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Eur J Cardiothorac Surg 2006;30:817-818
© 2006 Elsevier Science NL
Letters to the Editor |
David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue 62-258 CHS, Los Angeles, CA 90095-1741, United States
Received 24 August 2006; accepted 28 August 2006.
* Tel.: +1 310 206 1027; fax: +1 310 825 5895. (Email: gbuckberg{at}mednet.ucla.edu).
Key Words: Helical ventricular myocardial band • Biventricular pacing • Structure/function relationship • Functional mitral regurgitation
Insight into functional aspects of electrophysiology requires synthesis of form and motion during planning and enactment of pacing strategies [1]. Tomioka et al. [2] employed the helical ventricular myocardial band (HVMB) to determine if this spatial geometry model, together with prior knowledge about rapid axial and slower radial electro-physiologic conduction velocities, could explain cardiac resynchronization therapy benefits during heart failure.
A central theme is understanding how the anatomic distribution of the His Purkinje system that touches only a few millimeters of nerve myocyte connection, can effect sequential contraction following subsequent transmural impulse heart muscle transmission. Such knowledge requires recognizing differences between electrical activation and differentiating how impulse conduction along the radial versus axial pathway influences contraction. This understanding relates to Taccardi et al.'s studies [3] of spreading activation along spiral axial pathways that follow fiber orientation to create a sequential beat, rather than following traditional transmural endocardial to epicardial electrical stimulus activation patterns to produce a synchronous transmural beat that produces a more unphysiological contraction from Wiggers early studies.
The synchronous beat following cardiac resynchronization therapy differs (i.e., contraction without twisting) from the natural sequential beat following axial conduction by sinus rhythm, or during Tomioka's study of atrial-ventricular septal pacing; ventricular twisting follows sequential segment shortening along the helical ventricular myocardial band. Biventricular pacing improves function after producing a less physiologic transmural beat of synchronous without twisting contraction [2]. Insight into the HVMB and pacing conduction explains this paradoxical observation by matching this clinical observation with underlying mechanisms.
Patients with left bundle branch block have late septum stimulation and impaired contraction. Consequently, the tardy septum wall bulges toward the right ventricle during isometric contraction to cause functional mitral incompetence (FMR) by tethering the attached septal papillary muscle. Biventricular pacing introduces an abrupt transmural electrical stimulus for early transmural septal synchronous contraction, thereby placing the previously bulging septum into a midline position to reduce FMR by architecturally avoiding papillary muscle tethering. Unfortunately, the sequential contraction that underlies the more natural twisting motion is not restored.
Conversely, architectural correction of septal geometry can return mechanical sequential synchrony, without pacing, as shown by DiDonato et al. [4] following left ventricular restoration. Rebuilding natural sequential muscular contraction implies return of slower axial conduction, an event that does not occur with biventricular pacing. The supposition is that mechanically re-uniting form and function does not need a pacemaker. Conversely, this unity is not achievable by His bundle pacing a spherically dilated heart, where volume expansion introduces excitation contraction delays that pacer stimuli cannot correct [5]. I suspect Tomioka's report of employing a septal electrical stimulus will not correct this spherical architectural deficiency.
Future studies that couple exogenous electrical stimulus with returning sequential strain patterns that return normal twisting motion may allow development of novel pacing modalities for failing hearts. Rebuilding the HVMB seems to govern the sequential contraction pattern, and perhaps interfacing electrical events with restoring improved heart model architecture may unfold new and useful pacer therapies.
References
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