The revelation that the LCX was the culprit artery in the recent case study made me go back to the peer reviewed literature to see where I went wrong.
Let’s look at the evidence.
From Sgarbossa et al., Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician. Am Heart J. 2001;141:507-17:
“The typical electrocardiographic pattern of inferior infarction consists of ST-segment elevation in leads II, III, and aVF. The occlusion is in the RCA in 80% to 90% of cases and is in the LCX in the remaining patients. Higher ST elevation in lead III than in lead II strongly suggests compromise of the RCA.
A bedside differential diagnosis between culprit arteries can also be attempted by examining additional electrocardiographic leads. Because the only lead that faces the superior part of the left ventricle and directly opposes the inferior wall is aVL, ST depression in lead aVL is almost always determined by RCA occlusion (sensitivity, 94%; specificity, 71%), without indicating concomitant involvement of the posterior wall or the right ventricle. Injury in leads II, III, and aVF without ST depression in aVL indicates proximal LCX occlusion.
Several studies in the 1980s concluded that ST elevation in leads V5 through V6 during inferior injury signaled LCX occlusion. However, because most inferior infarctions are caused by RCA occlusion, the positive predictive value of this sign is poor. The arteries that supply the posterolateral region of the left ventricle are the obtuse marginal branch of the LCX, the posterolateral, and the LAD branches. Thus ST changes in leads V5 and V6 indicate rather posterolateral ischemia triggered by either RCA or LCX occlusion. When this ST elevation is significant (>2 mm), it is probably a sign of “mega-artery-related” (either the RCA or LCX) infarction with a large ischemic burden.”
Let’s look at the 12 lead ECG from the case study:
ST elevation in leads II, III and aVF? Check.
ST elevation lead III > ST elevation lead II?
Remember this table from Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory – Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004?
It states that when ST elevation in lead II is equal to ST elevation in lead III, you should consider the T wave amplitude!
Well, that’s no help either, since the T wave amplitude in leads II and III are also the same.
ST depression in lead aVL? Check.
ST elevation in leads V5 and V6? Less than 2 mm, but check.
If you had to venture a guess based on these criteria, the smart money would be on the RCA.
Now let’s look at modified leads V4R and V5R.
This created some cognitive dissonance for me. I was surprised not to see ST elevation in these leads, particularly with the clinical correlation of borderline bradycardia and hypotension.
Let’s look at our cheat sheet.
In the last analysis, you can’t always identify the culprit artery based on the 12 lead ECG (or in this case, the 14 lead ECG).
Either that, or you have to be smarter than I am (in which case you should leave a comment).
This patient’s unusual coronary anatomy (I’m tempted to call it a mega-LCX) seems to confound the commonly accepted criteria.
It’s still fun to guess!
I’ve often said that acute inferior STEMI should be treated as RV infarction until proven otherwise!
I still feel that way. It’s interesting that leads V4R and V5R correctly identified that the patient was not experiencing RV infarction, but with the hypotension, the patient still required a fluid bolus.
Was it worth the paramedic’s time collecting leads V4R and V5R?
I’m not sure it changed anything for the patient, but it is interesting from an academic perspective!