The Experts below are selected from a list of 1341 Experts worldwide ranked by ideXlab platform
Wen-jin Cherng - One of the best experts on this subject based on the ideXlab platform.
-
Sinus automaticity and Sinoatrial Conduction in severe symptomatic sick sinus syndrome.
Journal of the American College of Cardiology, 1992Co-Authors: San-jou Yeh, Fun-chung Lin, Chun-chieh Wang, Wen-jin CherngAbstract:Abstract Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 ± 2.8 s (mean ± SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete Sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional Sinoatrial block. Group II consisted of 22 patients with either 1:1 Sinoatrial Conduction (group IIa = 13 patients) or second degree Sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to >14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 ± 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 ± 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patient with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 ± 1, 121). Thus, abnormalities in both sinus node automaticity and Sinoatrial Conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete Sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive Sinoatrial exit block plays a major role in producing posttachycardia pauses.
J M Power - One of the best experts on this subject based on the ideXlab platform.
-
specific effects of zatebradine on sinus node function suppression of automaticity prolongation of Sinoatrial Conduction and pacemaker shift in the denervated canine heart
Journal of Pharmacology and Experimental Therapeutics, 1995Co-Authors: Jonathan M Kalman, Andrew M Tonkin, J M PowerAbstract:We evaluated the cardiac electrophysiological effects of zatebradine in eight anesthetized and autonomically denervated canines, with particular emphasis on the effects on sinus node automaticity and Sinoatrial Conduction (SACT), both at rest and after atrial overdrive pacing. Sinus node function was assessed by using the recorded sinus node electrogram and also by applying a previously validated mathematical model of sinus node function which allows separate evaluation of effects of pacing on SACT and suppression of automaticity. Other standard electrophysiological parameters also were measured. Tests were performed before and after incremental doses of zatebradine (0.0625, 0.125 and 0.25 mg/kg). Zatebradine caused a significant, dose-related increase in cardiac cycle length. There also was a significant, dose-related increase in both suppression of automaticity and SACT (independent of changes in cycle length) after zatebradine. The only other significant electrophysiological effect was a relatively minor increase in the ventricular effective refractory period (13%). Higher doses of zatebradine were associated with spontaneous pacemaker shift characterized by loss of the sinus node electrogram and variation in P-wave morphology. Our results confirm that the effects of zatebradine are relatively specific for the sinus node. These included: 1) prolongation of resting sinus cycle length; 2) enhanced suppression of automaticity after overdrive pacing; 3) prolongation of SACT; and 4) induction of sinus node pacemaker shifts. This agent should be used cautiously in patients with possible sinus node dysfunction.
Vadim V. Fedorov - One of the best experts on this subject based on the ideXlab platform.
-
Tachy-brady arrhythmias: The critical role of adenosine-induced Sinoatrial Conduction block in post-tachycardia pauses
Heart rhythm, 2012Co-Authors: Qing Lou, Alexey V. Glukhov, Brian J. Hansen, Lori T. Hage, Pedro Vargas-pinto, George E. Billman, Cynthia A. Carnes, Vadim V. FedorovAbstract:Background In patients with Sinoatrial nodal (SAN) dysfunction, atrial pauses lasting several seconds may follow rapid atrial pacing or paroxysmal tachycardia (tachy-brady arrhythmias). Clinical studies suggest that adenosine may play an important role in SAN dysfunction, but the mechanism remains unclear. Objective To define the mechanism of SAN dysfunction induced by the combination of adenosine and tachycardia. Methods We studied the mechanism of SAN dysfunction produced by a combination of adenosine and rapid atrial pacing in isolated coronary-perfused canine atrial preparations by using high-resolution optical mapping (n = 9). Sinus cycle length and Sinoatrial Conduction time (SACT) were measured during adenosine (1–100 μM) and DPCPX (1 μM; A1 receptor antagonist; n=7) perfusion. Sinoatrial node recovery time was measured after 1 minute of "slow" pacing (3.3 Hz) or tachypacing (7–9 Hz). Results Adenosine significantly increased sinus cycle length (477±62 ms vs 778±114 ms; P P P Conclusions These data directly demonstrate that adenosine contributes to post-tachycardia atrial pauses through SAN exit block rather than slowed pacemaker automaticity. Thus, these data suggest an important modulatory role of adenosine in tachy-brady syndrome.
-
complex interactions between the Sinoatrial node and atrium during reentrant arrhythmias in the canine heart
Circulation, 2010Co-Authors: Vadim V. Fedorov, Alexey V. Glukhov, Richard B. Schuessler, Roger Chang, Geran Kostecki, Deborah Janks, Igor R EfimovAbstract:Background— Numerous studies implicate the Sinoatrial node (SAN) as a participant in atrial arrhythmias, including atrial flutter (AFL) and atrial fibrillation (AF). However, the direct role of the SAN has never been described. Methods and Results— The SAN was optically mapped in coronary perfused preparations from normal canine hearts (n=17). Optical action potentials were recorded during spontaneous rhythm, overdrive atrial pacing, and AF/AFL induced by acetylcholine (ACh; 0.3 to 3 μmol/L) and/or isoproterenol (Iso; 0.2 to 1 μmol/L). An optical action potential multiple component algorithm and dominant frequency analysis were used to reconstruct SAN activation and to identify specialized Sinoatrial Conduction pathways. Both ACh and Iso facilitated pacing-induced AF/AFL by shortening atrial repolarization. The entire SAN structure created a substrate for macroreentry with 9.6±1.7 Hz (69 episodes in all preparations). Atrial excitation waves could enter the SAN through the Sinoatrial Conduction pathways a...
San-jou Yeh - One of the best experts on this subject based on the ideXlab platform.
-
Sinus automaticity and Sinoatrial Conduction in severe symptomatic sick sinus syndrome.
Journal of the American College of Cardiology, 1992Co-Authors: San-jou Yeh, Fun-chung Lin, Chun-chieh Wang, Wen-jin CherngAbstract:Abstract Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 ± 2.8 s (mean ± SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete Sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional Sinoatrial block. Group II consisted of 22 patients with either 1:1 Sinoatrial Conduction (group IIa = 13 patients) or second degree Sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to >14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 ± 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 ± 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patient with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 ± 1, 121). Thus, abnormalities in both sinus node automaticity and Sinoatrial Conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete Sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive Sinoatrial exit block plays a major role in producing posttachycardia pauses.
Jonathan M Kalman - One of the best experts on this subject based on the ideXlab platform.
-
specific effects of zatebradine on sinus node function suppression of automaticity prolongation of Sinoatrial Conduction and pacemaker shift in the denervated canine heart
Journal of Pharmacology and Experimental Therapeutics, 1995Co-Authors: Jonathan M Kalman, Andrew M Tonkin, J M PowerAbstract:We evaluated the cardiac electrophysiological effects of zatebradine in eight anesthetized and autonomically denervated canines, with particular emphasis on the effects on sinus node automaticity and Sinoatrial Conduction (SACT), both at rest and after atrial overdrive pacing. Sinus node function was assessed by using the recorded sinus node electrogram and also by applying a previously validated mathematical model of sinus node function which allows separate evaluation of effects of pacing on SACT and suppression of automaticity. Other standard electrophysiological parameters also were measured. Tests were performed before and after incremental doses of zatebradine (0.0625, 0.125 and 0.25 mg/kg). Zatebradine caused a significant, dose-related increase in cardiac cycle length. There also was a significant, dose-related increase in both suppression of automaticity and SACT (independent of changes in cycle length) after zatebradine. The only other significant electrophysiological effect was a relatively minor increase in the ventricular effective refractory period (13%). Higher doses of zatebradine were associated with spontaneous pacemaker shift characterized by loss of the sinus node electrogram and variation in P-wave morphology. Our results confirm that the effects of zatebradine are relatively specific for the sinus node. These included: 1) prolongation of resting sinus cycle length; 2) enhanced suppression of automaticity after overdrive pacing; 3) prolongation of SACT; and 4) induction of sinus node pacemaker shifts. This agent should be used cautiously in patients with possible sinus node dysfunction.