Atypical Chest Pain: Suspicious ECG, and a Left Main ACS is found in a 30-something
Posted May 07 2013 8:25am
A male in his 30s presented with chest pain, cough, and sore throat.
He had been seen in clinic the day prior for cough x 1 month and sore throat. A strep test was positive and he was treated with penicillin, and also with acetaminophen and ibuprofen.
On the day of ED (ER) presentation, he presented with 5 hours of intermittent sudden onset left side chest pressure unrelieved by ibuprofen, with associated vomiting and SOB. There was some association with moving and palpation, but also some improvement with NTG. An ECG was obtained immediately
Sinus rhythm. There is some inferior and lateral ST elevation that is very subtle, and is associated with a very small amount of ST depression in lead aVL (which we have found to always be associated with inferior MI). There are large T-waves in II, aVF, and V4-V6. There is also a tiny amount of terminal T-wave inversion in lead III (see comparison below). There is a deformed T-wave in V2 (see discussion and graphic below)
I was highly suspicious of MI, so an ACS workup was initiated and we recorded a bedside echo (unavailable) which showed no inferior wall motion abnormality (or anywhere else). He was given aspirin and clopidogrel 600 mg. Because of the absence of wall motion abnormality, the patient's age, and the atypical pain, we decided to serially evaluate him and not activate the cath lab. A second ECG was recorded at 37 minutes.
This is identical, except the terminal T-wave inversion in III is gone.
Around this time, the initial troponin returned at 2.0 ng/ml. Because he had persistent chest pain and persistent ECG abnormalities, we activated the cath lab. He was taken and found to have open coronaries. The angiographer was concerned about inadequate opacification of the distal left main and proximal LAD, and did intravascular ultrasound. He confirmed a plaque with fissure in the distal left main coronary artery. There was no indication for stenting, but aggressive and prolonged antithrombotic and antiplatelet therapy (to "cool down" the fissured plaque) was instituted for this very high risk lesion.
Here is the ECG after the cath
The STE and reciprocal ST depression are gone, and T-waves are smaller. The previously deformed T-wave in V2 is normal now.
Some have asked what I mean by deformed T-wave in V2. Here are V2 and V3 from the first 3 ECGs side-by-side
Notice in the 1st and 2nd recordings, the initial part of the T-wave is flattened, and the upright part is very small. This is possibly a result of anterior wall ischemia, or (what I initially thought and the interpretation I favor) a result of subtle posterior STEMI which is pulling the ST segment down (ST segment starting to elevate if recorded from posterior leads). I don't know that any of this interpretation is true, but is based on observing scores of ECGs with known posterior transmural ischemia and reperfusion.
Troponin I peaked at 8 ng/ml. A formal echo showed no wall motion abnormality. An ECG at 24 hours was recorded
This confirms inferior and lateral infarction, with increased ST elevation and evolution of T-waves (reperfusion T-waves).
At 48 hours
The troponins trended down from a peak of 8 ng/ml.
The ECG suggests inferolateral MI. The T-wave in V2 suggests either posterior or anterior ischemia. The angiogram is consistent with anterior (LAD) and posterolateral MI (left main supplies the LAD and circumflex), and of inferior MI if the the circumflex is dominant (the cath report did not specify this).
In any case, what would be considered by most to be a "nonspecific" ECG was highly suspicious and prompted rapid evaluation and management in a young man who might otherwise be thought "low risk" with young age and atypical chest pain. The finding of reciprocal ST depression in lead aVL confirmed the pathologic nature of the inferior ST elevation.