This patient with "NSTEMI" was not allowed to go to the cath lab. Then the ED provider obtained an emergent coronary CT angio. What do you think it showed?

 Submitted by Shakita Crichlow MD, edits by Meyers

A female in her 60s presented with chest pain off and on starting the day before presentation. The chest pain was left sided, pressure-like, intermittent, without aggravating or alleviating factors, and associated with mild shortness of breath. She become worried when she took her blood pressure at home and found it to be 200 systolic, so she decided to come to the ED at that point. 

Here is her initial ECG:

What do you think?

Raw findings:

 - Sinus rhythm

 - STE in leads II, III, and aVF, reaching at least 1.0 mm in III and aVF

 - Large Q wave in lead III

 - STD in aVL and I

 - Subtle STD in V2

Interpretation:

Diagnostic of inferoposterior transmural injury, with the most common etiology being Occlusion MI of the RCA until proven otherwise. The normal QRS complex followed by focal inferior STE and reciprocal STD in I and aVL is diagnostic of inferior involvement, while the subtle STD maximal in V2 is diagnostic of the posterior involvement. The Q wave in III is pathologic.

There is at least 1.0 mm of STE in leads III and aVF, objectively and unequivocally. In our recent study  we would have called this STEMI(+) OMI. Interestingly, many providers (including every single one involved in this case) would not call this STEMI even though it meets these objective (and ineffectively insensitive) criteria. Cases like this are why the cardiologist in our study classified EVEN FEWER cases as STEMI than Dr. Smith and I did. I am chronically at a loss for words to respond to the cardiologists who refuse to act according to the same paradigm they simultaneously refuse to give up.

1.0 mm STE in aVF.

The ED provider did not quite recognize the STEMI criteria on this ECG, but clearly was worried about the findings in the inferior leads. They immediately consulted interventional cardiology who refused to take the patient to the cath lab, stating that the patient has only an NSTEMI and does not benefit from emergent management. They asked the provider to call back with the initial troponin.

The initial troponin T (contemporary assay, URL less than 0.01 ng/mL) of course returned undetectable (less than 0.01 ng/mL), as is the case in a very large portion of OMI and STEMI with acute onset symptoms, especially with 4th generation (not high sensitivity 5th generation) assays. 

--Even with hs assays, 10-15% are below the 99th percentile URL at presentation, for both I and T.  

--25-40% are below the 52 ng/L level which the Eur Soc of Cardiology states has an adequate positive predictive value in high risk chest pain patients to diagnose acute MI)

The ED provider had another discussion with the cardiologist, who heard about the negative troponin and suggested that the patient didn't even need to be transferred to the cath lab center. After further discussion, the ED provider ordered a stat coronary CT angiogram. It is unclear to me whether the provider was thinking:

a) "I can see that there is acute high risk ACS, I'm worried about RCA occlusion MI, and if they don't believe it then I'll just prove it to them and keep trying to get her the care she needs."

or

b) "I don't see clear STEMI criteria, and the first troponin was negative, so maybe this isn't even ACS at all. Maybe I can rule her out for ACS with a normal CT angio."

I am not sure whether the patient had ongoing pain at this time, but a repeat ECG was ordered:

There is still active ongoing injury, but it looks slightly less than the prior ECG. I would not be surprised if the lesion were starting to open just barely.

The coronary CT angio was done within a few hours of her arrival:

Coronary CTA:

"Dominance: the patient is co-dominant.

Left main: no plaque or stenosis.

Left anterior descending: mild multifocal calcific narrowing of the LAD in the proximal and middle thirds with the most severe stenosis estimated at 30-35%.

Left circumflex: mild to moderate multifocal calcific narrowing of the circumflex in the proximal and middle thirds with the most sever stenosis estimated at 40-50%. 

Right coronary: There is minimal punctate calcific narrowing in the proximal third with luminal stenosis estimated at 20-25%. Probable high-grade narrowing in the mid RCA near the acute right marginal branch. Severe motion artifact and blurring at this level limits assessment in the majority of cardiac phases. Degree of maximal coronary stenosis - 70-99% in the mid RCA. 

Interpretation - ACS likely."

Around this time, a second troponin T resulted at 0.73 ng/mL (this is quite high, and rapidly rising, and surely would have peaked higher than 1.0 ng/mL if further troponins had been ordered, which has been repeatedly confirmed in multiple studies as a reasonable retrospective cutoff differentiating OMI peak troponins from non-occlusion MIs).

With this information in hand, the ED provider called the cardiologist back and they now both seemed to understand that the patient likely had an acute occlusion or near occlusion of a major coronary artery (OMI!). 

So the patient was then emergently transferred to the cath lab center, straight to the cath lab.

Another ECG was recorded before transfer:

Definitively reperfusing, with resolution of STE and STD, and with terminal T wave inversion in lead III. The lesion is at least barely open at this time.

Cath:

RCA culprit lesion with subtotal approximately "98%" lesion with TIMI 3 flow. A stent was deployed with 0% residual stenosis with brisk TIMI 3 flow. 

There was also a 70% LAD lesion which was not deemed a culprit lesion, but was also stented nonetheless.

"IMPRESSION: 65-year-old female patient admitted with non-ST-elevation myocardial infarction. Percutaneous coronary intervention with drug-eluting stent of the right coronary artery..."

The patient did well and was discharged home with a final diagnosis of "NSTEMI."

Learning Points:

This case demonstrates how acute coronary artery occlusion could be better understood if it were evaluated and treated analogously to acute cerebral artery occlusion: using the "Large Vessel Occlusion" (LVO) paradigm. If you present with symptoms of a possible acute occlusion in your MCA, providers universally understand that initial screening tests and exam is insufficient, and the patient must receive emergent imaging to identify LVO. But if you present with possible symptoms of acute occlusion in your RCA, everyone simply looks for millimeters on a piece of paper and calls it a day if they don't find it!

Why is that? It is because CT cerebral angiogram (or MRI, which is also easy) is the diagnostic test of choice for stroke and CT is so easy to do because it does not take a team or special vascular access, and because its only function is diagnosis. If treatment is required, only THEN do patients go to the cath lab.

Perhaps we should be managing MI like stroke: CT angio first, and cath lab activation if CT angio is concerning. One problem is this: imaging the heart with CT is far harder than the brain because of motion. It usually requires no atrial fibrillation and slower heart rate.

Read this post on coronary CT angio:

Management of MI can be similar to stroke: Use CT angiogram. Don't depend only on STE on ECG for reperfusion?

In this case, a patient with acute RCA OMI was not recognized by ECG (even though it could have been), but instead was recognized by emergent coronary CT angio. Although I and probably all patients would prefer expert level ECG interpretation to recognize OMI as soon as possible and noninvasively, I am very glad that the coronary CT angio was done quickly in this patient! If not, the patient likely would never have been recognized as active RCA occlusion, and would have had greatly delayed reperfusion. In this particular case, the patient reperfused just slightly before the cath. However, many STEMI(-) OMIs will not; furthermore, many reperfused OMIs like this patient will reocclude in the middle of the night and be ignored until the morning when it is too late. 

Ultimately, OMI is not about the ECG. OMI is about the actual, deadly, fixable pathology happening to the human beings we treat: the acute coronary Occlusion Myocardial Infarction. Any method of identifying this pathology (ECG, coronary CT angio, bedside ultrasound) can help the patient get the care they need.

In a normal QRS complex (without any reason for baseline ST segment abnormalities), STE in the inferior leads with reciprocal STD in aVL should be considered inferior OMI until proven otherwise. Similarly, STD maximal in V1-V4 should be considered posterior OMI until proven otherwise.