Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 289, Issue 4, Pages H1692-H1701Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00241.2005
Keywords
arrhythmias; antiarrhythmic drugs; simulation
Funding
- NHLBI NIH HHS [P50 HL-53219] Funding Source: Medline
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Na+ and K+ channel-blocking drugs have anti- and proarrhythmic effects. Their effects during fibrillation, however, remain poorly understood. We used computer simulation of a two-dimensional (2-D) structurally normal tissue model with phase I of the Luo-Rudy action potential model to study the effects of Na+ and K+ channel blockade on vulnerability to and termination of reentry in simulated multiple-wavelet and mother rotor fibrillation. Our main findings are as follows: 1) Na+ channel blockade decreased, whereas K+ channel blockade increased, the vulnerable window of reentry in heterogeneous 2-D tissue because of opposing effects on dynamical wave instability. 2) Na+ channel blockade increased the cycle length of reentry more than it increased refractoriness. In multiple-wavelet fibrillation, Na+ channel blockade first increased and then decreased the average duration or transient time ( ) of fibrillation. In mother rotor fibrillation, Na+ channel blockade caused peripheral fibrillatory conduction block to resolve and the mother rotor to drift, leading to self-termination or sustained tachycardia. 3) K+ channel blockade increased dynamical instability by steepening action potential duration restitution. In multiple-wavelet fibrillation, this effect shortened because of enhanced wave instability. In mother rotor fibrillation, this effect converted mother rotor fibrillation to multiple-wavelet fibrillation, which then could self-terminate. Our findings help illuminate, from a theoretical perspective, the possible underlying mechanisms of termination of different types of fibrillation by antiarrhythmic drugs.
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