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Chest pain, resolved: don't forget to look at the previous and the prehospital ECG

Posted Feb 14 2011 7:07am
This is a 58 year old woman with a history of inferior MI.  She has had a week of intermittent substernal chest pain.  Because it came again and lasted for one hour, she called 911.  The medics recorded a 12-lead, then gave her  aspirin and nitro, and her pain resolved completely.  It seems the physicians caring for her did not see this ECG, so I am not showing it first.  On arrival in the ED around midnight, she was pain free and had this ECG recorded
First ED ECG.  Sinus rhythm with a couple of PACs.  Heart rate is close to 100, so one must entertain hemodynamic etiologies of chest pain, such as pulmonary embolism.  There are Q-waves with  minimal ST elevation in inferior leads and reciprocal ST depression in aVL, not significantly changed from baseline (ECG below).  There is also minimal ST elevation in V1 and V2 with the beginnings of T-wave inversion suggestive of anterior NSTEMI ("Wellens' syndrome").
 The first ECG is substantially different from the previous ECG 3 years prior
Previous ECG from 3 years prior shows old inferior MI and baseline precordial ST elevation of early repolarization.  There is upward concavity and normally upright T-waves.

Prehospital ECG during chest pain, before nitro and aspirin.  There is ST elevation and a large upright T-wave in V1, different from the baseline T-wave.  LAD may well have been occluded during this recording. 

ECG 2.5 hours after presentation, no therapy other than aspirin: ECG is back to baseline of 3 years ago.  At this point, the troponin returned at 0.14 ng/ml (limit of detection: 0.012; 99% reference value: 0.034, so this is a "positive"), after which there was an appropriate rise and fall, with peak at 0.358 ng/ml.  An angiogram showed a 95% mid-LAD stenosis, culprit lesion.  A stent was placed.

The K was also 2.9 mEq/L, but this does not account for the ECG findings.  The patient had a negative PE workup and was admitted to the hospital.  As indicated in the legend above, she ruled in for MI.  She went for an angiogram the next AM; it showed mid-LAD culprit lesion with 95% stenosis and was stented.

After stenting, there was another rise and fall of troponin, which probably precipitated the new changes (T-wave inversion typical of Wellens' syndrome) in precordial leads.

T-wave inversion in LAD ACS
Wellens' syndrome is chest pain that is relieved with terminal T-wave inversion on the initial, pain-free, ECG.  There is preservation of R-waves, and there is evolution to deeper T-wave inversion.  It is due to bried LAD occlusion with reperfusion.  This last evolution did not occur in this case.  Instead, the T-waves normalized (not pseudonormalization, which would indicated re-occlusion).  Normalization of T-waves is likely with very small NSTEMI or unstable angina.  Usually, in cases like this there is enough infarction to result in evolution of T-wave inversion.
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