Friday, November 4, 2011

Left Bundle Branch Block (LBBB) with Chest Pain, concordant and excessively discordant ST depression V2-V6

A middle-aged male presented pain free after an episode of chest pain.  Here is the initial ECG (sorry some is cut off -- it is an iPhone shot from a friend):

There is LBBB with appropriate discordance of all ST segments.  Anterior ST elevation is appropriate, with highest ST/S ratio of 3.5/28 = 0.125 (mean normal = 0.11; normal up to 0.19).  There are concordant T-waves in V5 and V6.  This is a nonspecific sign of NonSTEMI.
 5 minutes later, the patient had crushing chest pain, and this ECG was recorded (again, some of limb leads are cut off):
Now there is concordant ST depression in V2 and V3.  This is a relative change of approximately 5 mm(!).   There is excessively discordant ST depression in V4-V6.   (V4 ratio is 2/6 = 0.33; V5 ratio = 2.5/6.5 = 0.38;  V6 = 2/6.5 = 0.31).  Thus, there is ischemic ST depression in V2-V6.   In normal conduction, ST depression from V2-V6 is often due to subendocardial ischemia, whereas when limited to V1-V4, it is usually posterior STEMI.  Either way, this is a patient with acute coronary syndrome with chest pain.  If you cannot control the symptoms with medical therapy, then the patient must go to the cath lab.   

I have written about excessively discordant ST elevation, but have not mentioned excessively discordant ST depression.  In our study of LBBB with and without coronary occlusion, just one lead with excessively discordant ST depression or ST elevation, as defined as a ratio of ST depression (or elevation) to the preceding R-wave (or S-wave), greater than 0.25, was very specific for ischemia (in our study, for occlusion).  More recent analysis of the data showed that 0.20 was probably a better cutoff.

The physician called the interventionalist, who did not agree there was ischemia on the ECG.  The patient was started on nitroglycerine IV and the pain subsided, as did the ECG findings. 

The patient was admitted pain free on nitro and no immediate cath was done.  The troponin I peaked later at 0.18 ng/ml. 

The next AM, the patient had another episode of pain that could not be resolved with maximal medical therapy.  He went for emergent cath, which showed a proximal lad 95% stenosis with deep ulcer and a 90% mid lad stenosis.  Both were stented.

Later, the troponin peaked at 5.6, and echo showed anteroseptal hypokinesis with EF <40%.

So this was LBBB with concordant and excessively discordant ST depression, representing ST depression in leads V2-V6, completely consistent with subendocardial ischemia due to profound LAD ischemia.


  1. Nice example of yet another Steve Smith BBB tracing with strongly suggestive signs of acute ischemia if not infarction. Tracing 1 is subtler, and interesting in its own right - with as Steve indicates abnormal concordant T waves in V5,V6. Of interest is that the QRS in V5,V6 isn't strict monophasic R wave (simultaneous time lines show there to be a small terminal S wave) - which complicates ST-T wave assessment a tad. In addition to the abnormal concordant T waves in V5,V6 - the ST segments look funny (scooped and a bit depressed) - though understandable that one might not take the patient to the cath lab on the sole basis of the history and Tracing 1.

    LESS understandable why the interventionist did not agree with Dr. Smith on Tracing 2. As per details under Figure 2 in Steve's blog - Steve has validated the findings suggesting acute coronary occlusion in the setting of LBBB with excessively discordant ST depression. But even simpler is the abnormal shape of the ST segment in V3,V4 (scooped & depressed) - especially in the context of accompanying "crushing chest pain" - and especially in comparison with the precordial leads in the Tracing 1 ECG done only minutes earlier when the patient was pain free

    THANKS again to Steve for his ongoing contributions to the illustrated BBB-Acute Coronary Occlusion literature. Hopefully more cardiologists will listen.

  2. This is a great case of a subtle STEMI equivalent. However, I think the most important point is that patients who have a suggestive history or a suggestive ECG for ACS and whose symptoms cannot be controlled with medical management need to go to the cath lab.

    What do you do with a 55 year old guy with a non-specific ECG, and a good history of stuttering chest pain that has become constant and 10/10 and with maximal medical therapy it becomes 4/10? I personally push them all to the cath lab, although many cardiologists require much persuasion.

    I love ECG's and their subtleties but we should remember that HPI trumps everything. If the history is ACS and the response to medical management is incomplete even an ECG showing only non-specific-junk should not disuade a push for early cath...

    My 2 cents,

  3. There is no literature to support (and it doesn’t even pass the common sense test) taking a patient to cath without objective evidence of ischemia by EKG or troponin or clinical instability (shock, pulmonary edema, etc). Objective evidence of ischemia on the ECG means ischemic ST depression or elevation or T-wave inversion or hyperacute T's, and does not include the many cases of ST depression, elevation or T wave abnormalities that are NOT ischemic. This is where some ECG expertise is important.

    If those are negative, then studies such as radionuclide stress or stress echo are pretty good, but they do not prove that pain was due to the stenosis which the test finds.

    And especially there is no literature to support emergent cath, even with ongoing chest pain, unless there is objective evidence of ischemia (positive EKG or biomarkers, or known severe CAD, or clinical instability.
    Of course you can take anyone to cath, but if your patient has esophageal spasm and also happens to have a 70% chronic lesion, you will stent it and you will think that you've done your patient a favor when you’ve done the opposite. The simple fact is that most patients with chest pain do not have myocardial ischemia, but some other cause.

    So chest pain alone, even if it sounds typical, is not enough.

  4. Even for LBBB, only 5-10% of patients with chest pain and LBBB rule in for MI, and only about 3% of these have acute occlusion.

  5. In this case, there is concordant ST dep. What if it is an isolated discordant ST dep? Discordant ST dep has never been part of Sgarbossa's either. Have you done any work on such patients? What would your comment be for isolated discordant ST dep that fulfills the ST/QRS ratio criteria of 0.2 or 0.25? BTW, could I have the references that demonstrated a cut-off of 0.2 as more sensitive compared to your abstract's of 0.25?

  6. In our study, isolated excessively discordant ST depression was the single best indicator of occlusion, by both sensitivity and specificity. However, this flies in the face of conventional wisdom and until someone else validates it, you're not going to make a lot of headway with the interventionalists. As far as 0.25 vs. 0.20, we ultimately, after much statistical analysis, found that 0.25 is best. However, 0.20 will be more sensitive just by commone sense (and less specific).

  7. Very nice presentation of the case..
    Dr smith ..Will you please elaborate that concordant STD in V-1 to V-3 as mentioned in sgarbossa criteria or excessive discordant STD as mentioned in your study..Does both mean STEMI or UA/NSTEMI ???

    1. In out study, they were found in patients with complete occlusion (equivalent to STEMI)

  8. Is there Cabrera's sign in V3?


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