A man in his 60s with chest pain. Cardiologist refuses to take to the lab. Obvious STEMI, even with criteria. Yet final diagnosis "NSTEMI". This happens far too often.

Submitted by Anonymous MD, edits by Meyers

A man in his 60s with past medical history of multiple sclerosis and hypertension was brought in by EMS from home for chest pain that started acutely just prior to arrival.  He rated the pain at 9/10, describes as pressure, radiates towards the left arm with associated shortness of breath, diaphoresis and had one episode of emesis. He did not have a prior history of CAD or other cardiac disease. His pain improved to 6/10 after EMS gave him 3 sprays of sublingual nitroglycerin and 324 mg of aspirin.

 

Prehospital ECGs:

What do you think?

Both ECGs are diagnostic of acute LAD OMI until proven otherwise, with STE in V1-3 and I/aVL, hyperacute T waves in V1-V4 and I/aVL, poor R wave progression, and reciprocal findings in inferior leads. Probably does not meet STEMI criteria in these ECGs, but it is obvious nonetheless. 

Smith: In addition, the 1st and 3rd complexes in V1-V3 are RBBB-like PVCs, and they are even more diagnostic than the conducted beats, with concordant STE in V1 and massive STE in V2. 

Prehospital STEMI was activated. 

Bedside ECG immediately upon patient arrival (with active chest pain):

Despite the poor quality, leads V1 and V2 have progressed to meet frank STEMI criteria.

 

Cardiology at bedside upon patient arrival and cancelled “Code STEMI”, despite the EM provider's concerns.

Initial troponin (the assay is Troponin I with reference range 0-0.045 ng/mL): <0.015 ng/mL.

A bedside echo reportedly showed an anterior and apical WMA (video not available).

In the next hour after cancellation, the patient received multiple doses of fentanyl without improvement in chest pain. Hydromorphone was given next, but the pain persisted. 

Cardiology was called again with concern for ongoing STEMI(+) OMI.

"Cardiology is adamant that this is not a STEMI and may instead be related to his underlying MS. Recommend continuing morphine and avoiding nitro given his currently low BP, trending troponin."

ECG @ 1 hr after arrival:

ECG @ 1.5 hours after arrival:

We could use this one to train medical students in their first lecture on the most obvious STEMI(+) acute coronary occlusions.

 

Second troponin I: elevated 0.453 @ 1.5 hours after arrival.

 "Cardiology re-paged after several previous discussions, did not want to take patient to cath lab as they do not feel this is STEMI, recommend treating as NSTEMI with therapies we have already initiated."

 

Cardiology consult note:

“On presentation to emergency room EKG reviewed.  Not consistent with a STEMI and a STEMI activation was canceled.  He continues to express chest discomfort which appears to be atypical, and he is actively vomiting.

EKG comment: EKG SR with NS-ST changes

TIMI score UA = 1. 

A very likely differential is Multiple sclerosis Hug (MS Hug), and that diagnosis would be likely in the setting of the patient ruled out of ACS."

After several attempts to convince cardiology to take patient to cath lab and several discussions with EM colleagues in the department, ED administration, house supervisor, cardiology leadership; the patient was admitted as NSTEMI on heparin gtt and remained with active chest pain. Receives CTA on the way to floor bed per cardiologists request to assess for dissection – unremarkable CTA.

 

ECG @ 4 hours after arrival:

Improvement, likely interval reperfusion.

ECG @ 5 hours after arrival (patient shaking):

Obvious reocclusion.

After admission: third troponin I not drawn until 2250 returns at 77 ng/mL. 

ECG @ 7 hours after arrival:

Interval reperfusion.

Despite the ECGs showing potential intermittent repefusion, the medical ICU was consulted for ongoing persistent chest pain requiring nitro drip.

The ICU team of course contacted the on call cardiologist again. This time the cardiologist stated that he did not feel that cath could be performed at this time due to "contractures of the lower extremities due to MS, such that he cannot lay flat on the cath table." The cardiologist reportedly advised the ICU to try valium and/or baclofen overnight to see if the patient could better tolerate positioning for the cath lab table in the morning.

ECG hours later:

 

Fourth troponin I during first night of admission: 131 ng/mL. (very large MI)

No further troponins measured, peak unknown.

 

ECG next morning:

QS-wave in V2 shows completed infarction

Angiogram for "NSTEMI" was performed the next morning at 9:30 AM. Apparently the patient had no difficulty tolerating the procedure at that time.

Total thrombotic occlusion of the left anterior descending artery right at the bifurcation of the first diagonal branch. s/p PCI with good angiographic results. Beyond that the artery is patent all the way down to the apex. 100% TIMI flow 0 pre intervention, TIMI 3 post intervention.

Also, 90% stenosis of the mid LCX which was also stented. 

ECG status post PCI: 

The patient survived the hospitalization. Long term outcome will likely not be obtained.

 

The ED provider involved brought the case to administrators for review. Reportedly, other cardiologists in the group reviewed the case and felt that no action needed to be taken. No perceivable action was taken from the point of view of the EM physician.

Learning Points:

Please do not write me to tell me that this case is unusual, or that there must have been other factors that we are not privy to, explaining the inaction. I envy you and your practice environment if you actually believe it is unusual. One day maybe it will be unusual, but not while we still live under the STEMI paradigm.

Many on Twitter will say something to the effect of "maybe you should bring this up with the hospital's QI process instead of posting it on social media." It was done in this case, and as usual in my experience, nothing significant happened. I feel it is vitally important to show these cases to the world. What else can we do? Answer: promote and research the OMI paradigm shift.

The STEMI criteria miss a significant number of acute coronary occlusions, but this patient is an example of one of the very obvious OMI patients who quickly develops STEMI(+) OMI. Notice that we can diagnose his OMI earlier using expert ECG interpretation.

In real life, malpractice cases like this one are easily swept under the rug by simply retrospectively continuing to call this patient an "NSTEMI." It doesn't matter whether the ECGs actually show STEMI criteria, as above. The cardiologist and the chart simply say "no, it is not STEMI," and in the STEMI paradigm that is the final word, that is the actual definition of the outcome. This is what happens when the Acute MI paradigm is defined based on an ECG finding instead of an actual pathophysiology or outcome. It doesn't matter what was obviously happening to the patient which was proven by the angiogram and troponins, all that matters was whether the cardiologist states the ECG was STEMI or NSTEMI. As we see in this case, retrospective adjudication and reconciliation does not happen. The final diagnosis does not change. No one cares what the EM or IM physician diagnoses.

No matter how difficult it may be to override the cardiologists decision, this patient would have benefitted from thrombolytics, or transfer to a facility or interventionalist that is actually interested in emergent management of acute coronary occlusion. It is easy to say this, and more difficult to do this when multiple cardiologists and supervisors tell you not to in real time. 

Multiple sclerosis "hug" is an interesting phenomenon in which thoracic cord involvement is postulated to cause a sensation of band-like constriction or pressure in the chest and/or abdomen. It can mimic ACS. See this article for further information.