An elderly woman with no prior known cardiac history presented with approxiately 9
hours of chest pain, much improved by arrival and essentially resolved
after a single sublingual Nitroglycerine. She was hemodynamically stable.
Here is her ECG:
Case continued
The physician only activated the cath lab after having a previously normal ECG faxed, and after the first troponin I returned at 41 ng/mL. This very elevated troponin shows that the infarct has been going on for quite a while and is consistent with the ECG.
He did record another ECG:
Outcome:
The RCA was 100% acutely occluded and was opened and stented.
Second troponin I was 70 ng/mL, Third was too high to measure.
An echocardiogram showed a new inferoposterior wall motion abnormality
Ischemic T-waves in LBBB
We showed that Concordant T-waves are weakly sensitive and specific indicators of MI [combination of STEMI and NonSTEMI] (1).
With reperfusion, even in LBBB, T-waves often invert with reperfusion. Here is a great case of STEMI in LBBB, with Reperfusion T-waves after PCI.
1. Dodd KW. Elm KD. Smith SW. Terminal T-Wave Concordance Increases the Sensitivity of Electrocardiographic Diagnosis of Acute MyocardialInfarction in Left Bundle Branch Block (full text link). (Abstract 15666) Circulation. 2014;130:A15666; November 2014.
Here is her ECG:
 |
| There is sinus bradycardia and Left Bundle Branch Block. The ST segments are appropriately discordant, except that in lead II there is some ST elevation; the QRS in lead II is a bit more positive than negative, so the ST segment should be negative or isoelectric, but it is elevated. This is a sign of STEMI. More importantly, though lead III has a discordant ST segment, it is out of proportion. The STE is 3 mm in the presence of a 12 mm S-wave, for a ratio of 0.25, thus highly likely to be STEMI. What is unusual is that the T-wave is concordant. This is likely due to prolonged (subacute) STEMI, or to some reperfusion (the patient is pain free after NTG), or both. There are also two signs of a fragmented QRS, which are equivalent to Q-waves in LBBB: "Cabrera's sign" (notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5), seen here in lead V3; also "Chapman's sign," (notch on the ascending limb of the R-wave in I, aVL, or V6), seen here in I, aVL, and V6. |
Case continued
The physician only activated the cath lab after having a previously normal ECG faxed, and after the first troponin I returned at 41 ng/mL. This very elevated troponin shows that the infarct has been going on for quite a while and is consistent with the ECG.
He did record another ECG:
 |
| No significant change |
Outcome:
The RCA was 100% acutely occluded and was opened and stented.
Second troponin I was 70 ng/mL, Third was too high to measure.
An echocardiogram showed a new inferoposterior wall motion abnormality
Ischemic T-waves in LBBB
We showed that Concordant T-waves are weakly sensitive and specific indicators of MI [combination of STEMI and NonSTEMI] (1).
With reperfusion, even in LBBB, T-waves often invert with reperfusion. Here is a great case of STEMI in LBBB, with Reperfusion T-waves after PCI.
1. Dodd KW. Elm KD. Smith SW. Terminal T-Wave Concordance Increases the Sensitivity of Electrocardiographic Diagnosis of Acute MyocardialInfarction in Left Bundle Branch Block (full text link). (Abstract 15666) Circulation. 2014;130:A15666; November 2014.
GREAT case (as usual)! Below is my interpretation of the initial ECG (as I wrote on the EKG Club page BEFORE I knew the history - and before I read Dr. Smith's discussion). My purpose in writing out my interpretation BEFORE reading the case is to hopefully emphasize how there often ARE important clues from the initial 12-lead ... THANK YOU Steve for another great discussion! - :)
ReplyDelete------------------
I will commit myself to commenting before reading Dr. Smith's Blog. I see sinus bradycardia with 1st degree AV block and LBBB. Without yet knowing the history - I see several findings of concern that transcend need (in my opinion) for numerical criteria ... These include: i) ST coving and slight-but-real elevation in leads III and aVF - associated with fairly deep T wave inversion in these leads that is NOT what I expect with "typical" LBBB; ii) Subtle-but-real ST segment coving that should-not-be-there with simply LBBB in lead II - that supports i) findings; iii) J-point depression with uncharacteristically FLAT ST segment in leads I,aVL (whereas with typical LBBB the ST segment isn't flat, but slowly upsloping) - associated with an upright terminal T wave in these leads (!) that is the "mirror-image" opposite of what I see in leads III, aVF; iv) An uncharacteristic-for-LBBB takeoff of the ST segment in lead V2 (is typically not so straight at takeoff); and v) 1-2mm of J-point ST depression in V5,V6 - that isn't what will usually be seen with typical LBBB.
My point of highlighting the above is that in addition to use of modified Smith-Sgarbossa Criteria (that I DO find helpful!) - assessment of QRST morphologic changes in context with overview of the entire 12-lead tracing is an invaluable part of the interpretation process that should not be overlooked. IMPRESSION: The findings I see here are VERY suspicious for something acute (possibly occlusion) going on, depending of course on the history, physical exam, time sequence, appearance of prior tracings and serial tracings, etc.
It's now time for me to read the full case on Dr. Smith's Blog ...
thanks, Ken!
DeleteAny thoughts on the Cabrera's sign and Chapman's sign on these ECGs? Both are not very sensitive, but my understanding is that both signs are pretty specific for injury when you see either one.
ReplyDeleteLarry,
DeleteExcellent point! These are really not signs of "injury" which is what we say when there is transmural ischemia at risk of infarction, but signs of infarction. I will put that in.
thanks, Steve