A 33 year old male with acute back pain radiating to the chest

Written by Pendell Meyers, with edits by Steve Smith

Case

I was called to the EMS control room to answer an RMA (Refusal of Medical Advice). After the call was over, just before I was about to go back to the grind in our acute emergency department, my fantastic EMS colleague paramedic Jess Boyle asked me for an opinion on these 2 ECGs from a single patient, one done immediately after the other, without any other clinical information:

What do you think?










Both of the ECGs show sinus rhythm with normal QRS complex morphology. There is ST segment depression in leads III and aVF with inappropriate large "volume" T-wave inversion. This is reciprocal to a small amount of ST elevation in lead aVL, with suspiciously large amount of area underneath the ST segment and T-wave, suspicious for hyperacute T-waves. In the context of the inappropriate (inappropriate for the QRS) STE in aVL with reciprocal inferior STD, these T-wave must be considered truly diagnostic for hyperacute T-waves. In the first ECG, take a close look at the PVC that occurs in leads aVR, aVL, and aVF just before the precordial leads start. What do you notice?


There is concordant ST elevation in that PVC in lead aVL. PVCs, like any other form of abnormal conduction (LBBB, ventricular paced rhythm, etc) generally follow the rule of appropriate discordance (which states that the ST segment and T wave will deviate away from the majority of the abnormally conducted QRS complex). So in the absence of superimposed ST elevation, the PVC in aVL should have an isoelectric or depressed ST segment following that large, abnormally conducted R wave. Instead, the J point is clearly above the baseline. This is concordant ST elevation, and we believe based on much experience with this exact question and many prior cases showing this, that this is also diagnostic of acute transmural ischemia just as it has been shown to be in LBBB (and soon, ventricular paced rhythm).

So this ECG is diagnostic for the fact that the high lateral wall has very recently lost its blood supply. The ECG reports the acute transmural thickness of the myocardium at the cellular level, and the cells do not know or care why they have acutely lost blood supply - any etiology of acute coronary occlusion, or even small vessel ischemia such as is seen in takotsubo stress cardiomyopathy, or in "No Reflow" phenomenon after opening of an occluded coronary artery, will produce the same ECG changes. On a population level, by far the most common etiology for acute coronary occlusion is type 1 ACS (plaque rupture causing acute thrombotic occlusion). But remember, the ECG just shows the fact that there is an occlusion, not the etiology of the occlusion.


Back to the case:

The EKG had been sent to medical control approximately 15 minutes prior to my review, and my paramedic friend had been worried by it so he took it immediately to an ED physician for review. Although he mentioned that he was worried about aVL and the inferior reciprocal changes, the reviewing attending disagreed and did not think that it warranted prehospital cath lab activation.

I was immediately worried about what might happen to the patient. I asked him which hospital the patient had been transported to (our medical control services oversees many different hospitals). Luckily, he responded that the patient had just arrived in our ED! So I went to find him and make sure that the receiving team had gotten copies of these prehospital ECGs.

As it turns out, the receiving team had not gotten a copy of these prehospital ECGs. I gave them the ECGs, told them my concerns, and asked for some info about the patient:

He was a 33 year old male with history of asthma and smoking who called EMS for sudden onset chest pressure beginning 1 hour prior to arrival. He stated he had just finished urinating when he was reaching to flush the toilet when he suddenly felt a cramping pain in his mid back. When he went immediately to lay down, the pain radiated into the center of his chest. He took tylenol with no improvement, then called EMS. EMS administered ASA, NTG, and 5mg morphine with improvement in pain. He adamantly denied any ingestions, drugs, cocaine, etc.


Here was his first ECG in the ED, during this time he supposedly had 2/10 pain which was improved since onset:

The findings are much more subtle compared to the prehospital ECGs, but still present. There is also a tiny new Q wave compared to the priors. Because the findings have decreased, but the T-wave is still upright, it is hard to say whether the artery is still fully occluded or whether we might be witnessing the beginning of the changes of reperfusion. 

If the artery is reperfusing, we should soon see complete resolution and/or the classic reperfusion sequence of terminal T-wave inversion followed by full T-wave inversion over time. 

Usually, improvement in pain is very helpful in this decision, however morphine may confound your assessment in the setting of ACS. Unlike aspirin, NTG, or other ACS medications, which improve pain by treating the underlying cause, morphine does not treat the occlusion, and unfortunately may be effective in masking the pain of acute coronary occlusion, inspiring less frequent serial ECGs and serial examinations of a sick patient. "Masking" of ischemia may be the reason that morphine is associated with worse outcomes in ACS (http://prdupl02.ynet.co.il/ForumFiles_2/14835373.pdf)

Overall, the treating team interpreted the clinical picture as improving, and did not immediately activate the cath lab but instead continued aggressive bedside evaluation and serial ECGs.

There was no appreciable wall motion abnormality upon bedside echo without contrast.

The iStat point of care troponin I returned at 0.38 ng/mL (elevated, normal less than 0.08 ng/mL). In general, iStat troponins can be unreliable, although the higher the result the more likely it is true. The initial troponin T returned at 0.04 ng/dL (also slightly elevated from normal which is less than 0.01 for this assay).

At this point, only ~20 minutes after arrival, they activated the cath lab.

The patient was taken immediately for cathetization, which showed "mid to distal 1st diagonal branch revealed 90% stenosis and mid-distal segment attenuated and appears in spasm, unresponsive to intracoronary NTG and intracoronary nicardipine." The RCA and LCX were normal. See the cath images below.

Normal RCA.

In this view you see the LAD (largest vessel coming down the center of the screen), with the large 1st diagonal  branching off and appearing robust until approximately halfway down its length, when it suddenly is extremely narrowed and then followed by downstream low attenuation. See next picture for annotation.

The arrow points out the beginning of the spasm of the D1.

The cath report states that he had improvement in symptoms and ECG findings despite the fact that the angiographic appearance was not improved after the intracoronary administration of NTG and nicardipine. Given this improvement and the suspected spasm as the etiology, they did not place a stent, but instead planned to treat the patient with medical therapy including amlodipine and NTG as needed.

His serial troponin T rose from initial 0.04 to 0.43 to 0.66, then started to trend back downward.

Here is his first post-cath ECG:

There appears to be no resolution of active injury on the ECG. Rather, it appears as though there is ongoing injury and progression along the classical pattern of OMI. This is concerning for persistent downstream ischemia despite an open artery angiographically.

Two more hours later. Now you can see the development of larger Q waves in lead aVL. There is persistent STE in aVL with reciprocal STD in III and aVF.

No longer any R wave in aVL, replaced entirely by Q wave. This does not necessarily mean that the full thickness of the high lateral wall has infarcted, because stunned but viable myocardium may also produce a Q wave and later recover.

The cardiologists plan on repeat catheterization in several weeks after medical therapy to reassess whether any other intervention will be necessary.


Learning Points:

Make sure you have a system in place so that your EMS ECGs get delivered to the receiving ED team every time, even when they are originally interpreted as normal.

The ECG cannot tell you the etiology of OMI. By the numbers, the etiology must be assumed to be one treated by immediate reperfusion therapy (in the absence of a specific known alternate cause). This is not a "false positive" OMI, rather this is one of the few patients who has something other than thrombus causing the OMI. The only appropriate way to differentiate occlusive spasm from occlusive thrombus is by performing an emergent angiogram. See our other cases of spasm here.

This patient never met the "STEMI criteria", like many other very significant acute coronary occlusions and near occlusions.

Young people can have acute MI.

Don't forget to look for the signs of OMI within PVCs.

I believe that even transient OMI/STEMI should ideally be taken to the cath lab if feasible, because it is unlikely that the patient will get serial ECGs and close monitoring enough to recognize reocclusion before more myocardium is lost, or worse, even in the best of hands.