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Challenges in Clinical Electrocardiography
August 26, 2019

Electrocardiographic Progression of Cardiac Conduction Disease: When So Much Depends on a Fascicle

Author Affiliations
  • 1Temple Heart and Vascular Institute, Temple University Hospital, Philadelphia, Pennsylvania
JAMA Intern Med. 2019;179(10):1422-1423. doi:10.1001/jamainternmed.2019.3547

A woman in her 70s with coronary artery disease and diabetes presented to the emergency department with sudden-onset severe chest pain and shortness of breath. Vital signs were unremarkable and the physical examination was notable for lower extremity edema and wheezing. Her initial troponin I level was 0.03 ng/mL (normal level, <0.045 ng/mL). The admission electrocardiogram (ECG) showed normal sinus rhythm with incomplete right bundle branch block (RBBB) and new ST elevations in V2 to V4. Urgent cardiac catheterization was performed revealing an acute 100% lesion of the proximal left anterior descending artery, which was treated with successful balloon angioplasty and placement of a stent. Nonetheless, the patient required placement of an Impella ventricular assist device (Abiomed) for cardiogenic shock. An echocardiogram revealed an ejection fraction of 20% with severe hypokinesis of the anterior and apical walls. The patient was transferred to intensive care and a repeat ECG was performed (Figure).

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    1 Comment for this article
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    Alternate Explanation
    Behzad Pavri, MD, FACC, FHRS | Thomas Jefferson University Hospital
    Dr. Sadek et al describe an interesting ECG presentation, and the explanation provided is reasonable, but the following observations should be made and need to be reconciled:
    1. There is QRS cycle length alternans.
    2. This appears to be driven by apparent PR interval alternans.
    3. The QRS complex ascribed to RBBB + LPFB shows a terminal NEGATIVE deflection in lead V1 and ABSENCE of a terminal negative deflection in lead I, both of which are inconsistent with RBBB (ECG diagnosis of RBBB requires a terminal positive deflection in V1 and a terminal negative deflection in lead
    I).

    The terminal negative deflection in V1 is NOT due to the "hidden" P wave, as it does not march out. It is difficult to invoke dual pathways physiology in the setting of AV block, and at this sinus rate, to explain the PR interval alternans.

    An alternate explanation that satisfies the above observations is that this is an example of "escape-capture bigeminy" with infra-nodal block during extreme sinus tachycardia. The RBBB + LAFB complex represents true AV conduction, and the other complex (ascribed to RBBB + PLFB) actually represents an accelerated escape complex arising from the (ischemic) left anterior fascicle. If true, then this ECG represents an even higher degree of AV block (more than 2:1, but not quantifiable due to the presence of the escape complex) that was missed.
    CONFLICT OF INTEREST: None Reported
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