Pay now (in the evening) or pay later with interest (in the middle of the night).

A 50 something male presented in the evening to ED for evaluation of chest pain that started at 1600. He states that it feels like burning and pressure, like GERD. He reports this was similar to how he felt when he had his heart attack 4 years prior, now s/p 4 stents. 

(The history gives a subtle hint that this might be another acute OMI.)

 

Patient normally takes lisinopril 40 mg daily, atorvastatin 80 mg daily, and ASA 81 daily. Has not taking lisinopril for 2 weeks because he ran out. 

An ECG was recorded 16 minutes after arrival:

What do you think?

Smith: clearly diagnostic of posterior and high lateral OMI (ST depression V2-V4, with hyperacute T-wave in aVL and recriproal STD in inferior leads).

PMCardio Queen of Hearts AI Model:

The Queen of course also thinks it is acute OMI, for the same reasons.

Note: the 2022 ACC Expert consensus Chest pain guidelines state that "posterior STEMI-Equivalent" is a sign of acute coronary occlusion. They do not give advice on how to diagnose it, but we have published that, in the context of acute chest pain, ANY ST depression maximal in V1-V4 was 96% specific for an OMI with need for PCI.  

The cath lab was not activated.

Instead, Cardiology was consulted and they recommended Nitro IV (and of course ASA and heparin). NTG was titrated to greater than 120 mcg/min.

The chest pain continued for hours.

At 2.5 hours, another ECG was recorded.  The patient was still having chest pain.

The findings have improved, especially in aVL/inferor leads.  

There is still some ST depression in V4 and V5.

Spontaneous reperfusion is likely, aided by aspirin and heparin. 

2.45 hours with posterior leads:

STD in V3 remains, though subtle

V4-V6 are really V7--V9.  

They show inverted T-waves, suggesting that the posterior MI has reperfused.

Here are the troponins while the patient is in the ED, with persistent pain:

Even if you don't believe the ECG, it should have been clear from the very first troponin that this is acute MI.  And with refratory (persistent) pain, the patient should go to the cath lab immediately.

It is very common for such patients with "VERY HIGH RISK NSTEMI" to not undergo guideine recommended ＜2 hour angiogram.  In this study by Lupu et al., only 6% of eligible patients were treated according to the guidelines.

The cath lab was not activated until the middle of the night, 7 hours after arrival.

By waiting, not only could the patient suffer harm, but the cath team needed to come in in the middle of the night rather than in the evening.

Shortly before angiogram:

Some ST depression remains in V2-V4

The pain finally resolved just before the angiogram.

Angiogram:

--"Suspected culprit for the patient's non-ST elevation myocardial infarction with refractory chest discomfort (although it had resolved prior to arrival to the cardiac catheterization lab), is a ruptured plaque in the distal circumflex with local embolic occlusion of the distal OM 3."

So apparently, the initial pain was due to occlusion in the distal circumflex.  The pain resolved when that reperfused, in spite of the fact that the thrombus embolized and occluded the small distal OM3.

"--Previously placed stents in the proximal LAD and RCA are patent, but there is a native vessel occlusion in the distal RCA beyond the most distal stent margin."

"--Severe disease of the second diagonal branch and suspected chronic total occlusion of a branch of LPL 1 are also noted."

Last troponin measured was 9500, a pretty large MI.  (2/3 of STEMI have a peak 4th generation troponin I greater than 10.0 ng/mL, but it is uncertain how well that correlates to high sensitivity troponin of 10,000 ng/L.)

Comment:

The first ECG is diagnostic of OMI that does not meet STEMI criteria.  ("NSTEMI-OMI").  Fortunately for the patient, the worst area of occlusion probably spontaneously reperfused.  But in order to follow the NSTEMI guidelines, which are that a diagnosed NSTEMI with persistent pain (refractory to medical therapy) should go to the cath lab emergently, they needed to take him even if they were not convinced of OMI by the ECG.

And, in doing so, it required the cath lab to be activated in the middle of the night rather than in the early evening.  

But early evening would be more convenient for the team AND better for the patient.

So one can choose to pay attention to the ECG and "pay now" (come in and do the procedure) or not pay attention to the ECG and thus "pay later" (be required to come in later in the middle of the night.)  

If there is no spontaneous reperfusion, the patient pays the interest by losing more myocardium.

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MY Comment, by KEN GRAUER, MD (2/20/2025):

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I fully realize that I was able to review today's case in the comfort of my home, sitting back in my desk chair as I reviewed the serial ECGs on my big computer screen. That said — errors were made that we need to learn from. And, the BEST way to learn is to pause for a moment — and put yourself to the test.

The Challenge:

Before looking at my thoughts below — Take another look at this case as it is presented above by Dr. Smith.

• What specific things should have been done sooner in the hope of reducing the time until cardiac to much less than the 7 hours it took?

Below are my thoughts — starting in Figure-1 with my labeling of the initial ECG.

Figure-1: Comparison between the first 2 ECGs in today's case.

MY Thoughts on What Should Have Been Done Sooner:

• It took 16 minutes after arrival in the ED to record the 1st ECG. As per Dr. Smith — this patient has known coronary disease from a previous MI, and in his words — his CP (Chest Pain) felt "like his previous heart attack". With that history — ideally, the order for recording the initial ECG would have been given within a minute or two on seeing this patient.

We are not told how ECG #1 was interpreted. We know only that the cath lab was not activated. Instead — cardiology was consulted as the patient was treated with progressively increasing doses of IV Nitroglycerine that failed to relieve his CP. It apparently was not until ~2.5 hours that a 2nd ECG was recorded (with the patient still having CP).

• The initial ECG was misinterpreted. As per Dr. Smith, despite the lack of ST elevation — ECG #1 is clearly diagnostic of acute postero-lateral OMI. Given the presenting history — the cath lab should have been activated immediately on seeing this ECG.
• There is no ST elevation with posterior OMI in conventional leads. Instead — there is maximal ST depression in leads V2 and/or V3 and/or V4 (exactly as we see in ECG #1). There will also often be a positive "Mirror" Test (as I show in the RED insert in ECG #1).
• There is no need to delay further by getting posterior leads that are lower in sensitivity and more difficult to interpret than the standard 12 leads (These concepts on ECG assessment of posterior OMI illustrated in My Comments in the September 21, 2020  — January 3, 2022 — and December 18, 2022 posts in Dr. Smith's ECG Blog, among many other posts).
• In addition to maximal ST depression in V2-V4 — the ST segment straightening in lead aVL of ECG #1 is clearly abnormal — with reciprocal ST depression in the inferior leads — suggesting lateral (as well as posterior) involvement. 

Regardless of how the initial ECG was interpreted — the ECG should have been repeated long before 2.5 hours:

• The very suggestive history for an acute event + unrelieved CP alone (even without ECG abnormalities) is indication for prompt cath to determine the anatomy. Ideally — a 2nd ECG is obtained with 15-20 minutes after the initial tracing in such a patient.
• As per Dr. Smith — significant persistent Troponin elevation in association with persistent CP continued ...

The 2nd ECG was not correctly compared to the 1st ECG:

As we repeatedly emphasize — unless interpretation of serial ECGs is accomplished by placing both tracings you are looking at together, important findings will be missed.

• Prove this to yourself. How many leads in ECG #2 show a difference in ST-T wave morphology compared to ECG #1? (To facilitate this comparison — I put these first 2 tracings in today's case together in Figure-1).

ANSWER:

It should be obvious from comparing ECGs #1 and #2 in Figure-1 — that all 12 leads show change in ST-T wave morphology.

• ST depression is less in leads II,III,aVF; V2,V3,V4 in ECG #2.
• The T waves have flattened in leads I,aVL and in each of the chest leads.
• There is less ST elevation in aVR.
• In addition to suggesting some degree of spontaneous reperfusion in the posterior wall — this difference between ECG #1 and ECG #2 represents a "dynamic" ST-T wave change in this patient with ongoing CP and elevated Troponins ==> yet one more indication for prompt cath.