A middle aged man with several CAD risk factors presented with one week of intermittent shortness of breath and then sudden severe SOB. There was no chest pain.
Here is the initial ECG:
There is grouped beating, which should always make you think of Wenckebach (2nd degree, Mobitz type I). This is indeed Wenckebach, which is common in inferior MI. The rhythm itself is stable -- there is little danger of progression to complete AV block. It is a sign that pathology is present, and this is confirmed with the ST elevation (< 1 mm in inferior leads and reciprocal ST depression in aVL). There is also ST depression in V2 and V3, diagnostic of simultaneous posterior STEMI. There is T-wave inversion which suggests reperfusion. There is a pathologic Q-wave already in lead III.
The patient went for immediate angiography and PCI of a 100% occluded RCA. Why was there T-wave inversion if the artery was 100% occluded? Because there was good collateral circulation
Wellens' first described the T-wave inversion bearing his name in 1982 and it was in connection with "unstable angina" of the LAD, with stenosis in all cases progressing to complete infarction within a couple weeks. In 1989, he published a much larger case series of 180 cases (out of 1260 consecutive cases of unstable angina), and 33 of these had 100% occluded arteries (the other 147 had open arteries). But in all 33 cases, there was good collateral circulation. The ECG tells you what is going on at the cellular level (ischemia or not), but not why there is or is not ischemia. So whether the myocardium under those leads is reperfused through collaterals or through opening of the artery (spontaneous or due to therapy), there may be T-wave inversion.
By the way, completed transmural infarction that has no reperfusion at all will also present with (shallow) T-wave inversion, but in the presence of well-formed, deep Q-waves. Wellens' waves do not have pathologic Q-waves.
The initial troponin I was 14.1, indicating recurrent or prolonged MI. TnI peaked at 28 ng/ml.
Echo showed EF of 53% and an inferior wall motion abnormality.
Here is the initial ECG:
 |
There is grouped beating, which should always make you think of Wenckebach (2nd degree, Mobitz type I). This is indeed Wenckebach, which is common in inferior MI. The rhythm itself is stable -- there is little danger of progression to complete AV block. It is a sign that pathology is present, and this is confirmed with the ST elevation (< 1 mm in inferior leads and reciprocal ST depression in aVL). There is also ST depression in V2 and V3, diagnostic of simultaneous posterior STEMI. There is T-wave inversion which suggests reperfusion. There is a pathologic Q-wave already in lead III.
The patient went for immediate angiography and PCI of a 100% occluded RCA. Why was there T-wave inversion if the artery was 100% occluded? Because there was good collateral circulation
Wellens' first described the T-wave inversion bearing his name in 1982 and it was in connection with "unstable angina" of the LAD, with stenosis in all cases progressing to complete infarction within a couple weeks. In 1989, he published a much larger case series of 180 cases (out of 1260 consecutive cases of unstable angina), and 33 of these had 100% occluded arteries (the other 147 had open arteries). But in all 33 cases, there was good collateral circulation. The ECG tells you what is going on at the cellular level (ischemia or not), but not why there is or is not ischemia. So whether the myocardium under those leads is reperfused through collaterals or through opening of the artery (spontaneous or due to therapy), there may be T-wave inversion.
By the way, completed transmural infarction that has no reperfusion at all will also present with (shallow) T-wave inversion, but in the presence of well-formed, deep Q-waves. Wellens' waves do not have pathologic Q-waves.
The initial troponin I was 14.1, indicating recurrent or prolonged MI. TnI peaked at 28 ng/ml.
Echo showed EF of 53% and an inferior wall motion abnormality.
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