Monday, November 25, 2013

CHF Exacerbation with Old LBBB: Is There New Infarction or Not?

An very elderly woman with a h/o CAD with stents to the RCA and circ, mild aortic stenosis, h/o ischemic cardiomyopathy, EF 25%, and h/o heart failure, and with ICD for primary prevention, presented with a c/o chest and back pain intermittent for several nights, relieved by isosorbide.  On the evening of admission, she could not find her isosorbide and she became progressively SOB, in addition to chest and back pain.  She called 911, and she felt better on CPAP by EMS.  On arrival, her O2sat was 88%, then rose to 100% on BiPAP in the ED.  Her BP was 140/50, pulse 90.  She clearly had pulmonary edema.  She also had some peripheral pitting edema.  She was treated with intravenous nitroglycerin and furosemide.

Here is her initial ECG:
What do you think?  Discussion below.  

Multiple interpreters read this as left bundle branch block without any change or evidence of ischemia.

There was a previous ECG for comparison.
There is Left Bundle Branch Block.  All ST segments have appropriate and proportionate discordance.  

There is left axis deviation, and the QRS duration is 179 ms (quite long for LBBB), both of which are associated with poor ejection fraction (EF) in LBBB.   

There is a fragmented QRS, in this case "Cabrera's sign" (notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5) in V4 and V5.  

A "fragmented QRS" is a sign of infarction, either new or old, analogous to Q-waves.  

This ECG does not have "Chapman's sign," (notch on the ascending limb of the R-wave in I, aVL, or V6), but it does have, in addition to Cabrera's sign, other unnamed types of QRS fragmentation in many other leads: a notch in the ascending limb of the S-wave in III and aVF, and in the descending limb of the R-wave in I, II, and aVL.  V6 is also very fragmented.  

There is little angiographic data on fragmented QRS in LBBB.  The only one I know of was published recently as an abstract and had a small number of asymptomatic LBBB patients who otherwise were well match.  Among these patients, a fragmented QRS was highly specific for the presence of coronary artery disease.  In this study by Hands et al., QRS criteria were quite specific for MI of indeterminate age.

It is unlikely that a fragmented QRS on an isolated ECG with LBBB has good diagnostic utility for acute MI, but it is much more likely to be significant if there is NEW fragmentation

Here is the initial ECG again, annotated:
There is sinus rhythm and LBBB.  There is still left axis deviation and the QRS is now 193 ms. 
There are multiple signs of new, acute ischemia.  
--The black arrow shows concordant ST depression in V3, and it is also clearly changed from the previous.
--The blue arrow shows even more concordant ST depression in V4.
--The red arrow shows an increase in QRS fragmentation.  Increased (new) fragmentation can also be seen in many other leads: Rsr' in I and aVL, Qrs in II, III, and aVF.
--The green arrow shows excessively discordant ST depression in lead V5.  This is also present in V6.

The concordant ST depression meets the second Sgarbossa criteria for STEMI in LBBB.  The other signs are supportive of MI.  The excessively discordant ST depression, as defined by a ratio of 30% of the preceding R-wave, had a sensitivity of 100% and specificity of 88% for coronary occlusion in our study of coronary occlusion in LBBB.

None of these signs were seen.  Fortunately, the woman was not a good candidate for, and did not want, invasive therapy. 

However, in a patient who is a candidate for PCI, these signs can be very helpful.

Her troponin I peaked at 28 ng/mL.  She improved on supportive and medical therapy.  Her subsequent echo showed new posterior and anterior (in addition to old inferior) wall motion abnormalities and a decrease in EF from 25% to 20%.

Here is her next day ECG:
The ischemia has resolved.  It is quite similar to the old ECG.

Finally, it is possible that the CHF exacerbation was the cause, not the result, of the ischemia; that there is severe stable CAD and that along with the hypoxia of a CHF exacerbation, she developed coronary ischemia.  ECG findings and positive troponin tell you there is infarction, but not definitively whether there is ACS.  However, concordant ST segments, and troponin values that high are almost always due to occlusion, which may or may not be transient.


In LBBB, there are many signs one can look for in order to diagnose, or strongly suspect, MI or coronary occlusion.   However, this is still not widely known by clinicians.  To illustrate this, one note said "LBBB, so no new ECG findings."

Had this been someone who could undergo angiogram and PCI, one would not want to miss these findings.  They could very well be signs of a coronary occlusion that could be opened and spare some myocardium.


  1. Thank you so much! Your explanations are amazing!

  2. Thank you so much, your explanations are amazing!

  3. Doesn't her next day ECG still shows concordant ST depressions in V5 and V6?


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