scholarly journals Differential effective refractory period as a useful marker of multiple accessory pathways

2019 ◽  
Vol 35 (2) ◽  
pp. 296-299
Author(s):  
Robert H. Helm ◽  
Santosh C. Varkey ◽  
Ankur A. Karnik
Keyword(s):  
Refractory Period ◽  
Effective Refractory Period ◽  
Accessory Pathways

Characteristics of antegrade-only accessory pathways in children and adolescents

2021 ◽  
pp. 1-5
Author(s):  
Minh B. Nguyen ◽  
Allison C. Hill ◽  
Yaniv Bar-Cohen ◽  
Michael J. Silka
Keyword(s):  
High Risk ◽  
Refractory Period ◽  
Accessory Pathway ◽  
Young Patients ◽  
Atrioventricular Node ◽  
Effective Refractory Period ◽  
Accessory Pathways ◽  
Electrophysiology Study ◽  
Minimal Data ◽  
Subsequent Comparison

Abstract There is minimal data regarding antegrade-only accessory pathways in young patients. Given evolving recommendations and treatments, retrospective analysis of the clinical and electrophysiologic properties of antegrade-only pathways in patients <21 years old was performed, with subsequent comparison of electrophysiology properties to age-matched controls with bidirectional pathways. Of 522 consecutive young patients with ventricular pre-excitation referred for electrophysiology study, 33 (6.3%) had antegrade-only accessory pathways. Indications included palpitations (47%), chest pain (25%), and syncope (22%). The shortest value for either the accessory pathway effective refractory period or the pre-excited R-R interval was taken for each patient, with the median of the antegrade-only group significantly greater than shortest values for the bidirectional group (310 [280–360] ms versus 270 [240–302] ms, p < 0.001). However, the prevalence of pathways with high-risk properties (effective refractory period or shortest pre-excited R-R interval <250 ms) was similar in both study patients and controls (13% versus 21%) (p = 0.55). Sixteen patients had a single antegrade-only accessory pathway and no inducible arrhythmia. Six patients had Mahaim fibres, all right anterolateral with inducible antidromic reciprocating tachycardia. However, 11 patients with antegrade-only accessory pathways and 3 with Mahaim fibres had inducible tachycardia due to a second substrate recognised at electrophysiology study. These included concealed accessory pathways (7), bidirectional accessory pathways (5), and atrioventricular node re-entry (2). Antegrade-only accessory pathways require comprehensive electrophysiology evaluation as confounding factors such as high-risk conduction properties or inducible Supraventricular Tachycardia (SVT) due to a second substrate of tachycardia are often present.

scholarly journals Angiotensin-(1–7) attenuates atrial tachycardia-induced sympathetic nerve remodeling

2017 ◽  
Vol 18 (3) ◽  
pp. 147032031772928 ◽  
Author(s):  
Wenfeng Shangguan ◽  
Wen Shi ◽  
Guangping Li ◽  
Yuanyuan Wang ◽  
Jian Li ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Tyrosine Hydroxylase ◽  
Sympathetic Nerve ◽  
Refractory Period ◽  
Atrial Tachycardia ◽  
Effective Refractory Period ◽  
Sympathetic Nerve Stimulation ◽  
Atrial Effective Refractory Period

Introduction: The effect of Angiotensin-(1–7) (Ang-(1–7)) on atrial autonomic remodeling is still unknown. We hypothesized that Ang-(1–7) could inhibit sympathetic nerve remodeling in a canine model of chronic atrial tachycardia. Materials and methods: Eighteen dogs were randomly assigned to sham group, pacing group and Ang-(1–7) group. Rapid atrial pacing was maintained for 14 days in the pacing and Ang-(1–7) groups. Ang-(1–7) was administered intravenously in the Ang-(1–7) group. The atrial effective refractory period and atrial fibrillation inducibility level were measured at baseline and under sympathetic nerve stimulation after 14 days of measurement. The atrial sympathetic nerves labeled with tyrosine hydroxylase were detected using immunohistochemistry and Western blotting, and tyrosine hydroxylase and nerve growth factor mRNA levels were measured by reverse transcription polymerase chain reaction. Results: Pacing shortened the atrial effective refractory period and increased the atrial fibrillation inducibility level at baseline and under sympathetic nerve stimulation. Ang-(1–7) treatment attenuated the shortening of the atrial effective refractory period and the increase in the atrial fibrillation inducibility level. Immunohistochemistry and Western blotting showed sympathetic nerve hyperinnervation in the pacing group, while Ang-(1–7) attenuated sympathetic nerve proliferation. Ang-(1–7) alleviated the pacing-induced increases in tyrosine hydroxylase and nerve growth factor mRNA expression levels. Conclusion: Ang-(1–7) can attenuate pacing-induced atrial sympathetic hyperinnervation.

Effects of infarction, procainamide, coupling interval, and cycle length on refractoriness of extrastimuli

1985 ◽  
Vol 248 (5) ◽  
pp. H606-H613
Author(s):  
F. E. Marchlinski ◽  
M. E. Cain ◽  
R. A. Falcone ◽  
R. F. Corky ◽  
J. F. Spear ◽  
...  
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Narrow Range ◽  
Left Ventricular ◽  
Effective Refractory Period ◽  
Stimulation Site ◽  
Refractory Periods ◽  
Coupling Interval ◽  
Cycle Lengths ◽  
Site Of Stimulation

The effects of prematurity, cycle length, site of stimulation, and procainamide on ventricular refractoriness following an extrastimulus (S2) were assessed in 10 dogs with and 10 dogs without infarction. Extrastimuli were introduced at preselected coupling intervals (S1-S2) from normal right and left ventricular sites and from left ventricular sites of infarction during drive cycle lengths (S1-S1) of 350 and 250 ms. At each S1-S2 interval, the effective refractory period of S2 was determined by introducing a second extrastimulus (S3). At all stimulation sites, cycle lengths, and before and during infusion of procainamide (mean concn 18.6 +/- 3.5 micrograms/ml), shortening (greater than 10 ms change) in refractoriness was most marked over a narrow range of closely coupled S1-S2 intervals. Regardless of stimulation site, the effective refractory period of S2 was less during a cycle length of 250 ms compared with a cycle length of 350 ms. In dogs without infarction, the effective refractory periods of S2 from left ventricular sites tended to be longer than from right ventricular sites, particularly during procainamide administration. The refractory period of S2 at sites of infarction did not differ consistently from those at normal sites. Finally, at all stimulation sites and cycle lengths, procainamide prolonged refractoriness of S2 at each S1-S2 interval and blunted the total shortening in refractoriness in response to S2.

Frequency- and voltage-dependent effects of disopyramide in canine Purkinje fibers

1989 ◽  
Vol 67 (7) ◽  
pp. 710-721 ◽  
Author(s):  
Matthew A. Flemming ◽  
Betty I. Sasyniuk
Keyword(s):  
Potassium Channels ◽  
Action Potential ◽  
Sodium Channel ◽  
Action Potential Duration ◽  
Refractory Period ◽  
Drug Effect ◽  
Effective Refractory Period ◽  
Slow Inactivation ◽  
Purkinje Fibers ◽  
Rate Dependent

The voltage- and frequency-dependent blocking actions of disopyramide were assessed in canine Purkinje fibers within the framework of concentrations, membrane potentials, and heart rates which have relevance to the therapeutic actions of this drug. [Formula: see text] was used to assess the magnitude of sodium channel block. Disopyramide produced a concentration- and rate-dependent increase in the magnitude and kinetics of [Formula: see text] depression. Effects on activation time (used as an estimate of drug effect on conduction) were exactly analogous to effects on [Formula: see text]. A concentration-dependent increase in tonic block was also observed. Despite significant increases in tonic block at more depolarized potentials, rate-dependent block increased only marginally with membrane potential over the range of potentials in which propagated action potentials occur. Increases in extracellular potassium concentration accentuated drug effect on [Formula: see text] but attenuated drug effect on action potential duration. Recovery from rate-dependent block followed two exponential processes with time constants of 689 ± 535 ms and 15.7 ± 2.7 s. The latter component represents dissociation of drug from its binding site and the former probably represents recovery from slow inactivation. A concentration-dependent increase in the amplitude of the first component suggested that disopyramide may promote slow inactivation. There was less than 5% recovery from block during intervals equivalent to clinical diastole. Thus, depression of beats of all degrees of prematurity was similar to that of basic drive beats. Prolongation of action potential duration by therapeutic concentrations of drug following a long quiescent interval was minimal. However, profound lengthening of action potential duration occurred following washout of drug effect at a time when [Formula: see text] depression had reverted to normal, suggesting that binding of disopyramide to potassium channels may not be readily reversed. Variable effects on action potential duration may thus be attributed to a block of the window current flowing during the action potential being partially or over balanced by block of potassium channels. Purkinje fiber refractoriness was prolonged in a frequency-dependent manner. Disopyramide did not significantly alter the effective refractory period of basic beats but did increase the effective refractory period of sequential tightly coupled extra stimuli. The results can account for the antiarrhythmic actions of disopyramide during a rapid tachycardia and prevention of its initiation by programmed electrical stimulation.Key words: action potential duration, effective refractory period, upstroke velocity, conduction, rate of sodium channel unblocking.

Sign in / Sign up

Export Citation Format

Share Document