A male in his 40's complained of 4 hours of chest pain.
Here is his initial ECG
There is ST elevation in II, III, and aVF, with a minimal amount of reciprocal ST depression in aVL. There is also minimal ST elevation in V2-V4, with a QTc of 375 and STE at 60 ms after the J-point is 2 mm. R-wave is 14.5 mm. So the equation value is only 19.75. Not an LAD occlusion. However, the Q-wave in V4 is unusual. The equation study excluded ECGs with Q-waves in V2-V4, so this must be evaluated with that in mind.
There was a previous ECG on file
This one has no ST elevation anywhere, and no ST depression in aVL, and smaller Q-waves in V4-V6.
Here are all the leads side-by-side for easier comparison. For each lead, the presentation ECG complex is on the left and the old ECG complex on the right
Now the difference is more apparent. One can also see now that the T-waves in V1-V6 are larger, and in V2-V4 are really hyperacute.
While you may not want to activate the cath lab based on this, you should certainly order serial ECGs every 15 minutes if the pain is ongoing.
80 minutes after the initial ECG, the troponin returned elevated. At this point, it would be again important to obtain a repeat ECG. This was not done. It is now clear that the chest pain and ECG findings are due to ACS, and it is high risk ACS.
If there is any increase in ST elevation, the patient should go to the cath lab emergently.
In any case, given that the pain is ongoing, and there is no doubt that it is ACS, aggressive antiplatelet, antithrombotic, and anti-ischemic therapy is indicated. The patient should be started on aspirin, high dose clopidogrel (600 mg), a GP IIb-IIIa inhibitor like eptifibatide (Integrilin), and Heparin (LMWH or unfractionated, depending on the institution), and a nitroglycerine drip if the pain is still ongoing.
If these do not relieve the symptoms, or at least resolve the ECG findings, consult the interventionalist for possible emergent angiography.
The management above was undertaken and the patient's pain resolved. The STE also resolved
Most STE is resolved. ST depression in aVL is resolved. Q-waves persist.
Troponin I peaked at 23 ng/ml. Echo showed an apical and distal inferior wall motion abnormality. Angiogram showed a wraparound LAD supplying the apex and inferior wall. There was a proximal LAD culprit with thrombus, but open with TIMI III flow. It had embolized to the distal LAD (which supplies the inferior wall) resulting in 100% occlusion there,and hence inferior infarction with ST elevation.
Here is the ECG Immediately after angiogram
There is terminal T-wave inversion identical to Wellens' type A