Adaptive diastolic interval control of cardiac action potential duration alternans.
BACKGROUND
Recent experimental and computational studies have shown that beat-to-beat alternation in action potential duration can trigger cardiac reentry, suggesting that such "alternans" is a mechanistic precursor to arrhythmias. Given such a link, termination of alternans may help prevent the onset of arrhythmias. To this end, recent efforts have shown that chaos control methods can modulate the timing of electrical stimulation to eliminate alternans.


RESULTS
We have developed an alternative control method founded entirely in cardiac electrophysiology (rather than borrowing techniques from the control of physical systems as with existing control techniques). Using computer simulations, we show that this method, which exploits the rate-dependent behavior of cardiac tissue, can be used to control alternans (and higher-order) rhythms, and is robust to drift and noise. When applied to individual model cells exhibiting alternans, the algorithm converges to the period-1 rhythm over as wide, and in some cases a wider, range of feedback proportionality constant values relative to existing methods. Control success comparable to existing methods is achieved when the algorithm is applied to a simulated one-dimensional Purkinje fiber exhibiting alternans.


CONCLUSIONS
We have developed a method that adaptively controls the timing of electrical stimulation to rapidly eliminate action potential duration alternans in cardiac tissue. This control method may prove valuable in future arrhythmia prevention therapies.
Department of Physiology and Biophysics, Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10021, USA.
Peter N
PN
Jordan
David J
DJ
Christini
D000200:Action Potentials; D000465:Algorithms; D001145:Arrhythmias, Cardiac / Q000503:physiopathology / Q000628:therapy*; D003198:Computer Simulation; D003971:Diastole / Q000502:physiology; D022062:Electrophysiologic Techniques, Cardiac; D006339:Heart Rate / Q000502:physiology; D008962:Models, Theoretical; D009206:Myocardium / Q000166:cytology