A middle-aged male presented with acute chest pain:
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| There is sinus rhythm. There is LVH by voltage in aVL, with what may appear to be secondary repolarization abnormalities (so-called "LVH with strain", but this is a misnomer because it implies ischemia. "LVH with secondary repolarization abnormalities" is more appropriate). It has the "hockey stick" morphology typical of LVH with secondary repolarization abnormalities. What do you think? |
Here is the ECG of another middle-aged male with acute chest pain:
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| It is similar, but notice how the T-waves are not nearly as proportionately large as in the above ECG. What do you think? |
The bottom ECG is that patient's baseline LVH.
The top ECG is LVH with superimposed inferior acute MI. The T-waves (both upright and negative ones) are far too large in proportion to the QRS. There is also a concordant T-wave in lead II, and ischemic appearing biphasic T-waves in V4-V6, with a flattened ST segment in V3, all suggesting posterior and lateral involvement.
Notice also the ischemic biphasic T-waves in V4 and V5.
Technically, it is not "STEMI" because the ST elevation at the J-point is less than 1 mm.
Technically, it is not "STEMI" because the ST elevation at the J-point is less than 1 mm.
But it is an OMI!!
This (top) ECG was missed by several interpreters and the patient had very delayed reperfusion therapy.
The culprit was 100 % thrombotic occlusion of the mid RCA. The peak troponin I was 47 ng/ml (very high). There was a regional wall motion abnormality in the inferior and posterior walls. The LAD was not involved.
The patient was discharged with a diagnosis of NonSTEMI.
There actually was a previous ECG for comparison, which proves the point. Here it is:
Here is the post-PCI ECG:
Learning point
Know the T-wave to QRS proportions in LVH vs. LVH with superimposed MI.
This (top) ECG was missed by several interpreters and the patient had very delayed reperfusion therapy.
The culprit was 100 % thrombotic occlusion of the mid RCA. The peak troponin I was 47 ng/ml (very high). There was a regional wall motion abnormality in the inferior and posterior walls. The LAD was not involved.
The patient was discharged with a diagnosis of NonSTEMI.
There actually was a previous ECG for comparison, which proves the point. Here it is:
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| Very different from LVH with superimposed inferior STEMI. |
Here is the post-PCI ECG:
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| Notice inferior reperfusion (inverted) T-waves Notice precordial large T-waves (posterior reperfusion T-waves) Notice lateral reperfusion T-waves. These are "Wellens' waves" of inferior, posterior, and lateral walls. |
Learning point
Know the T-wave to QRS proportions in LVH vs. LVH with superimposed MI.
Dear Dr. Smith in the basal old ecg,is not atypical to see strain pattern with st elevation of the j point in right precordial leads(v1-v3) without clearly signs of strain pattern with hockey sign in lateral precordial leads? Thank you
ReplyDeleteIt is less common for sure, but is not necessary to have the "hockey" sign.
DeleteRelation between QRS & T wave in II,III, AVF , tall ,positive so called hyper acute T wave ,very much suggestive of earliest stages of ischemia , before ST elevation.
ReplyDeleteSerial ECGs, changing ECGs with ischemia,LVH shouldn't change unless also ischemia
ReplyDeleteGreat case! The ST-T waves in leads I, aVL in the 1st (Top) tracing look potentially consistent with secondary ST-T wave abnormalities in this patient with obvious LVH (R wave in lead aVL ~20mm). In contrast, the ST-T waves in the chest leads for this 1st (Top) ECG look either due to ischemia (that may be acute) or a repolarization variant. But it would be rare to see this type of chest lead ST-T wave repolarization variant in a patient with seemingly “typical LV strain” changes in lead aVL — so something “isn’t right”. One look at the inferior lead should confirm this impression. The R wave in lead aVL is markedly taller than the S wave in lead III is deep. As a result, the amount of ST-T wave peaking in lead III (and in the other inferior leads) should be correspondingly less than the depth of ST-T depression in aVL. Instead, there is decidedly more relative inferior T wave peaking — with inferior T waves that are clearly broader (“fatter”)-than-they-should be. These are hyperacute T waves. Putting this all together in a patient with new chest pain — and the onus falls on us to rule out an acute event. Finding a baseline tracing (2nd ECG shown) then confirms this impression by documenting that we are indeed seeing acute ECG changes.
ReplyDeleteP.S. I wonder why there is such dramatic change in chest lead QRS amplitude between the first 2 tracings in this patient with acute RCA occlusion but no anterior infarction … ?
THANKS again Steve for posting this highly insightful case!