosis at the new LCX stent being the obvious culprit.
This patient had countless indications for emergent cath, and several advocates who tried to get this patient the correct care. But still was denied proper treatment and died.
I get these cases all the time. Sadly, it is a normal event in 2021 under the STEMI paradigm, despite the fact that it is so easily diagnosable, and even when it is not diagnosed on ECG, there are multiple guidelines that indicate that this patient deserves angiogram for ongoing ACS despite medical management and ACS with cardiogenic shock.
If you are a cardiologist reading this case, I would really appreciate your insights for the following questions: given the fact that this case was most likely an occlusion at the site of his LCX stent that had just been placed 1 week ago, what are the "repercussions" of that event in terms of metrics and statistics? Is the cardiologist disincentivized to cath the patient for fear of diagnosing a "complication" of the stent 1 week ago? What actual, tangible repercussions happen to the cardiologist? to the cardiology department? Please help us understand why these seemingly easy decisions are more complicated than we can see.
Learning Points:
Use the modified Sgarbossa criteria for LBBB (studied and proven), ventricular paced rhythm (studied and proven), and also for other LBBB-like QRS complexes (not yet studied). The principles of appropriate discordance can be applied to all wide QRS complexes in general.
In the setting of ACS clinically, whether in LBBB or in normal conduction, STD max in V1-V4 is posterior OMI until proven otherwise.
Regardless of the ECG, patients with ACS with ongoing ischemia (as shown by ECG ischemia or ongoing symptoms) despite medical management, or with electrical instability or cardiogenic shock, should receive emergent angiogram as per all guidelines.
"NSTEMI" OMIs have almost double the mortality of NSTEMIs without OMI. Patients like this one make it obvious why this is.
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