Friday, February 18, 2011

New LBBB and Massive ST elevation: Do not automatically jump to activate the cath lab!

This 50 year old male presented with some atypical chest pain and a blood pressure of 220/150.

There is Left Bundle Branch Block with up to 6 mm of discordant ST elevation in V2 and V3.  Limb leads have neither concordance nor discordance, and that is because  the QRS is neutral: neither definitely positive nor negative.  There  are some biphasic T-waves in II and aVF, suggesting ischemia.  The discordant ST elevation in precordial leads, though large, is proportional to a very high voltage S-wave (50 mm, or 5 mV).  The ratio of the ST elevation as measured at the J-point = 6 divided by 50 = 0.12.  The mean in my studies of LBBB without occlusion (either no MI or NSTEMI) was 0.10 +/- 0.1 (95% CI), so this is very close to a normal ratio.

This is a previous ECG from months ago, showing that the presentation ECG is indeed New LBBB.  Here there is profound LVH with secondary ST/T abnormalities.

This did not alarm me.  In ED patients with symptoms of ischemia and New LBBB, only about 2-4% have acute coronary occlusion (need for immediate reperfusion therapy).  Many more have MI as diagnosed by biomarkers.   This is typical evolution of severe LVH to LBBB in a patient with severe HTN.  There may well be MI as diagnosed by biomarkers, but it is not due to acute coronary occlusion, rather most likely to demand ischemia from severe hypertension (afterload, "type II" MI).

Troponin I had a rise and fall, but never went above the 99% reference value for the VITROS assay (in ng/ml): 0.017, 0.018, 0.029, 0.020.  So this also represents a case that had some tiny amount of myocardial necrosis but is by current definition not an MI. 

11 comments:

  1. In the presentation EKG, how do you come up with 5mV s wave? I count 5 large boxes in V1 which would be 2.5 mV, right? I cannot see where the S stops in any other lead. Thanks.

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  2. I'm measuring the largest S-wave, where there is also the largest ST elevation: 50 mm in V2 at 0.1 mV per mm = 5 mV. V1 has 2.5 mm STE divided by 25 mm (2.5mV) which also = a ratio of 0.10.

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  3. Could you cover the different types of myocardial infarction? In the pre-hospital setting we really only receive education on AMIs (STEMI vs NSTEMI). Thanks!

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  4. This is quoted from Universal Definition of MI: Circulation 2007;116;2634-2653. Free full text at: http://circ.ahajournals.org/cgi/reprint/116/22/2634


    Type 1
    Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection.

    Type 2
    Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension.

    Type 3
    Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new STelevation, or new LBBB, or
    evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of
    cardiac biomarkers in the blood.

    Type 4a
    Myocardial infarction associated with PCI.

    Type 4b
    Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy.

    Type 5
    Myocardial infarction associated with CABG

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  5. Without having a previous ECG would you have activated the cath lab?

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  6. The previous ECG makes it MORE likely to activated the cath lab, because the LBBB is new, which is one (very poor) criterion for activating the cath lab.

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  7. Dear Dr. Smith, I am new to your blog and myself an ECG addicted, am totally fascinated by the works you have done here. I have always wanted a good reference on rebutting the AHA recommendation of reperfusing new LBBB per se. And as you have mentioned it is only about 2 - 4% with documented coronary occlusion. As often, even our Malaysian guidelines would blindly follow what AHA says. Do you have reference to support that?

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  8. I am writing a couple papers on this with many many references. There is no single one, but Chang et al. showed 5% of old LBBB with chest pain have AMI and 7% of new LBBB with chest pain have AMI. THis is by biomarkers (troponin), and since only about 30% of patients with AMI by troponin have STEMI-equivalent, only 2-4% have occlusion.

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  9. Here is the reference: http://emresokc.org/resources/READING-SCHEDULES/lbbb.pdf

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