TY - JOUR

T1 - Nonlinear modeling of the atrioventricular node physiology in atrial fibrillation

AU - Rashidi, Armin

AU - Khodarahmi, Iman

PY - 2005/2/21

Y1 - 2005/2/21

N2 - A nonlinear model of the atrioventricular (AV) node physiology in atrial fibrillation (AF) is proposed based on three assumptions: (1) normal distribution of atrial impulses, (2) right-skewed distribution of R-R intervals, (3) increase in the refractory period of the AV node due to rapid bombardment from the atria. Simulation resulted in the following conclusions, all of which are in agreement with previous experience: (1) the entry speed of atrial impulses into the AV node in AF is inversely proportional to the ventricular rate, (2) the autocorrelation function of R-R intervals is zero at all delays, (3) a newly introduced index, sign of first difference, has a negative autocorrelation function at the first delay and zero ones at all others. In spite of its simplicity, the model is able to explain what happens in atrial premature complexes, sinus tachycardia and sinus bradycardia. Different rhythms, some of which rarely seen clinically, can be reproduced by changing input patterns or by slightly manipulating the model parameters. In order to make possible a long irregular time series of R-R interval, aperiodic changes in atrial signals are shown to be necessary. In conclusion, we proposed a simple model for the AV node physiology capable of explaining the previously known facts about AF as well as predicting interesting properties of some other supraventricular arrhythmias.

AB - A nonlinear model of the atrioventricular (AV) node physiology in atrial fibrillation (AF) is proposed based on three assumptions: (1) normal distribution of atrial impulses, (2) right-skewed distribution of R-R intervals, (3) increase in the refractory period of the AV node due to rapid bombardment from the atria. Simulation resulted in the following conclusions, all of which are in agreement with previous experience: (1) the entry speed of atrial impulses into the AV node in AF is inversely proportional to the ventricular rate, (2) the autocorrelation function of R-R intervals is zero at all delays, (3) a newly introduced index, sign of first difference, has a negative autocorrelation function at the first delay and zero ones at all others. In spite of its simplicity, the model is able to explain what happens in atrial premature complexes, sinus tachycardia and sinus bradycardia. Different rhythms, some of which rarely seen clinically, can be reproduced by changing input patterns or by slightly manipulating the model parameters. In order to make possible a long irregular time series of R-R interval, aperiodic changes in atrial signals are shown to be necessary. In conclusion, we proposed a simple model for the AV node physiology capable of explaining the previously known facts about AF as well as predicting interesting properties of some other supraventricular arrhythmias.

KW - Autocorrelation

KW - Logistic

KW - R-R interval

KW - Right-skewed

KW - Time series

UR - http://www.scopus.com/inward/record.url?scp=9644290793&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=9644290793&partnerID=8YFLogxK

U2 - 10.1016/j.jtbi.2004.08.033

DO - 10.1016/j.jtbi.2004.08.033

M3 - Article

C2 - 15588634

AN - SCOPUS:9644290793

SN - 0022-5193

VL - 232

SP - 545

EP - 549

JO - Journal of Theoretical Biology

JF - Journal of Theoretical Biology

IS - 4

ER -