A 50 yo male presented with chest pain. This ECG was recorded at 0415.
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There is sinus tachycardia. There is left bundle branch block (LBBB). All ST-T complexes are discordant. However, the ST-T in V1-V4 is excessively discordant: with 6 mm ST elevation, V3 meets criterion 3 of Sgarbossa's criteria (giving 2 points, not enough for a diagnosis of "MI"). By the Smith modification of Sgarbossa's criteria, the ratio of the ST elevation at the J-point (6 mm) to the S-wave (24 mm) is 0.25. Since this is greater than the cutoff of 0.20, it would be diagnostic not just of MI, but of LAD occlusion.
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The occlusion was not appreciated by the treating physicians, and another ECG was recorded at 0457:
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Now the R-wave in V3 is gone (QS-wave), the S-wave is "fragmented" (an indication of infarction analogous to Q-waves), and the ST elevation remains at 6mm, with an S-wave of only 12 mm, for a ratio of 0.50. The injury is worsening.
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The notching in V3 is also known as "Cabrera's sign" (prominent notching of at least 40 msec in the ascending limb of the S-wave in any of leads V3-V5).
The patient was taken to the cath lab and a 100% LAD occlusion was opened.
Here is the ECG after reperfusion:
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There is less tachycardia, as the stroke volume is now higher with improved myocardial function. The ST elevation has mostly resolved. There are now concordent T-waves diffusely, especially in the LAD territory.
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Such T-wave inversion is a frequent sign of reperfusion even in LBBB, and when seen alone (without the preceding ECGs diagnostic of STEMI) is a common sign of NSTEMI. T-wave concordance can be normal, so it is not a very specific nor sensitive sign of ischemia. But it should raise your suspicion. In the context of this case and the preceding ECGs, it is diagnostic of reperfusion and is definitely the result of ACS.
Excellent case as always by Dr. Smith. Just to point out a number of additional clues to support Steve's premise that the initial (0415) and subsequent (0457) tracings with LBBB suggest need for acute cath lab activation in a patient with new chest pain: i) Lead V6 is distinctly abnormal in both the 0415 and subsequent 0457 tracings for a patient with LBBB. Not only is there ~3mm of J-point ST depression, but there is abnormal coving of the depressed ST segment prior to the biphasic T wave. This reflects acute reciprocal ST depression. ii) In the 2nd (0457) tracing - there is evolution in leads V3 and V4, which now show more suggestive morphologic ST coving of acute injury; iii) There are 2 PVCs seen on the 0457 rhythm strip. These are fusion beats (note that both are preceded by P waves with a slightly shorter PR interval than the PR for the sinus beats conducted with pure LBBB. Note again the unusual morphology with ST coving of the depressed ST segments in these 2 PVCs. On occasion - clue/support to acute MI is provided by ST-T wave changes in PVCs - and in this case these fusion-PVCs show similar marked reciprocal ST depression supporting acute coronary occlusion. iv) Finally - evidence of acute event evolution in the final (post-reperfusion) ECG which shows dramatic evolutionary change in ST segments with ST coving and T wave concordance (180 degree change in T wave morphology) - plus a wide new Q and suggestion of ST elevation in lead aVL (the new Q in aVL in a patient with LBBB being a further marker that damage has occurred). v) Interesting to follow the ST elevation in lead aVR through the above evolutionary changes. BOTTOM LINE: Another gorgeous series of evolutionary tracings provided by Steve Smith to support his modified Smith-Sgarbossa criteria for assessing LBBB tracings for likelihood of acute coronary occlusion (and need for immediate cath activation). For those still skeptical - or who have trouble seeing the subtle transition point between the J-point ST elevation and T (excessive discordance) on the initial LBBB tracing - the clinical context (new CP in a LBBB patient) in conjunction with other clues can assist. Frequent repetition of ECGs early on with careful review of these serial tracings (as in this case) show evolution may occur in as little as 40 minutes or less (differences between the 0415 and 0457 tracings). CREDIT again to Dr. Smith! - Ken Grauer, MD
ReplyDeleteGreat case Dr. Smith...
ReplyDeletemy question is in regard to the comment that in the second ECG, the injury is worsening because the ST elevation/S wave ratio is worsening... this is due to a smaller S wave, and in fact in the second ECG i see S wave attenuation in many leads, most notably in V5 and V6 (S wave has been almost obliterated in V6)... i have heard you talk about S wave attenuation with regard to MI and concurrent LVH, and i am wondering if there is significance to S wave attenuation in the context of AMI... thanks!
-David
Good observation. But I don't know for certain (yet) about my LVH hypothesis, but if it is true, this could also be an analogous example.
ReplyDeleteHi Dr. Smith, just to confirm - Cabrera sign (as well as Chapman's sign) are only suggestive of previous MI and not acute MI, right? Actually such notchings are rather commonly seen in LBBB, does that mean that in the absence of clinical picture suggestive of MI, such notchings are of no significant? Thanks!
ReplyDeleteYes, these are signs of old MI. Chapman's sign is a 50 ms notch in the upstroke of the R-wave in I, aVL, V5 or V6. However, their accuracy in diagnosing previous MI is not great. See these references:
Deletehttp://circep.ahajournals.org/content/early/2008/07/14/CIRCEP.107.763284.full.pdf+html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764818/