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Nodal Conduction (nodal + conduction)
Selected AbstractsAutonomic Blockade Unmasks Maturational Differences in Rate-Dependent Atrioventricular Nodal Conduction and Facilitation in the MouseJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2003SAMIR SABA M.D. Maturational Differences in Murine AVN Conduction. Introduction: In large animals, rate-dependent AV nodal (AVN) properties of conduction are modulated by autonomic inputs. In this study, we investigated whether the properties of AVN conduction and facilitation are altered by autonomic blockade in the mouse and whether this effect is age dependent. Methods and Results: Young (age 4,6 weeks; n = 11) and adult (age 8,9 months; n = 11) female mice underwent in vivo electrophysiologic testing, before and after autonomic blockade. After autonomic blockade, the adult mice had significantly longer AVN effective refractory period (AVNERP; 67 ± 14 msec vs 56 ± 4 msec, P = 0.05) and functional refractory period (AVNFRP; 81 ± 10 msec vs 72 ± 4 msec, P = 0.05). With autonomic blockade, the increase from baseline of AVN Wenckebach cycle length (,AVW; 1.8 ± 8.1 msec vs 8.8 ± 3.3 msec, P = 0.04), as well as of AVNERP (,AVNERP; 3.5 ± 3.5 msec vs 21.4 ± 12.6 msec, P = 0.002) and AVNFRP (,AVNFRP; 2.3 ± 3.2 msec vs 12.8 ± 9.0 msec, P = 0.008), was significantly larger in adult than in young mice. Compared with young mice, adult mice were less likely to exhibit AVN facilitation (44% vs 90%, P = 0.03) and had smaller maximal shortening of AVN conduction times after the "test beat" for any coupling of the "facilitating beat" (4 ± 4 msec vs 7 ± 3 msec, P = 0.05). Conclusion: Complete autonomic blockade significantly increases AVN conduction times and refractory periods in adult but not in young mice. Adult mice also exhibit less AVN facilitation. Our results confirm that, like in larger animals, rate-dependent murine AVN properties of conduction are under autonomic regulation. Adult mice have higher sympathetic AVN inputs at baseline, leading to slower conduction after autonomic blockade. (J Cardiovasc Electrophysiol, Vol. 14, pp. 191-195, February 2003) [source] Utilization of Retrograde Right Bundle Branch Block to Differentiate Atrioventricular Nodal from Accessory Pathway ConductionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2009SURAJ KAPA M.D. Introduction: Defining whether retrograde ventriculoatrial (V-A) conduction is via the AV node (AVN) or an accessory pathway (AP) is important during ablation procedures for supraventricular tachycardia (SVT). With the introduction of ventricular extrastimuli (VEST), retrograde right bundle branch block (RBBB) may occur, prolonging the V-H interval, but only when AV node conduction is present. We hypothesized that when AP conduction was present, the V-A interval would increase less than the V-H interval, whereas with retrograde nodal conduction, the V-A interval would increase at least as much as the V-H interval. Methods and Results: We retrospectively reviewed the electrophysiological studies of patients undergoing ablation for AVN reentrant tachycardia (AVNRT) (55) or AVRT (50), for induction of retrograde RBBB during the introduction of VEST, and the change in the measured V-H and V-A intervals. Results were found to be reproducible between independent observers. Out of 105 patients, 84 had evidence of induced retrograde RBBB. The average V-H interval increase with induction of RBBB was 53.7 ms for patients with AVRT and 54.4 ms for patients with AVNRT (P = NS). The average V-A interval increase with induction of RBBB was 13.6 ms with AVRT and 70.1 ms with AVNRT (P < 0.001). All patients with a greater V-H than V-A interval change had AVRT, and those with a smaller had AVNRT. Conclusions: Induction of retrograde RBBB during VEST is common during an electrophysiological study for SVT. The relative change in the intervals during induction of RBBB accurately differentiates between retrograde AVN and AP conduction. [source] Orthodromic Pacemaker-Mediated Tachycardia in a Biventricular System Without an Atrial ElectrodeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2004ANTONIO BERRUEZO M.D. Pacemaker-mediated tachycardia is a well-known complication of dual-chamber devices. In this report, we describe for the first time a case of orthodromic pacemaker-mediated tachycardia in a patient in whom a biventricular system without an atrial electrode had been implanted. Retrograde atrial activation was directly produced by the dislodged coronary vein electrode in the AV groove, resulting in simultaneous capture of the left atrium and left ventricle. During tachycardia, AV nodal conduction was via the anterograde pathway of the circuit and limited the ventricular response. Subsequently, right ventricular activation was sensed by the right ventricular electrode that triggered biventricular pacing and left atrial capture, perpetuating the tachycardia. Because the left atrial threshold was higher than the left ventricular threshold, the problem could be resolved easily by lowering the output of the coronary vein electrode. [source] Effects of Estrogen on Cardiac Electrophysiology in Female MiceJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2002SAMIR SABA M.D. Estrogen and Cardiac Electrophysiology.Introduction: Understanding the molecular mechanisms that underlie gender- and hormonal-related differences in susceptibility to cardiac arrhythmias has been hampered by the lack of a suitable animal model. We examined the effect of hormonal status on the electrophysiologic (EP) properties of the mouse heart in an in vivo, closed chest model. Methods and Results: Fifty-three female C57/J mice aged 10 to 12 weeks were studied. Thirty-six mice underwent bilateral ovariectomies; 18 received estrogen (OVX + E) and 18 received placebo (OVX). Seventeen female mice underwent only sham surgery. All animals underwent in vivo EP studies. Select EP parameters were measured after quinidine treatment. Data were analyzed by a blinded observer. Compared with the intact female mice, the PR and AH intervals were significantly shorter in the OVX mice, and these parameters normalized with estrogen replacement (PR = 45.9 ± 4.5 msec in the intact mice, 42.1 ± 4.3 msec in the OVX group, and 46.9 ± 3.5 msec in the OVX + E group, P < 0.005; AH = 36.5 ± 4.9 msec in the intact mice, 34.4 ± 4.7 msec in the OVX group, and 38.8 ± 2.7 msec in the OVX + E group, P = 0.03). The right ventricular effective refractory period was significantly shorter in the OVX mice versus the intact mice, and this also normalized with estrogen replacement. Hormonal status did not significantly affect any other EP variable, including QT interval. Conclusion: In female mice, estrogen prolongs AV nodal conduction and the right ventricular effective refractory period. Taken together, these data suggest that hormonal status affects aspects of cardiac EP function. Future application of this mouse model will be helpful in determining the molecular pathways that mediate hormonal differences in cardiac EP. [source] Connexin40-Deficient Mice Exhibit Atrioventricular Nodal and Infra-Hisian Conduction AbnormalitiesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000BRIAN A. VANDERBRINK B.S. AV Nodal and Infra-Hisian Conduction in Cx40 Mice. Introduction: Previous electrophysiologic investigations have described AV conduction disturbances in connexin4(Cx40)-deficient mice. Because expression or(Cx40 occurs predominantly in the atria and His-Purkinje system of the mouse heart, the AV conduction disturbances were thought to be secondary to disruption in His-Pnrkinje function. However, the lack of a His-bundle electrogram recording in the mouse has limited further investigation of the importance of Cx40. Using a novel technique to record His-bundle recordings in Cx40-deficient mice, we define the physiologic importance of defciencies in Cx40. Methods and Results: Ten Cx40 -/- mice and 11 Cx40+/+ controls underwent a blinded, in vivo, closed chest electrophysiology study at 9 to 12 weeks of age. In the Cx40+/+ mice, the PR interval was significantly longer compared with Cx40+/+ mice (44.6 ± 6.4 msec vs 36.0 ± 4.1 msec, P = 0.002). Not only the HV interval (14.0 ± 3.0 msec vs 10.4 ± 1.2 msec, P = 0.003) but also the AH interval (33.2 ± 4.8 msec vs 27.1 ± 3.7 msec, P = 0.006), AV Wenckebach cycle lengths, and AV nodal effective and functional refractory periods were prolonged in Cx40 -/- compared with Cx40+/+ mice. Conclusion: Cx40-deficient mice exhibit significant delay not only in infra-Hisian conduction, as would be expected from the expression of Cx40 in the His-Purkinje system but also in the electrophysiologic parameters that reflect AV nodal conduction. Our data suggest a significant role of Cx40 in atrionodal conduction and/or in proximal His-bundle conduction, [source] Maturational Atrioventricular Nodal Physiology in the MouseJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2000COLIN T. MAGUIRE B.S. Mouse AV Nodal Maturation. Introduction: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. Methods and Results: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 ± 12 msec, 2:1 block pacing cycle length was 61 ± 11 msec, and mean AVERP100 was 54 ± 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2, conduction curves or AV nodal echo heats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). Conclusion: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, hut they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population. [source] Atrial, SA Nodal, and AV Nodal Electrophysiology in Standing Horses: Normal Findings and Electrophysiologic Effects of Quinidine and DiltiazemJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2007Colin C. Schwarzwald Background: Although atrial arrhythmias are clinically important in horses, atrial electrophysiology has been incompletely studied. Hypotheses: Standard electrophysiologic methods can be used to study drug effects in horses. Specifically, the effects of diltiazem on atrioventricular (AV) nodal conduction are rate-dependent and allow control of ventricular response rate during rapid atrial pacing in horses undergoing quinidine treatment. Animals: Fourteen healthy horses. Methods: Arterial blood pressure, surface electrocardiogram, and right atrial electrogram were recorded during sinus rhythm and during programmed electrical stimulation at baseline, after administration of quinidine gluconate (10 mg/kg IV over 30 minutes, n = 7; and 12 mg/kg IV over 5 minutes followed by 5 mg/kg/h constant rate infusion for the remaining duration of the study, n = 7), and after coadministration of diltiazem (0.125 mg/kg IV over 2 minutes repeated every 12 minutes to effect). Results: Quinidine significantly prolonged the atrial effective refractory period, shortened the functional refractory period (FRP) of the AV node, and increased the ventricular response rate during atrial pacing. Diltiazem increased the FRP, controlled ventricular rate in a rate-dependent manner, caused dose-dependent suppression of the sinoatrial node and produced a significant, but well tolerated decrease in blood pressure. Effective doses of diltiazem ranged from 0.125 to 1.125 mg/kg. Conclusions and Clinical Importance: Standard electrophysiologic techniques allow characterization of drug effects in standing horses. Diltiazem is effective for ventricular rate control in this pacing model of supraventricular tachycardia. The use of diltiazem for rate control in horses with atrial fibrillation merits further investigation. [source] | ||||||||||