Cardiologists need to keep an open mind and be capable of listening to, and learning from, the Emergency Physician

This was sent by a reader.  He wanted to remain anonymous but also wanted to express appreciation for the great job his 4th year resident did.  She immediately recognized OMI and did everything she could, in multiple conversations with cardiology, to advocate for the patient and the need for the cath lab.  

Unfortunately, they did not listen or learn.

I would like to commend our own cardiologists at Hennepin who are not only extremely well informed, but very open to new information from us Emergency Physicians.  We appreciate it!

68 female presented at 3PM with chest pain that, by history, sounded like ischemic discomfort:

The part of the computer read that is cut off says:

"Atrial sensed, ventricular paced rhythm." 

You can see it also says "No further analysis attempted due to paced rhythm"

What do you think?

This is clearly a positive ECG in the setting of paced rhythm by BOTH the Sgarbossa criterial and the Modified Sgarbossa criteria.

It is positive in 6 leads!!  (There is concordant ST elevation in II, III, aVF and V4-V6).  There is concordant reciprocal ST depression in aVL.  Unmistakable!!

There is almost 1 mm of concordant ST depression in V2.

The emergency physician activated the cath lab.

What do you think the cardiologist said?

You guessed it!!

Cardiology "declined" cath lab despite extensive conversations.  He/she kept stating to the ED resident, "Why do you keep bringing up Sgarbossa?"

The initial contemporary troponin I returned negative at 0.01 ng/mL.  Remember that the initial troponin, even if high sensitivity, is often normal in OMI and even in STEMI (+) OMI!! 

A stat echo was performed on the floor after admission.  It showed an inferolateral wall motion abnormality.  Duh.  What did they think it would show?

By 5 AM, the troponin I was at 28 ng/mL.  This is a typical level for a STEMI.

Another ECG was recorded:

All ischemic findings are gone.

This could be due to spontaneous reperfusion (autolysis) or to completed MI, but not after significant myocardial loss.

Up to 36% of STEMI have autolysis at emergent angiogram (1).

A much higher percent will reperfuse by the next day, but not after a lot of damage is done.

The fact that 25% (2) of NonSTEMI still have an occluded artery at next day angiogram (2) implies that many far more than 25% of STEMI (-) OMI have an occluded artery at presentation.

She was taken for an angiogram at 11 AM:

mid LAD 80%, circ OM1 90%, RCA 70%.  All open.  

The culprit was not mentioned; it could have been the OM1 or the RCA.

She was referred for eval for CABG. 

Comment:  I am critical of the cardiologist not because he/she did not know about the Modified Sgarbossa Criteria, or did not recognize the OMI.  Everyone has areas of knowledge they are unfamiliar with.  This is what I am critical of:  He/she was arrogant.  He/she did not listen. He/she did not stop to think that perhaps he/she could learn something from the Emergency Physician.  He/she did not have an open mind.  He/she could have said: "Could you tell me more about the Sgarbossa criteria?"  Although it is difficult for specialists to admit there is something that they do not know about their specialty that an Emergency Physician does know, it is not acceptable.

In 2016, an informal poll on Medscape by my mentor, K. Wang showed that only half of physicians believe you can diagnose MI in the setting of a ventricular paced rhythm.  We showed in the PERFECT study (3) that the ECG is quite accurate using the Modified Sgarbossa Criteria.  The manuscript is under revision for Annals of EM.

1.  Rakowski T, Dudek D, Dziewierz A, et al. Impact of infarct-related artery patency before primary PCI on outcome in patients with ST-segment elevation myocardial infarction: the HORIZONS-AMI trial. EuroIntervention [Internet] 2013;8(11):1307–14. Available from: http://dx.doi.org/10.4244/EIJV8I11A199

2.  Khan AR et al. 2017. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. doi:10.1093/eurheartj/ehx418

3. Perfect Study

While it is true that old MI, as diagnosed by Q-waves, is greatly obscured by LBBB and paced rhythm, acute occlusive MI appears to be fairly readily diagnosable, almost as much as in normal conduction.  In normal conduction, (i.e., no LBBB or paced rhythm), acute coronary occlusion MI (OMI) is diagnosed in approximately 75% of cases.  The other 25% are not diagnosed until rule-in by troponin and next day angiography.(1)

1. Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis.  European Heart Journal 38(41):3082-3089; November 1, 2017.  In this study, of 40,000 patients with NonSTEMI, 10,000 had OMI that was not diagnosed until the next day.

We have shown the ACO (OMI) can indeed be diagnosed in paced rhythm with comparable sensitivity and specificity.   It is important to realize however that many OMI may be difficult to diagnose in any ECG rhythm, and that NOMI (non-occlusive MI) is often impossible to diagnose on the ECG.

Here is our abstract from SAEM 2018.  We are writing the manuscript right now, with more patients enrolled.

The Smith-Modified Sgarbossa Criteria Accurately Diagnose Acute Coronary Occlusion in Emergency Department Patients With Ventricular Paced Rhythm.  

Kenneth W. Dodd1 , Deborah L. Zvosec2 , Michael A. Hart1 , Laura Bannister3 , Gary Mitchell4 , George Glass5 , Brooks Walsh6 , Harvey P. Meyers7 , David Miranda8 , James Corbett-Detig9 , Vaishal M. Tolia10, Louise Cullen11, Stuart Zarich6 , Sally Aldous12, William Brady5 , Timothy Henry13, Adam J. Singer14, Stephen W. Smith15, and PERFECT Study Author Group 1 Hennepin County Medical Center, 2 Minneapolis Medical Research Foundation, 3

Background: The Smith-modified Sgarbossa criteria (MSC) are frequently recommended for diagnosing acute coronary occlusion (ACO; STEMI-equivalent) in the setting of ventricular paced rhythm (VPR). The MSC are positive if one of the following criteria are met in at least 1 lead: concordant ST Elevation (STE) of at least 1 mm, concordant ST depression of at least 1 mm in V1-V3, or ST/S ratio less than -0.25 in leads with at least 1 mm STE. We hypothesized that the MSC will have higher sensitivity for diagnosis of ACO in VPR when compared to the original Sgarbossa criteria. Methods: The PERFECT study (#NCT02765477) is a retrospective, 16 center, international investigation of ED patients from 1/2008 - 12/2016 with VPR on the ECG and symptoms of acute coronary syndrome (ACS). Data from ten sites are presented here. Acute myocardial infarction (AMI) was defined by the Third Universal Definition of AMI. For this analysis, ACO was defined as angiographic evidence of coronary thrombosis with peak cardiac troponin-I (cTn-I) at least 10 ng/mL or cTn-T ≥ 1 ng/ mL. Blinded physicians adjudicated angiogram reports for coronary lesions and thrombolysis in myocardial infarction (TIMI) flow score. Separate, blinded physicians performed ECG measurements. Trained abstractors recorded data on standardized forms. Statistics were by Mann Whitney U, Chi-square, and McNemar’s test. Results: There were 46 encounters in the ACO group (median age 76 [IQR 65-82], 36 (76%) male) and 79 in the No-AMI group (median age 70 [61-75], 48 (61%) male). For ACO, median peak cTn-I was 65 ug/L [IQR 35-239] and cTn-T 3.3 ng/mL [IQR 2.2-8.3]. For No-AMI, median peak cTn-I was 0.015 ug/L [IQR 0-0.09]. For ACO, the sensitivity and specificity of the MSC and the original Sgarbossa criteria were 83% (95%CI 68-91) versus 63% (48-76; p less than 0.005) and 99% (92-100) versus 99% (92-100; p = 0.5). In pre-defined subgroup analysis of patients with TIMI 0-1 flow and peak cTnI at least 10 ug/L or peak cTnT at least 1 ng/mL (n = 29), the sensitivity was 87% (69-96) for the MSC versus 58% (39-75) for original Sgarbossa criteria (p less than 0.05). Conclusion: This represents the largest study of patients with VPR and angiographically-proven ACO. The MSC were highly sensitive and specific for the diagnosis of ACO in patients presenting to the ED with VPR and symptoms of acute coronary syndrome.

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MY Comment by KEN GRAUER, MD (10/5/2020):

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Today’s case provides a superb example of how acute OMI can sometimes be definitively recognized even in the presence of pacing. Unfortunately, this was not recognized by the cardiology team despite a typical ischemic-sounding history + clear evidence on ECG — and stat Echo consistent with ECG findings.

• As we’ve shown in numerous cases on Dr. Smith’s ECG Blog — Modified Smith-Sgarbossa Criteria can be used to objectively identify acute OMI in both LBBB and paced tracings. Dr. Smith emphasizes how the initial ECG in today’s case is positive for these criteria in no less than 6/12 leads.
• I would add that from a qualitative standpoint — the initial ECG in today’s case shows clear ECG abnormalities suggestive of acute OMI in no less than 10/12 leads!

For clarity — I’ve put both of the ECGs from today’s case together in Figure-1.

• Please TAKE another LOOK at ECG #1. In the context of an older patient who presents with new-onset ischemic-sounding chest pain — WHICH leads in ECG #1 are abnormal?
• WHICH anatomic lead areas are affected?

Figure-1: The 2 ECGs in today’s case (See text).

MY Thoughts on ECG #1: As per the computer interpretation — there is an atrial-sensed, ventricular-paced rhythm with 100% ventricular capture.

• The rate is ~70-75/minute.
• Without knowing what the pacing parameters are, and what this patient’s unpaced ECG looks like — it’s hard to know to what extent the QRS complexes we see here might reflect some component of fusion between spontaneous conduction of sinus P waves vs ventricular-paced complexes (ie, the PR interval appears to be no more than 0.15 second). Regardless — the point to emphasize is that at times, one can assess ST-T wave changes for acute ischemia, even when there is 100% pacing.

No less than 10/12 leads in ECG #1 show abnormal ST-T waves.

• There is 1 mm of ST elevation with a hyperacute-looking T wave in each of the 3 inferior leads = in leads II, III and aVF. This is not a normal ST-T wave appearance in either a paced or spontaneous rhythm. To the extent that spontaneous P waves are conducting — the T waves in inferior leads clearly look fatter-at-their-peak than should be expected. To the extent that inferior lead QRS complexes are paced — one would normally expect ST-T waves to be oppositely-directed to the upright QRS complexes (and one would not expect there to be any ST elevation).
• That these inferior lead ST-T wave changes are “real” — is supported by the mirror-image ST-T wave depression we see in lead aVL.
• Acute inferior lead changes are often accompanied by acute posterior involvement. This posterior involvement is suggested in ECG #1 by the abnormal ST-T wave appearance in leads V1 and V2.
• ST-T waves in leads V3, V4, V5 and V6 look similar to each other — and similar to the abnormal ST-T wave appearance we saw in each of the inferior leads.
• IMPRESSION: Regardless to what extent QRS complexes in ECG #1 are paced or conducted — the abnormal ST-T wave changes we see in this older woman with new chest pain suggest acute infero-postero-lateral OMI.

MY Thoughts on ECG #2: Putting the 2 ECGs in today’s case together makes it easy to appreciate the serial changes:

• The inferior lead ST elevation and hyperacute T wave changes have almost completely resolved.
• I see essentially no change in ST-T wave appearance in high lateral leads I and aVL between ECG #1 and ECG #2.
• In the chest leads — the T waves in leads V1 and V2 are now upright. There is probably no significant change in the ST-T wave appearance in leads V3 and V4 — but the slight ST elevation and hyperacute T wave changes seen in leads V5 and V6 in ECG #1 have been replaced by ST segment flattening in lead V5, and shallow T wave inversion in lead V6.
• BOTTOM Line: Seeing indisputable changes in 7 leads between the time ECGs #1 and #2 were obtained convincingly shows that the ST-T wave abnormalities noted above in ECG #1 were truly acute changes. As per Dr. Smith — these changes in ECG #2 are consistent with some degree of spontaneous reperfusion.

Learning Points: A picture is worth 1,000 words. Regardless to what extent QRS complexes in ECG #1 were paced vs conducted — the “picture” to memorize is that the combination of ST elevation, hyperacute T waves and ST-T depression seen in so many (ie, 10/12) leads in a patient with new chest pain has to be interpreted as an OMI until proven otherwise.