A dynamic control technique was used to suppress a cardiac arrhythmia called an alternans rhythm in a piece of dissected rabbit heart. Our control algorithm adapted to drifting system parameters, making it well suited for the control of physiological rhythms. Control of cardiac alternans rhythms may have important clinical implications since they often precede serious cardiac arrhythmias and are a harbinger of sudden cardiac death.[S0031-9007 (97)03337-1] PACS numbers: 87.22. -q, 05.45. + b, 07.05.Dz, 87.10.+e Control techniques from the field of nonlinear dynamics [1] have been used to control both chaotic [2] and nonchaotic [3] dynamical systems. Since these control methods do not require knowledge of the system's governing equations, they are particularly applicable in biology where detailed mathematical models are usually unavailable. Control of biological dynamics is important for medical science since abnormal physiological rhythms can be life threatening [4]. Attempts have already been made to control both experimental [5] and model [6,7] biological systems. However, none of these studies used control algorithms which adapted to evolving system parameters. Since physiological environments typically drift over time, practical biological control schemes must adapt to these changes. Here, we utilize an algorithm which controls an evolving cardiac arrhythmia called an alternans rhythm in the rabbit heart.Cardiac alternans rhythms are characterized by an alternation of the timing or morphology of the heart's electrical activity from one beat to the next. While the clinical importance of cardiac alternans has only recently been recognized [8], their discovery dates back to the earliest recordings of cardiac electrical signals [9]. We generated cardiac alternans by electrically stimulating a piece of dissected rabbit heart [10]. Each stimulus delivered to the upper atrium caused a wave of electrical activity to propagate through the atrium, the atrioventricular (AV) node and out the His bundle which is the output of the AV node [ Fig. 1(a)]. We measured the electrical activity near an atrial input of the AV node and at the His bundle output [ Fig. 1(b)]. X was the time for the impulse to pass through the AV node. The output impulse was reinjected into the atrium after a time delay l. When l was made sufficiently small, the conduction time through the AV node began to alternate [11] [ Fig. 1(b)].The dynamics of AV nodal conduction can be characterized by a one-dimensional mapwhere X n is the AV nodal conduction time following the nth atrial stimulus, l is the time delay from His bundle activation to the next atrial stimulus, and f is a nonlinear, decreasing function of both arguments which relates the successive conduction times [11]. The map is represented as a graph in Fig. 2(a). This map determines the sequence of AV nodal conduction times, X 1 , X 2 , X 3 , . . . , X n given some initial conduction time, X 0 , for fixed l. The intersection of the curve with the line of identity (X n11 X n ) defines the period-...

Background-The AV node is frequently the site of reentrant rhythms. These rhythms arise from a slow and a fast pathway for which the anatomic and functional substratum remain debated. This study proposes a new explanation for dual-pathway physiology in which the posterior nodal extension (PNE) provides the substratum for the slow pathway. Methods and Results-The anatomic and functional properties of the PNE were studied in 14 isolated rabbit heart preparations. A PNE was found in all studied preparations. It appeared as an elongated bundle of specialized tissues lying along the lower side of Koch's triangle between the coronary sinus ostium and compact node. No well-defined boundary separated the PNE, compact node, and lower nodal cell bundle. The electric properties of the PNE were characterized with a premature protocol and surface potential recordings from histologically controlled locations. The PNE showed cycle-length-dependent posteroanterior slow activation with a shorter refractory period (minimum local cycle length) than that of the compact node. During early premature beats resulting in block in transitional tissues, the markedly delayed PNE activation could propagate to maintain or resume nodal conduction and initiate reentrant beats. A shift to PNE conduction resulted in different patterns of discontinuity on conduction curves. Transmembrane action potentials recorded from PNE cells in 6 other preparations confirmed the slow nature of PNE potentials. Conclusions-The PNE is a normal anatomic feature of the rabbit AV node. It constitutes a cycle-length-dependent slow pathway with a shorter refractory period than that of the compact node. Propagated PNE activation can account for a discontinuity in conduction curves, markedly delayed AV nodal responses, and reentry. Finally, the PNE provides a substratum for the slow pathway in dual-pathway physiology. (Circulation. 1998;98:164-174.)

To study the intranodal origin of the functional properties of the atrioventricular node, progressive changes in nodal cell activation time and cycle length occurring during complete sequences of periodic premature stimulation of the atrium were determined for 419 nodal cells recorded in 11 isolated rabbit heart preparations. The conduction time in proximal nodal cells including the N cells increased only at very short coupling intervals. Conduction time in the distal node (NH and H cells) first increased and then decreased with increasing prematurity. The major fraction of the basic and premature delays developed between N and NH cell activation, a period devoid of upstrokes. The effective and functional refractory periods were related to the minimum intervals between successive upstrokes at the node entrance and outlet, respectively. These results suggest that the cycle-length dependency of nodal conduction is the result of complex changes in propagation time occurring at three levels in the node, whereas the effective and functional refractory periods reflect reactivation limits of cells located at the node entrance and outlet, respectively.