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Role of Wavelength Adaptation in the Initiation, Maintenance, and Pharmacologic Suppression of Reentry
Author(s) -
GIROUARD STEVEN D.,
ROSENBAUM DAVID S.
Publication year - 2001
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2001.00697.x
Subject(s) - reentry , medicine , cardiology , reentrancy , tachycardia , orthodromic , stimulation , physics , condensed matter physics
Wavelength Adaptation and Reentry.Introduction: The stability of reentry is thought to depend on a critical balance between the spatial extent of refractory tissue in a reentrant wave (i.e., wavelength λ) and the reentrant path length. Because considerable evidence suggests that λ changes continuously in space and time during abrupt rate changes associated with the onset of tachycardia, we hypothesized that beat‐by‐beat adaptation of λ to the dimensions of the reentrant path plays a central role in the mechanism of initiation of reentry. Methods and Results: To investigate the dynamic relationship between λ and path length during initiation of reentry, optical mapping with voltage‐sensitive dyes was used in a guinea pig model of reentrant ventricular tachycardia (VT). In this model, a computer‐guided laser obstacle precisely controlled the position and dimensions of the reentrant path. Under control perfusion and after addition of 15 μ M d‐sotalol, λ was monitored during steady‐state pacing, premature stimulation, and the initiating beats leading to nonsustained and sustained VT. During control perfusion, reentrant VT was reproducibly induced in 8 of 8 hearts, whereas in the presence of d‐sotalol, reentry could only be initiated in 1 of 8 hearts due primarily to the failure of λ to adapt to the reentrant path length. During successful initiation of VT, a consistent sequence was observed. The sequence was characterized by antidromic and orthodromic propagation around both sides of the anatomic obstacle, followed by unidirectional block of the antidromic impulse and persistence of reentry only if the λ of the orthodromic impulse adapted to the reentrant path (λ < path length). d‐Sotalol prevented initiation of VT by altering λ adaptation of the orthodromic wave; however, it failed to terminate ongoing VT because reverse use‐dependence developed after several beats of tachycardia. Conclusion: In an experimental model where λ, path length, and cellular action potentials were monitored during initiation of reentry, we found that, in contrast to termination, the initiation of reentry and the transition from nonsustained to sustained VT is strongly dependent on beat‐to‐beat adaptation of λ to the dimensions of the reentrant path.