A middle aged male with no significant past medical history complained of several hours of chest pain.
Here is his initial ED ECG:
--There is a large pathologic QR-wave in I and aVL, and small ones in V3-V6. (Leads V2 and V3 must be reversed, as the QR progression is interrupted and only makes sense if one interprets them as switched). These are diagnostic of MI of unknown age.
--The STE in aVL, with minimal reciprocal ST depression in inferior leads, in the setting of well-formed Q-waves, is also of unknown age, but very likely to represent old lateral MI with persistent ST elevation.
--There is less than 1 mm of STE in I, aVL, V5 and V6, but these leads are notoriously insensitive for coronary occlusion. Only about 50% of occlusion of arteries supplying this area of myocardium have ST elevation that meets "criteria" of 1mm or more.
--However, the T-waves in V5 and V6 make this diagnostic of coronary occlusion. They are far too tall and fat to be normal. They are hyperacute.
The cath lab was activated. At cath, a nearly occluded (TIMI-1 flow) first diagonal was found and stented. Peak troponin I was 41.84 ng/mL.
Echo showed mid-anterior and anterolateral akinesis, with an EF of 58%.
Here was the post PCI ECG:
Hyperacute T-waves in V5 and V6 are occasionally the only indication of coronary occlusion.
See V5 and V6 in this case, which is even more interesting.
Also this case
Here is his initial ED ECG:
 |
| The computer read: left anterior fascicular block and old anterior MI. No other comment. What do you think? |
--There is a large pathologic QR-wave in I and aVL, and small ones in V3-V6. (Leads V2 and V3 must be reversed, as the QR progression is interrupted and only makes sense if one interprets them as switched). These are diagnostic of MI of unknown age.
--The STE in aVL, with minimal reciprocal ST depression in inferior leads, in the setting of well-formed Q-waves, is also of unknown age, but very likely to represent old lateral MI with persistent ST elevation.
--There is less than 1 mm of STE in I, aVL, V5 and V6, but these leads are notoriously insensitive for coronary occlusion. Only about 50% of occlusion of arteries supplying this area of myocardium have ST elevation that meets "criteria" of 1mm or more.
--However, the T-waves in V5 and V6 make this diagnostic of coronary occlusion. They are far too tall and fat to be normal. They are hyperacute.
An ED bedside ultrasound confirmed anterior wall motion abnormality.
The cath lab was activated. At cath, a nearly occluded (TIMI-1 flow) first diagonal was found and stented. Peak troponin I was 41.84 ng/mL.
Echo showed mid-anterior and anterolateral akinesis, with an EF of 58%.
Here was the post PCI ECG:
 |
| Now the T-waves are much more normal. Q-waves are more well developed in V5 and V6. The STE in aVL is still present and may well have been due to old MI (which is also, again, strongly suggested by the well-formed, deep and wide Q-waves). |
Hyperacute T-waves in V5 and V6 are occasionally the only indication of coronary occlusion.
See V5 and V6 in this case, which is even more interesting.
Also this case
Hello Dr. Smith,
ReplyDeletecase very instructive.
it is interesting to note that the anterior fascicular block present the phenomenon of "reverse progression" r wave in the inferior leads DII, DIII.
In block fascolare front isolated SIII> SII and rII> RIII.
This phenomenon we can find it in the anterior fascicular block and IMA inferior or while the sort is associated with IMA lateral. (Changes in direction of carriers)
Thanks Dr. Smith.
Greetings from Italy.
Vittorio
Thanks, Vittorio. Greetings to you as well!
DeleteSteve
Great case Steve. The morphologies of both the ST-elevations as well as the T-waves in I & aVL also jumped out at me. Although the T-waves aren't all that large, their broadness & symmetry really stuck me as hyperacute.
ReplyDelete-SG