AV Nodal (av + nodal)

Distribution by Scientific Domains

Terms modified by AV Nodal

  • av nodal pathway
  • av nodal physiology
  • av nodal reentrant tachycardia

  • Selected Abstracts


    Connexin40-Deficient Mice Exhibit Atrioventricular Nodal and Infra-Hisian Conduction Abnormalities

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000
    BRIAN 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]


    Phytanic Acid Accumulation Is Associated with Conduction Delay and Sudden Cardiac Death in Sterol Carrier Protein-2/Sterol Carrier Protein-x Deficient Mice

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2004
    GEROLD MÖNNIG M.D.
    Introduction: The sterol carrier protein-2 gene encodes two functionally distinct proteins: sterol carrier protein-2 (SCP2, a peroxisomal lipid carrier) and sterol carrier protein-x (SCPx, a peroxisomal thiolase known as peroxisomal thiolase-2), which is involved in peroxisomal metabolism of bile acids and branched-chain fatty acids. We show in this study that mice deficient in SCP2 and SCPx (SCP2null) develop a cardiac phenotype leading to a high sudden cardiac death rate if mice are maintained on diets enriched for phytol (a metabolic precursor of branched-chain fatty acids). Methods and Results: In 210 surface and 305 telemetric ECGs recorded in wild-type (C57BL/6; wt; n = 40) and SCP2 null mice (n = 40), no difference was observed at baseline. However, on diet, cycle lengths were prolonged in SCP2 null mice (262.9 ± 190 vs 146.3 ± 43 msec), AV conduction was prolonged (58.3 ± 17 vs 42.6 ± 4 ms), and QRS complexes were wider (19.1 ± 5 vs 14.0 ± 4 ms). In 11 gene-targeted Langendorff-perfused hearts isolated from SCP2 null mice after dietary challenge, complete AV blocks (n = 5/11) or impaired AV conduction (Wenckebach point 132 ± 27 vs 92 ± 10 msec; P < 0.05) could be confirmed. Monophasic action potentials were not different between the two genotypes. Left ventricular function studied by echocardiography was similar in both strains. Phytanic acid but not pristanic acid accumulated in the phospholipid fraction of myocardial membranes isolated from SCP2 null mice. Conclusion: Accumulation of phytanic acid in myocardial phospholipid membranes is associated with bradycardia and impaired AV nodal and intraventricular impulse conduction, which could provide an explanation for sudden cardiac death in this model. [source]


    Autonomic Blockade Unmasks Maturational Differences in Rate-Dependent Atrioventricular Nodal Conduction and Facilitation in the Mouse

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2003
    SAMIR 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]


    Connexin40-Deficient Mice Exhibit Atrioventricular Nodal and Infra-Hisian Conduction Abnormalities

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000
    BRIAN 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]


    Biventricular Pacing for Severe Mitral Reguritation Following Atrioventrgicular Nodal Ablation

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2p1 2003
    PATRICK J.S. DISNEY
    DISNEY, P.J.S., et al.: Biventricular Pacing for Severe Mitral Regurgitation Following Atrioventricular Nodal Ablation. A 69-year-old woman developed acute pulmonary edema and severe mitral regurgitation (MR) 2 days following an uncomplicated AV nodal (AVN) ablation and insertion of VVI pacemaker for chronic atrial fibrillation. There was no history of significant mitral valve disease. Left ventricular function was normal and there was no evidence of an acute cardiac ischemic event. Transthoracic echo and right heart catheterization studies showed reduction in the severity of MR with biventricular pacing as opposed to RV pacing alone. A permanent pacemaker configured for biventricular pacing was implanted with complete resolution of symptoms and significant reduction in degree of MR. (PACE 2003; 26[Pt. I]:643,644) [source]


    Effects of Sex and Age on Electrocardiographic and Cardiac Electrophysiological Properties in Adults

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001
    TARESH TANEJA
    TANEJA, T., et al.: Effects of Sex, and Age on Electrocardiographic and Cardiac Electrophysiological Properties in Adults. Although differences in patient sex in heart rate and QT interval have been well characterized, sexual differences in other cardiac electrophysiological properties have not been well defined. The study population consisted of 354 consecutive patients without structural heart disease or preexcitation who underwent clinically indicated electrophysiological testing in the drug-free state. Atrial, AV nodal, and ventricular effective refractory periods (AERP, AVNERP, VERP) were determined at a pacing cycle length of 500 ms using an 8-beat drive train and 3-second intertrain pause. There were 124 men and 230 women with a mean age of 45 ± 19 and 47 ± 18 years, respectively The sinus cycle length (SCL) was longer in men than in women (864 ± 186 and 824 ± 172 ms, respectively, P < 0.05). The QRS duration was significantly longer in men (90 ± 12 ms) than women (86 ± 13 ms) (P < 0.005). The HV interval was 48 ± 9 ms in men and 45 ± 8 ms in women (P < 0.05). The sinus node recovery time (SNRT) was significantly longer in men than in women (1215 ± 297 ms and 1135 ± 214 ms, respectively, P < 0.05). AERP and VERP were similar in both sexes. Aging did not influence sexual differences in cardiac electrophysiological properties, although, it independently prolonged the SCL, PR, and QT intervals, AH and HV intervals, SNRT, AVNERP, and the AV Wenckebach cycle length. The SCL, QRS duration, HV interval, and SNRT were significantly longer in men than in women. Aging prolonged cardiac conduction and increased the SCL but the effects were similar in both sexes. AERP and VERP were unaffected by aging or sex. [source]