Key result
In 12 isolated animal hearts, LH potentials arose from asynchronous activation near the coronary sinus, while HL potentials arose from asynchronous activation of atrial and nodal-type cells.
HL double potentials near the tricuspid annulus are caused by asynchronous activation of atrial and nodal-type cells, which may represent the substrate of the slow AV nodal pathway.
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Animal data links HL potentials to slow pathway substrate; leaves open whether they guide AVNRT ablation in patients.
McGuire et al. (1994) studied Atrioventricular junctional reentrant tachycardia (n=12). Electrophysiological mapping and histology was evaluated on Origin of double potentials (LH and HL). In 12 isolated animal hearts, LH potentials arose from asynchronous activation near the coronary sinus, while HL potentials arose from asynchronous activation of atrial and nodal-type cells.
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