Complex AV nodal dynamics during ventricular-triggered atrial pacing in humans

David J. Christini, Kenneth M. Stein, Steven M. Markowitz, Suneet Mittal, David J. Slotwiner, Sei Iwai, Bruce B. Lerman
2001 American Journal of Physiology. Heart and Circulatory Physiology  
Complex AV nodal dynamics during ventricular-triggered atrial pacing in humans. Am J Physiol Heart Circ Physiol 281: H865-H872, 2001.-In vitro experiments have shown that the complexity of atrioventricular nodal (AVN) conduction dynamics increases with heart rate. Although complex AVN dynamics (e.g., alternans) have been observed clinically, human AVN dynamics during rapid pacing have not been systematically investigated. We studied such dynamics during ventricular-triggered atrial pacing in 37
more » ... atrial pacing in 37 patients with normal AVN function (18 patients with dual AVN pathway physiology and 19 patients without). Alternans, which always resulted from single pathway conduction, occurred in 18 patients. In 16 patients (3 of whom also had alternans), quasisinusoidal AVN conduction oscillations occurred (mean frequency 0.02 Hz); such oscillations have not been previously reported. There were no significant differences in the dynamics for patients with or without dual AVN pathways. To illuminate the governing dynamic mechanism, a second atrial pacing trial was performed on 12 patients after autonomic blockade. Blockade facilitated alternans but inhibited oscillations. This study suggests that rapid AVN excitation in vivo can lead to autonomically mediated AVN conduction oscillations or single pathway alternans that are a function of inherent nonlinear dynamic AVN tissue properties. atrioventricular node; alternans; oscillations; autonomic nervous system; nonlinear dynamics THE INHERENT ELECTROPHYSIOLOGICAL functional characteristics of atrioventricular (AV) nodal (AVN) tissue have been carefully studied in vitro (1, 2, 4, 13, 29, 32). One of the major factors that governs AVN conduction is AVN recovery time (which is defined in this context as the time between when one impulse exits the AVN and the next impulse enters the AVN) (5, 30, 34). AVN conduction dynamics are a function of the interaction of three intrinsic properties of AVN tissue: recovery, facilitation, and fatigue (2, 4, 25, 34) . Recovery is the process of reestablishing excitability after excitation (3, 29) . Facilitation is the process that produces a short AV interval after a long AV interval that was preceded by a short recovery time (9, 23, 26, 32) . Fatigue is the gradual slowing of AVN conduction during rapid repetitive excitation (21, 32). As the excitation rate increases, it has been shown that recovery, facilitation, and fatigue can interact in a nonlinear fashion to produce increasingly complex AVN conduction dynamics. The idea that AVN dynamics are nonlinear is not new, having been suggested in the early 1900s by Mobitz (24) and incorporated into most AVN conduction models since that time. The nonlinear dynamic mechanistic theory for AVN conduction, which is consistent with the expanding body of evidence supporting the influence of nonlinear dynamics on cardiac electrophysiological behavior (7, 12), is supported by the observation that AVN conduction time can bifurcate (such bifurcations are hallmarks of nonlinear dynamic systems) and settle into a beat-tobeat AVN conduction time alternation known as alternans. Alternans occurs when conduction fatigues beyond a critical value, after which recovery and facilitation interact in a nonlinear fashion to produce alternating long and short intervals. (For a detailed mathematical analysis of this mechanism, see Ref. 32.) Although alternans has often been attributed clinically to the presence of dual AVN pathways (11, 31, 33, 35) , the aforementioned in vitro studies, along with observations of single AVN pathway alternans in humans during AV orthodromic reciprocating tachycardia (ORT) (8, 19, 27, 28) , have provided evidence that the inherent electrophysiological properties of a single AVN pathway may also produce alternans. [ORT is a repetitive reentrant arrhythmia in which normal anterograde ventricular excitation via the AVN is followed by reexcitation of the atria via a pathological retrograde accessory ventriculoatrial (VA) pathway.] Although experimental studies have provided invaluable information about the functional nature of complex AVN dynamics in vitro, knowledge of complex in vivo dynamics in which autonomic influences are also present (17) is lacking. Most in vitro studies have investigated nodal conduction dynamics in the absence of autonomic influences [e.g., the preparations for the experiments that produced the aforementioned nonlin-
doi:10.1152/ajpheart.2001.281.2.h865 pmid:11454592 fatcat:g6yk2qcxzncnzn2fkkpkaucnxm