I was doing some light reading the other day and stumbled upon this article by R. Shinde et al, entitled Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. I don’t have access to Pacing and Clinical Electrophysiology, but the authors’ original manuscript is available for free here and can’t be too different from the finished product. In the end I wasn’t too intrigued by their whole J-wave hypothesis, but an ECG in their case study did catch my eye.
In the paper, they describe these ECG’s:
Electrocardiogram (ECG) recorded during pain was unremarkable except for presence of “J Waves” in leads I and aVL (emphasis mine). There was no pain thereafter. However, suspecting ischemia, he was kept under observation. Repeat ECG after 12 hours showed no change. However, the ECG after 24 hours showed positive recruitment in R wave voltage in lead V1 along with ST-T changes in inferior and lateral wall leads. The “J Waves” in leads I and aVL were absent. A diagnosis of true posterior wall infarction was made from the ECG. Serum Troponin-T was 3.5 ng/dL (Normal < 0.05 ng/dL). 2D echocardiographic examination of the heart revealed postero-inferior hypokinesia with an ejection fraction of 40%. Subsequently, he underwent coronary angiography, which revealed complete occlusion of left circumflex coronary artery (LCx) after the origin of the first obtuse marginal branch.
As you may have figured by this point, instead of being “unremarkable,” the initial ECG is quite close to being diagnostic for acute coronary occlusion. Why can I say that? Let’s take a look at some of the precordial leads again.
Walking stepwise through what we see:
- The R-wave transition starts a little early with a decent sized R-wave in V2, but this could just be normal-variant for a 28 year-old.
- There are abnormally horizontal ST-segments from V2-V5.
- There is a small amount of ST-depression from V2-V5 (0.5 – 1 mm).
- Accompanying the ST-depression, there are upright T-waves.
- There is a good amount of baseline sway complicating things in V6, but the T-wave shape is unusually convex with a slightly high takeoff when compared to V2-V5. This may be an “injury pattern.”
- The other seven leads are otherwise normal.
All of these findings point to one thing: isolated posterior STEMI. You don’t need fancy J-wave recognition to tell you there is an acute coronary artery occlusion. All you need are posterior leads V7-V9.
Here we don’t have them to confirm that they would have shown ST-elevation, but with the standard 12-lead, coronary angiography, and echocardiogram all pointing towards posterior MI, I feel quite confident that V7-V9 would have been abnormal.
So what does this case highlight?
- Approach everything you read with a critical eye, even peer-reviewed journals.
- The 12-lead ECG doesn’t pick up every MI, but with a trained eye you can spot very subtle STEMI’s and greatly increase its sensitivity.
- Have a low threshold for running posterior leads, especially if the patient has ST-segments that are abnormally horizontal or show even slight depression from V2-V4.