I was shown this ECG with the history that the patient had chest pain:
This is what I said: “This is not anterior STEMI; it is normal variant, though it is unusual in appearance.”
If you wanted to use the formula, the computerized QTc on all ECGs was 360 ms – 370 ms
4-variable formula value = 12.14 (this is VERY low).
Then I was told that the first troponin I was 14.0 ng/mL (very high!)
Here is the history:
A 40-something male presented with pleuritic left-sided chest pain, radiating to the neck, on and off for 3 days. He has also noted some dull generalized chest pain which he locates more so on the right side of his chest with some associated fatigue and shortness of breath. He does feel generally unwell and notes chills at home.
As soon as the ECG was seen, the patient was moved to the critical care area and cardiology was consulted. They stated that the ECG was normal variant, and the patient was moved out of the critical care area. Then that troponin returned at 14 ng/mL, and he was moved back to the critical care area.
Comment: When I heard all this, I thought it must be myocarditis. But before assuming myocarditis with chest pain and a positive troponin, one must ascertain absence of wall motion abnormality (WMA) or, if there is a WMA, then one must prove by angiography that it is not due to occlusion MI (OMI), acute occlusion of a coronary artery.
If it is OMI, then it is subacute OMI, as the troponin is already very high.
There were several further ECGs, and all looked the same. Here is one:
An emergent formal echo was obtained:
Normal estimated left ventricular ejection fraction .
Regional wall motion abnormality-inferolateral.
There was no anterior wall motion abnormality.
At this point, in a patient with persistent pain, wall motion abnormality, and high troponin, I would think that an emergent angiogram would be done.
It was not and the patient was treated medically.
He was taken for angiogram the next day and found to have a 100% obtuse marginal occlusion (OMI). This was opened and stented.
His ECG never evolved in any way, over several days. When STE is due to ischemia, the ECG always evolves. Absence of evolution is proof that the first ECG showed no evidence of ischemia.
Troponins did not rise any further, which is a bit atypical even for subacute OMI. Opening the artery usually releases troponin into the circulation.
What do we make of this?
The outcome tells us that this ECG was the patient’s baseline ECG. This ECG, though there was ST Elevation, was this patient’s NORMAL ECG! He has normal variant ST Elevation AND an occlusive MI that is invisible on the ECG.
Remember that an ECG can be completely normal in the presence of OMI, especially in the circumflex distribution.
Remember that one of the manifestations of completely normal is normal variant.
Other similar situations:
A patient with ST elevation due to LVH can have OMI and present with his baseline ECG that shows pseudoSTEMI due to LVH.
A patient with ST elevation due to LV Aneurysm can have OMI and present with his baseline ECG that shows pseudoSTEMI due to LV Aneurysm.
The patient needed cath lab activation, but not because of the ECG. He needed it because of refractory chest pain and elevated troponin, and also with a new inferior wall motion abnormality!