Controlling reentrant arrhythmias in cardiac tissue
Ekaterina Zhuchkova* and Harald Engel
Institut für Theoretische
Physik, Technische Universität zu Berlin, Berlin, Germany
*ekaterina@physik.tu-berlin.de
Ventricular
tachyarrhythmias (tachycardias
and fibrillations) caused by rotating waves (reentry) in the heart can lead to
highly rapid and uncoordinated contractions, resulting in dysfunction of the
blood pumping by the heart. For
terminating these pathologies devices surgically implanted in high-risk cardiac
patients are used. Modern implantable cardioverter
defibrillators possess pacing, cardioversion and
defibrillation capabilities, and in the case of ventricular tachycardia may try
to pace the heart faster than its intrinsic rate in order to break it before
the latter proceeds to fibrillation. This local forcing is known as
anti-tachycardia pacing (ATP). It locally applies one or more series of
low-power stimuli to return a racing heart to its normal rhythm. So far, ATP is
the only low-energy therapy for both types of ventricular tachyarrhythmias
and it would be desirable since it prevents destruction of the cardiac and
surrounding tissues and adverse side effects.
However,
we have systematically analyzed and have shown that the low-voltage
non-feedback local forcing is not a robust method to terminate reentrant arrhythmias.
Even in homogeneous isotropic tissue simulated by a simplified ionic model it
was found that success/failure of the
“point” pacing strongly depends on the type of reentry, location of the
electrode, phase of stimuli during the rotation period, stimulation frequency
and waveform and the size of tissue. Along with elimination of spiral waves,
shift of spiral cores closer to unexcitable boundaries or no effect, the local
forcing may also cause spiral-wave turbulence (fibrillation) and prolong existence
of an otherwise self-terminating single spiral wave (reentrant tachycardia).
Finally
we propose feedback-mediated control of reentry as an alternative realistic
low-energy defibrillation strategy.