Is there a Right Ventricular MI in addition to Infero-postero-lateral MI?

A 40-something woman had sudden chest pain.  She called 911.  This prehospital ECG was recorded:


Here are limb leads:

Here are precordial leads:

Diagnosis?

This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria.

But which myocardial walls are affected?

Inferior
Posterior (as manifested with T-wave inversion)
Lateral (subtle ST elevation)
Is there also RV MI?  Can you tell from this ECG?  (hint: no, you can't tell from this ECG)

When this was shown to me, I said "Activate the Cath Lab."

The providers had been uncertain until I gave my opinion, but then went ahead and activated.

Then this was recorded in the ED 10 minutes after the first:

Now there is massive STE
Many inferior MI are associated with RV MI.  Is there RV MI here?

The left sided 12-lead is imperfect for diagnosing RV MI.  The same week this case arrived, I submitted a revision of a manuscript that is under consideration in which we found:

1) ST depression in lead I is useless in differentiating RCA occlusion with vs. without RV MI
2) ST elevation in V1 is pretty specific (~83%) for RV MI in the setting of inferior MI.
3) ST elevation in V1 is not sensitive for RVMI, and is very insensitive if there is ST depression in V2 (posterior MI pulls the ST segment down and negates any ST elevation that might otherwise be present in V1 during RV MI).

So, if you have the time while waiting for the angiography team, you should record a right sided ECG, because RV MI have higher mortality, are more likely to be hypotensive, and are more nitroglycerin sensitive.

So we recorded a right sided ECG:

V1 = V1R = same position as V2 on left side ECG
V2 = V2R = same position as V1 on left side ECG
V3 = V3R
etc.
Now you can see that there is much STE in V4R-V6R, diagnostic of RV MI.

At angiogram, there was a culprit just distal to the RV marginal branch (not proximal), and so it was called a mid-RCA occlusion.  By the ECG, it should be a proximal occlusion, proximal to the RV marginal branch.

I saw this result the next day and it perplexed me, so I inquired with the cardiologists.

Today, they viewed the angiogram and concluded that the thrombus at the mid RCA must have extended proximally from the culprit ruptured plaque, extending proximal to the RV marginal branch and temporarily occluding it.  However, by the time of the angiogram it had embolized distally,  and had only done so after the right sided ECG was recorded.

See this case in which I saw STE in V1 and called the angiographer to suggest he look more closely at the angiogram.  He did, found the true culprit, and went back in to stent it.

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

This is the ECG.  You can listen to my explanation by playing the video.

Learning Points:

1. To reliably diagnose RV MI, you need a right sided ECG.
2. In inferior MI, ST elevation in V1 is specific for RVMI.  False negatives could be partly due to misleading angiograms!
3. In inferior MI, ST elevation in V1 is not sensitive for RVMI, and is particularly insensitive when there is ST depression (due to posterior MI) in V2.
4. ST depression in lead I is NOT useful in determining the presence of right ventricular MI
5.  The condition of the coronary artery at the time of angiogram may be different than it was 30 minutes prior during recording of the ECG.

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My Comment, by KEN GRAUER, MD (7/11/2018):

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Insightful blog post by Dr. Smith regarding ECG criteria for recognizing acute RV involvement in patients with inferior STEMI. I’ll highlight a few additional points:

• As per Dr. Smith — the initial ECG is diagnostic of acute coronary occlusion MI (OMI). This initial tracing is a superb example of Hyperacute ST-T wave changes. By this, we mean that while there is relatively little ST segment elevation — the T waves in each of the inferior leads are extremely prominent, and much fatter-than-expected at their peak. It is almost as if you can imagine the prominent T wave peak beginning to lift up the ST segment — which then becomes dramatically obvious in the 2nd ECG recorded in the ED just 10 short minutes later! I find it humbling to appreciate how RAPIDLY acute ST-T wave changes may sometimes evolve ...
• Hyperacute ST-T wave changes are transient. In this case, they were gone within 10 minutes. The reason it is so important to recognize hyperacute changes for the brief time they are present — is that when they are seen in “patterns of leads” (ie, in all 3 inferior leads), in association with reciprocal changes — they can be diagnostic of acute OMI before frank ST elevation occurs.
• Confirmation that suspected hyperacute changes are real — is forthcoming once you identify mirror-image reciprocal changes (Figure-1). With acute inferior STEMI — there is an almost magic “mirror-image” picture for the ST-T waves in lead III compared to lead aVL. To better appreciate this concept — I’ve placed a mirror image picture of lead III within the BLUE rectangle — and a mirror image picture of lead aVL within the YELLOW rectangle. Thus, lead aVL shows how reciprocal ST-T depression can also manifest a hyperacute picture.
• Hyperacute changes are also seen in other leads in Figure-1. Note how lead V6 shows a disproportionately large and fatter-than-expected T wave peak. Little wonder this picture in V6 was soon to evolve into significant ST elevation in the 2nd ECG. Hyperacute changes are more subtle in lead V5 — but given the concept of “neighboring leads”, they are nevertheless present. That is, the ST segment in lead V4 is clearly abnormal (ie, coved instead of concave up) — so the ST-T wave picture in V5 reflects a “transition” between what we see in neighboring leads V4 and V6.
• Finally — leads V2 and V3 in Figure-1 manifest a similar ST-T wave shape as is seen in lead aVL. This reflects the mirror-image ST-T wave reciprocal picture in anterior leads that is so commonly seen in association with acute infero-postero OMI.

Figure-1: Initial ECG, obtained pre-hospital from this 40-ish year old woman with new-onset chest pain (See text).

Comparing the First 2 Tracings:

It is interesting follow the evolution of the hyperacute changes seen in the initial ECG. To facilitate this comparison — I’ve put both images into a single figure (Figure-2).

• Note that all leads showing hyperacute changes in the initial ECG (within the RED rectangle) — now show dramatic ST deviation (elevation or depression) in the 2nd tracing (within the BLUE rectangle).
• Localization of the “culprit artery” to the RCA is suggested in the 2nd ECG by: i) More ST elevation in lead III compared to lead II (the opposite tends to be true when the LCx is the culprit artery); ii) marked reciprocal ST depression in lead aVL; and iii) Less ST elevation in lead V6 compared to what is seen in the inferior leads.
• As per Dr. Smith — right-sided leads were needed to diagnose acute RV involvement. However, once right-sided leads confirmed associated RV MI — identification of the RCA as the “culprit artery” is solidified.

Figure-2: TOP — Initial ECG obtained pre-hospital. BOTTOM — 2nd ECG obtained 10 minutes later in the ED (See text).  

PS (7/15/2018): In a July 11 post to the EKG Club — Peter Calvert raised the excellent point about development of prominent J-waves in the 2nd ECG — noting that no J waves were seen on the initial ECG (Figure-2). His astute observation is worthy of brief discussion:

• Rituparna et al document a case study report, in which J waves appeared to be induced by ischemia (Pacing Clin Electrophysiol 30(6):817-819, 2007). The proposed mechanism is complex. The “bottom line” conclusions of their case report were that transient J waves may on occasion be induced by an acute injury current from impending myocardial infarction. Recognition of such J waves may assist in localization of the likely “culprit artery”. The presence of such J waves may be associated with malignant ventricular arrhythmias.
• In Figure-2 — prominent J waves are seen in each of the leads that show ST elevation. In addition, there is prominent notching at the onset of ST depression in lead aVR. In view of the lack of J waves in the pre-hospital tracing — it would certainly seen that these J waves were ischemia-induced, and markers of the “culprit artery”. In the future — I’ll be on the look-out for this interesting ECG sign! (See P.S. below)

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P.P.S.: I believe I found another example of ischemia-induced J waves (See Oct. 24, 2018 ECG Blog — Please scroll down to the bottom of the page to My Comment, in the section "Beyond-the-Core" ...).

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion

This is a video I made a while back.  I thought it was worth a re-post.  For those who don't have time to watch a video, you'll have to read the ECG as shown on this still frame because I lost it and cannot post it.

See down below for explanation if you don't want to watch the video.

See video here:

RV MI diagnosed by ST elevation in V1 from HQMedEd on Vimeo.

 

There is inferior STEMI.  But there is also ST elevation in leads V1 and V2.  When you see this, think right ventricular (RV) MI.  The hypotension is further evidence for RV MI.  There was no right sided ECG.

I heard about the case, and saw the ECG, shortly after the patient left for the cath lab.  I called the interventionalist while the patient was on the table and he told me that the occlusion was not in the proximal RCA, but further down.  I asked if he was sure about this, because the ECG would indicate a proximal RCA occlusion with RV MI.  He took another look and realized that the culprit was indeed in the proximal RCA and that the thrombus had embolized distally.  And so he put the stent in the proximal RCA.

Learning point: Even when you have an angiogram, the ECG findings make a difference.

A 56 year old woman with chest pain and hypotension:

https://vimeo.com/18680419