Novel Approaches for the Diagnosis of Concealed Nodo-Ventricular and His-Ventricular Pathways

Author:

Higuchi Satoshi12ORCID,Gerstenfeld Edward P.1ORCID,Hsia Henry H.1ORCID,Wong Christopher X.1ORCID,Ho Reginald T.3ORCID,Tchou Patrick J.4ORCID,Nissan Batel5,Shauer Ayelet5,Belhassen Bernard5ORCID,Scheinman Melvin M.1ORCID

Affiliation:

1. Division of Cardiology, University of California San Francisco (S.H., E.P.G., H.H.H., C.X.W., M.M.S.).

2. Department of Cardiology, Tokyo Women’s Medical University, Japan (S.H.).

3. Division of Cardiology, Department of Medicine, Thomas Jefferson University Hospital, Philadelphia, PA (R.T.H.).

4. Heart and Vascular Institute, Cleveland Clinic, OH (P.J.T.).

5. Heart Institute, Hadassah University Hospital, Jerusalem, Israel (B.N., A.S., B.B.).

Abstract

Background: Confirming the presence and participation of concealed nodo-ventricular (cNV) or concealed His-ventricular (cHV) pathways in tachyarrhythmias is challenging. We describe novel observations to aid in diagnosing cNV or cHV pathways. Methods: We present 7 cases of cNV and cHV pathway-mediated arrhythmias and focus on several laboratory observations: (1) differential ventricular overdrive pacing (VOD) from the base versus apex, (2) response to His refractory premature ventricular complexes, (3) paradoxical atriohisian response (shorter atriohisian interval during tachycardia than that during sinus rhythm) in long RP tachycardia, and (4) the role of adenosine to aid in the diagnosis. Results: Three cases underwent differential VOD during tachycardia. All demonstrated a shorter postpacing interval minus tachycardia cycle length during basal pacing than apical pacing with one case exhibiting apical VOD results compatible with atrioventricular nodal reentrant tachycardia. Basal VOD was useful for localizing the ventricular connection in a case with cHV pathway. In 3 cases, His refractory premature ventricular complexes reset the tachycardia without conduction to the atrium, which excluded the involvement of an atrioventricular pathway or atrial tachycardia, or atrioventricular nodal reentrant tachycardia alone. One case had His refractory premature ventricular complexes followed by subsequent constant AA interval and then tachycardia termination, suggesting a bystander cNV pathway involvement. Two cNV pathway cases presented with long RP tachycardia had paradoxical atriohisian shortening of >15 ms, suggesting parallel activation of the atrium and the atrioventricular node. Adenosine terminated the tachycardia with retrograde block in 2 cases with cNV pathways but had no response on a cHV pathway. Conclusions: cNV and cHV pathways mediated tachyarrhythmias can present with variable clinical presentations. We emphasize the important role of differential VOD sites, His refractory premature ventricular complexes that reset or terminate the tachycardia without conduction to the atrium, paradoxical atriohisian response in long RP tachycardia, and the use of adenosine for diagnosing cNV and cHV pathways.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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