A male in his 50s presented with Chest pain on and off during the day. At the time of presentation, he had only some jaw pain. An ECG was recorded:
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There are inferior and lateral T-wave inversions (reperfusion T-waves, analogous to Wellens' waves which were described in the LAD distribution, V2-V4, but this also applies also to other coronary distributions). There is also ST depression in V2 and V3: this is of course really ST elevation of the posterior wall, as recorded from the anterior wall.
T-waves are upright in V2 and V3 because, just like the inferior and lateral walls, the posterior wall is also reperfused. If we had posterior leads, it would show posterior T-wave inversion. Instead, we have anterior lead recordings, which superimpose a positive anterior T-wave with the opposite (because recorded from the opposing anterior chest) of a negative posterior T-wave (reperfusion of the posterior wall). Thus, we have the oppositve of a negative, which is positive; this positive is added to the anterior positive, which is two positives, and so the T-wave is upright with some added voltage.
This had me very worried, so even though the patient had no new symptoms, within 15 minutes I recorded another ECG to be certain that the artery was not re-occluding. Here it is:
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Now the T-waves are upright in inferior and lateral leads (pseudonormalization), indicating re-occlusion of the infarct-related artery. There is new minimal ST elevation in II, III, aVF and reciprocal ST depression in aVL. This is diagnostic of inferior MI (though technically not a "STEMI" because it does not meet the artibrary "criteria" for STEMI which we know are useless numerical cutoffs.
This is another NonSTEMI that needs the cath lab now, as the ECG shows signs of coronary occlusion even without 1 mm of ST elevation.
The T-waves in V2 and V3 are still upright. The predominant forces are still from the anterior wall, which is closest to the overlying leads, so any small amount of posterior positivity (which would result in a negative T-wave as recorded anteriorly) is overwhelmed by the anterior wall positive T-waves.
I activated the cath lab immediately.
Shortly thereafter, the patient reported no pain at all, including absence of neck pain. We recorded this ECG:
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On arrival in the cath lab he was pain free. The angiogram showed an ulcerated thrombotic plaque in the distal RCA with good flow, plus a very tight lesion in a right posterolateral branch to the posterior and lateral walls.
Diagnosis: Infero-postero-lateral MI due to dynamic ACS of the RCA.
Peak troponin I was 1 ng/mL.
Standard management in these cases is to admit the patient on medical management for ACS: aspirin, heparin or LMWH, P2Y12 inhibitor. If the patient rules in, then he/she goes to the cath lab the next day. But this is not adequate for a significant percentage of NonSTEMI patients; namely, those who have evidence of coronary occlusion or an artery that is opening and closing. There are no randomized trials of this management strategy, but there are several studies showing that when NonSTEMI patients do get their next day cath after a rule in by troponins, the infarct related artery is closed about 25-30% of the time. These patients have higher biomarkers, worse LV function, and higher mortaility than patients whose artery is open.
1. Wang T et al. Am Heart J 2009;157(4):716-23.
2. From AM, et al. Am J Cardiol 2010;106(8):1081-5.
3. Pride YB et al. JACC: Cardiovasc Interventions 2010; 3(8):806-11.
Lessons:
1. Wellens' syndrome has analogous findings in the inferior and/or lateral walls.
2. T-wave changes of the posterior wall record in the opposite direction from the anterior wall.
3. Reperfusion T-waves indicate a very unstable plaque that can instantly re-occlude at any moment. The re-occlusion is signaled by a "pseudonormalization" of T-waves.
4. Many coronary occlusions do not have 1 mm of ST segment elevation
5. Many NonSTEMIs need the cath lab now.
