It has been suggested that sick sinus syndrome, which is due to the dysfunction of the sinus node, may result from the sparser gap junctions and/or lower intrinsic frequencies of pacemaker cells that occur with aging....It has been suggested that sick sinus syndrome, which is due to the dysfunction of the sinus node, may result from the sparser gap junctions and/or lower intrinsic frequencies of pacemaker cells that occur with aging. Hence, in this paper, the synchronization mechanism of pacemaker cells that lie in the sinus node of the heart is examined using a modified Kuramoto phase model. Although each element always interacts with all the others in the Kuramoto phase model, in the proposed model, each element interacts only with the neighbors over a certain time (called the interaction time) during Phase 4 of the action potential. The pacemaker cell elements are arranged on a square lattice, and each element connects with the elements surrounding it. The results indicate that the diversity of intrinsic frequencies of pacemaker cells may be necessary for synchronization. Moreover, increasing the proportion of invalid connections causes the elements to take more time to synchronize until eventually they do not synchronize at all, and decreasing the intrinsic frequencies of the elements prevents them from synchronizing. Probably these elucidate the cause of sick sinus syndrome.展开更多
Most of atrial fibrillation(AF)pts have organic artrial injury which ismaintained at modified AV conduction as an AV substrate.Nevertheless this procedure allows to control ventricular contractionsrate(VCR)in AF pts.S...Most of atrial fibrillation(AF)pts have organic artrial injury which ismaintained at modified AV conduction as an AV substrate.Nevertheless this procedure allows to control ventricular contractionsrate(VCR)in AF pts.Supposing that "slow" pathways potentials arepotentials of atrial fibers eonneated with the AV node we used highfrequency current in the meadseptal right atrial area in 24 pts aged 52-74(mean 66±4.9 yrs)having paroxysmal(n=16)and chronic(n=8)AF.AF was induced in pts who had sinus rhythm before ablation andif VSR exceeded 50-70 beats/min the procedure was repeated.Favourable results were obtained in 18(75% of pts).These pts didnot reveal decreased Wenekebach point or increased effectiverefractory period of the AV junction.VSR decreased from 163±27 to65±9(p=0.001)during AF.Then atropine was given and if VSRexceeded 120/min we considered the procedure to be ineffective.Digoxine and beta-blockers which were ineffective before ablationbecame effective to control VSR after it.From 6 to 12 months afterthe procedure,these pts underwent exercise testing(AF was inducedin the sinus rhythm pts):maximum VCR was 116±10.8/min.Becauseof the procedure inefficacy,complete AV block was reached duringablation in 2(8%)pts in whom artificial pacemaker was implanted.Thus modification of AV conduction is an effective procedure tocontrol VSR in AF pts and allows to flee 75% of pts fromantiarrhythmic drugs.展开更多
文摘It has been suggested that sick sinus syndrome, which is due to the dysfunction of the sinus node, may result from the sparser gap junctions and/or lower intrinsic frequencies of pacemaker cells that occur with aging. Hence, in this paper, the synchronization mechanism of pacemaker cells that lie in the sinus node of the heart is examined using a modified Kuramoto phase model. Although each element always interacts with all the others in the Kuramoto phase model, in the proposed model, each element interacts only with the neighbors over a certain time (called the interaction time) during Phase 4 of the action potential. The pacemaker cell elements are arranged on a square lattice, and each element connects with the elements surrounding it. The results indicate that the diversity of intrinsic frequencies of pacemaker cells may be necessary for synchronization. Moreover, increasing the proportion of invalid connections causes the elements to take more time to synchronize until eventually they do not synchronize at all, and decreasing the intrinsic frequencies of the elements prevents them from synchronizing. Probably these elucidate the cause of sick sinus syndrome.
文摘Most of atrial fibrillation(AF)pts have organic artrial injury which ismaintained at modified AV conduction as an AV substrate.Nevertheless this procedure allows to control ventricular contractionsrate(VCR)in AF pts.Supposing that "slow" pathways potentials arepotentials of atrial fibers eonneated with the AV node we used highfrequency current in the meadseptal right atrial area in 24 pts aged 52-74(mean 66±4.9 yrs)having paroxysmal(n=16)and chronic(n=8)AF.AF was induced in pts who had sinus rhythm before ablation andif VSR exceeded 50-70 beats/min the procedure was repeated.Favourable results were obtained in 18(75% of pts).These pts didnot reveal decreased Wenekebach point or increased effectiverefractory period of the AV junction.VSR decreased from 163±27 to65±9(p=0.001)during AF.Then atropine was given and if VSRexceeded 120/min we considered the procedure to be ineffective.Digoxine and beta-blockers which were ineffective before ablationbecame effective to control VSR after it.From 6 to 12 months afterthe procedure,these pts underwent exercise testing(AF was inducedin the sinus rhythm pts):maximum VCR was 116±10.8/min.Becauseof the procedure inefficacy,complete AV block was reached duringablation in 2(8%)pts in whom artificial pacemaker was implanted.Thus modification of AV conduction is an effective procedure tocontrol VSR in AF pts and allows to flee 75% of pts fromantiarrhythmic drugs.
