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Yuan F Pinto J. Characteristics of I K and its response to quinidine in experimental healed myocardial infarction J. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.
Volume Article Contents 1 Introduction. Dispersion of ventricular repolarization and refractory period. Oxford Academic. Select Format Select format. Permissions Icon Permissions. Arrhythmia mechanisms , Hypertrophy , Infarction , Repolarization , Ventricular arrhythmias.
Table 1 Techniques for measurement of repolarization time and refractory period. Can be used in vivo? Maximum simultaneous recordings. Spatial resolution. Temporal resolution. Open in new tab. Open in new tab Download slide. Table 3 Changes in ionic currents and action potential in epicardial myocytes isolated from the infarct border zone. Change s in currents. Effect on AP. Table 4 Changes in ionic currents and APD in remodelled myocardium remote from infarct zone in chronic infarction.
Species, time postocclusion. Effect on APD. Google Scholar Crossref. Search ADS. Cellular mechanisms of arrhythmias in hypertrophied and failing myocardium. The cardiac ventricular myocyte as a substrate for sudden death. The regional lecture in Bath Google Scholar PubMed. Identifying patients at risk of sudden death after myocardial infarction: value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction.
Mechanism of death in heart failure: the vasodilator-heart failure trials. Results of a Veterans Administration Cooperative Study. Changes in the topology of gap junctions as an adaptive structural response of the myocardium. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. The role of non-uniform recovery of excitability in the occurrence of unidirectional block as studied with multiple microelectrodes. The Sicilian gambit.
Effect of 2,3-butanedione 2-monoxime on slow inward and transient outward currents in rat ventricular myocytes. Differential effects of cytochalasin d and 2,3 butanedione monoxime on isometric twitch force and transmembrane action potential in isolated ventricular muscle: implications for optical measurements of cardiac repolarization. Enhanced dispersion of repolarization and refractoriness in transgenic mouse hearts promotes reentrant ventricular tachycardia. In vitro validation of a new cardiac catheter technique for recording monophasic action potentials.
Relation of monophasic action potential recorded with contact electrode to underlying transmembrane action-potential properties in isolated cardiac tissues: a systematic microelectrode validation study.
Correlation between in vivo transmembrane APDs and activation-recovery intervals from electrograms: effects of interventions that alter repolarization time. Ability of activation recovery intervals to assess action potential duration during acute no-flow ischemia in the in situ porcine heart. QT dispersion: An indication of arrhythmia risk in patients with long QT intervals. Dispersion of ventricular repolarization: reality?
Dispersion of QT intervals: a measure of dispersion of repolarization or simply a projection effect? Electrocardiographic indexes of dispersion of ventricular repolarization: an isolated heart validation study. Comparative reproducibility of QT, QT peak, and T peak-T end intervals and dispersion in normal subjects, patients with myocardial infarction, and patients with hypertrophic cardiomyopathy.
Dispersion of effective refractory period during abrupt reperfusion of ischemic myocardium in dogs. Effects of sympathetic stimulation.
Effect of sustained stretch on dispersion of ventricular fibrillation intervals in normal rabbit hearts. Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Fast Fourier transform analysis of ventricular fibrillation intervals to predict ventricular refractoriness and its spatial dispersion. Intracellular recording from the in situ working dog heart in physiological conditions and during acute ischemia and fibrillation.
Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction. The mechanism of termination of reentrant activity in ventricular fibrillation. Regional capture of fibrillating ventricular myocardium: evidence of an excitable gap.
Quantification of spatial inhomogeneity in conduction and initiation of reentrant atrial arrhythmias. Hypoxia and hypothermia enhance spatial heterogeneities of repolarization in guinea pig hearts: analysis of spatial autocorrelation of optically recorded action potential durations. Quantitative indexes of dispersion of refractoriness for identification of propensity to reentrant ventricular tachycardia in a canine model of myocardial infarction.
Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T-wave.
Heterogeneity within the ventricular wall: electrophysiology and pharmacology of epicardial, endocardial, and M cells. Electrophysiologic characteristics of cells spanning the left ventricular wall of human heart: evidence for presence of M cells. Characteristics of the delayed rectifier current I Kr and I Ks in canine ventricular epicardial, midmyocardial, and endocardial myocytes: A weaker I Ks contributes to the longer action potential of the M cell.
Larger late sodium current contributes to the longer action potential of the m cell in canine ventricular myocardium.
Regional differences in the delayed rectifier current I Kr and I Ks contribute to the differences in action potential duration in basal left ventricular myocytes in guinea-pig. Electrophysiological properties of the canine peripheral A—V conducting system. Interactions of transmembrane potentials in canine Purkinje fibres and at Purkinje fiber-muscle junctions. Modulation of ventricular repolarization by a premature stimulus: role of epicardial dispersion of repolarization kinetics demonstrated by optical mapping of the intact guinea-pig heart.
Optical mapping reveals that repolarization spreads anisotropically and is guided by fiber orientation in guinea-pig hearts. Regional changes in ventricular excitability during load manipulation of the in situ pig heart. I K of rabbit ventricle is composed of two currents: evidence for I Ks. Implications of inhomogeneous distribution of I Ks and I Kr channels in ventricle with respect to effects of class III agents and beta-agonists.
Effect of sustained load on dispersion of ventricular repolarization and conduction time in the isolated intact rabbit heart. I to and action potential notch are smaller in left vs. Electrotonic influences on action potentials from isolated ventricular cells. Effects of I Kr and I Ks heterogeneity on action potential duration and its rate dependence: a simulation study.
Effects of the gap junction uncoupler palmitoleic acid on the activation and repolarization wavefronts in isolated rabbit hearts. Effects of sympathetic and vagal nerves on recovery properties of the endocardium and epicardium of the canine left ventricle.
Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic. Informal observations suggested that the effective refractory period lengthened with a prolongation of the time in sinus rhythm basic cycle length time between successive runs of drive stimuli S1S1s. If this were true, failure to control the basic cycle length time could affect the results and interpretation of electrophysiologic testing.
To study this phenomenon, the effective refractory period was studied in 20 patients during sinus rhythm and two ventricular paced rates with up to three extrastimuli, while varying the basic cycle length time from 2 to 3, to 10 to 20 s.
With each of the stimulation sequences used, the effective refractory period lengthened as the basic cycle length time increased "basic cycle length time-effective refractory period effect". The effect was most pronounced when extrastimuli were used during the two ventricular paced rates. As the basic cycle length time increased from 2 to 3 to 20 s, the mean effective refractory period determined during sinus rhythm increased from to ms; with the first ventricular paced rate, the effective refractory period increased from to ms p less than 0.
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