This is the conclusion to 49 year old male CC: Chest pain.
Let's take another look at the 12-lead ECG (the one with lead V4 in the position of right-sided lead V4R).
I had thought the original ECGs were lost but I found them in a folder when I was cleaning out my guest bedroom last week.
So let's take a look at the 12-lead ECG.
At first glance, ST-elevation is clearly present in leads II, III and aVF. ST-elevation is also present in leads V5 and V6.
The R/S ratio is > 1 in lead V2 which could suggest posterior infarction.
What appears to be hyperacute T-waves in the right precordial leads (and lead V2 in particular) could represent so-called posterior reperfusion T-waves secondary to a precarious clot.
So why isn't this ECG a slam dunk?
The thing that makes this ECG both unusual and difficult is the lack of reciprocal changes in the high lateral leads I and aVL.
Consider this comment by Stephen Smith, M.D. (from Dr. Smith's ECG Blog) on the EMCrit podcast.
"…we looked at 160 consecutive inferior STEMIs proven by angiographic occlusion…in 99% of all those occlusions there was either ST-depression or T-wave inversion in lead aVL…"
The absence of ST-depression or T-wave inversion in lead aVL in the setting of acute inferior STEMI is unusual.
Does that mean that no reciprocal changes are present on this ECG?
That depends on whether or not you're willing to accept leads aVR and V1 as reciprocal changes. Some authors contend that these leads should be considered.
Unfortunately, you can also have ST-depression in leads aVR and V1 with pericarditis.
Cases like this are difficult because they don't follow the expected pattern. But sometimes they're still sick patients who require immediate reperfusion!
This patient was in fact experiencing an acute STEMI.
The culprit artery was the circumflex (LCX).