Interaction of sequential stimuli applied during the relative refractory period in relation to determination of fibrillation threshold in the canine ventricle.

Tamargo, J; Moe, B; Moe, Gordon K.

doi:10.1161/01.res.37.5.534

Cited by 56 publications

(13 citation statements)

References 9 publications

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“…Studies on anaesthetized dogs demonstrate that RV stimulations are associated with lower VF threshold and higher inducibility of arrhythmia upon ectopic activation, compared to the spatially matched (either epicardial or endocardial) LV stimulations . In human patients with a documented history of spontaneous arrhythmia, a sustained ventricular tachycardia is more often inducible by programmed electrical stimulation applied to the RV compared to the LV endocardium .…”

Section: Impact Of Ventricular Pacing Site On Arrhythmic Vulnerabilitymentioning

confidence: 99%

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Osadchii

2017

Acta Physiologica

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In cardiac patients, life-threatening tachyarrhythmia is often precipitated by abnormal changes in ventricular repolarization and refractoriness. Repolarization abnormalities typically evolve as a consequence of impaired function of outward K currents in cardiac myocytes, which may be caused by genetic defects or result from various acquired pathophysiological conditions, including electrical remodelling in cardiac disease, ion channel modulation by clinically used pharmacological agents, and systemic electrolyte disorders seen in heart failure, such as hypokalaemia. Cardiac electrical instability attributed to abnormal repolarization relies on the complex interplay between a provocative arrhythmic trigger and vulnerable arrhythmic substrate, with a central role played by the excessive prolongation of ventricular action potential duration, impaired intracellular Ca handling, and slowed impulse conduction. This review outlines the electrical activity of ventricular myocytes in normal conditions and cardiac disease, describes classical electrophysiological mechanisms of cardiac arrhythmia, and provides an update on repolarization-related surrogates currently used to assess arrhythmic propensity, including spatial dispersion of repolarization, activation-repolarization coupling, electrical restitution, TRIaD (triangulation, reverse use dependence, instability, and dispersion), and the electromechanical window. This is followed by a discussion of the mechanisms that account for the dependence of arrhythmic vulnerability on the location of the ventricular pacing site. Finally, the review clarifies the electrophysiological basis for cardiac arrhythmia produced by hypokalaemia, and gives insight into the clinical importance and pathophysiology of drug-induced arrhythmia, with particular focus on class Ia (quinidine, procainamide) and Ic (flecainide) Na channel blockers, and class III antiarrhythmic agents that block the delayed rectifier K channel (dofetilide).

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Section: Impact Of Ventricular Pacing Site On Arrhythmic Vulnerabilitymentioning

confidence: 99%

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Osadchii

2017

Acta Physiologica

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“…However, there are certain drawbacks to this technique which have recently been investigated. 8 ' 15 One of the problems associated with using trains of stimuli is that anodal stimuli placed in the absolute refractory period can shorten its duration and cathodal stimuli can lengthen it. 8 This would heighten the disparity of cathodal and anodal refractory periods and hence the use of trains of stimuli may not be a desirable method for the comparison of the ability of cathodal and anodal stimuli to evoke fibrillation.…”

Section: Harris and Moe In 1942mentioning

confidence: 99%

Vulnerability of the mildly ischemic ventricle to cathodal, anodal, and bipolar stimulation.

Mehra¹,

Furman²,

Crump³

1977

Circulation Research

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SUMMARY We studied the difference between myocardial vulnerability to arrhythmias caused by cathodal, anodal, and bipolar stimulation in 29 dogs with partial right coronary artery ocdusion. We used 2-msec duration stimuli of up to 8 mA to determine the ventricular vulnerable periods, their relationship to the refractory periods, and the fibrillation or multiple response thresholds for unipolar anodal and cathodal stimulation after two premature ventricular contractions. The vulnerable period for arrhythmias began at the end of the respective refractory periods and terminated at a specific time within the cardiac cycle. Within this period the arrhythmia and excitation thresholds were equal. Because shorter refractory periods were obtained with anodal stimulation than cathodal, the vulnerable periods for anodal stimulation were longer. This indicated that the vulnerable periods for bipolar stimulation also would be longer than for unipolar cathodal stimulation since bipolar and anodal refractory periods are equal when the cathode and anode are of similar surface area. Results from seven of the experiments showed that a dual focus of excitation, which can only occur with bipolar stimulation, did not make the ventricle more vulnerable to arrhythmias than did unifocal stimulation. These results indicate that the difference between the arrhythmia vulnerability to unipolar cathodal, anodal, and bipolar stimulation is dependent on the relationship between their excitability characteristics, i.e., their strength-interval curves.THE EXISTENCE of a brief period in the ventricular cycle during which electrical stimulation can induce arrhythmias such as ventricular fibrillation was demonstrated in animals by Wiggers and Wegria, 1 and often has been verified. -3The extensive clinical use of cardiac stimulation has made the circumstances under which such electrical stimulation may cause an arrhythmia of importance. Although most investigations indicate that the minimum energy required to precipitate ventricular fibrillation in the normal myocardium exceeds that delivered by a clinical cardiac pacemaker, there have been clinical reports of ventricular fibrillation and tachycardia associated with a pacemaker stimulus falling in the "vulnerable period" of the cardiac cycle. This suggests the presence of pathophysiological and pharmacological factors that lower the threshold to arrhythmias such as myocardial ischemia, sympathetic activity, and premature ventricular beats. 4~6Aside from these factors, the effects of electrode and stimulus characteristics on myocardial vulnerability are not yet well understood.A recent analysis of cases of ventricular fibrillation and tachycardia attributed to pacemaker stimuli found that most such arrhythmias arose in patients undergoing bipolar rather than unipolar cathodal stimulation. 7 In our own review of the literature, 8 we found 26 cases in which the initiation of ventricular fibrillation or tachycardia (defined as at least a run of 3 premature ventricular contractions) was illustrated. In ...

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“…Lewis and Drury2 made similar observations in the dog atrium. Tamargo et al 3 demonstrated that subthreshold stimuli could inhibit threshold stimuli from activating canine ventricle.…”

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confidence: 99%

Inhibition in the human heart.

Prystowsky¹,

Zipes²

1983

Circulation

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Subthreshold electrotonic depolarizations have been shown to exert inhibitory actions on impulse conduction and generation in isolated cardiac tissues. We performed this study to determine whether inhibition occurs in human myocardium, and to investigate the effects of time and voltage, as well as distance, on myocardial inhibition. Sixteen subjects were studied in the clinical electrophysiology laboratory by standard techniques. Atrial and ventricular pacing were performed with the use of a quadripolar catheter. The basic drive train (S ) and premature stimulus (S2) were introduced at the distal bipolar electrode pair through one current output generator and the subthreshold conditioning stimulus (SC) was introduced before S2 at the distal or proximal bipolar pair through a separate current output generator. When 707-713, 1983. THAT AN electrical stimulus that does not completely depolarize myocardium has the ability to interact with a subsequent stimulus that activates myocardium has been known for some time. Drury and Love' showed in the frog ventricle that a subthreshold electrical stimulus initiated before a threshold stimulus could prevent the threshold stimulus from evoking a recordable ventricular depolarization. Lewis

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Interaction of sequential stimuli applied during the relative refractory period in relation to determination of fibrillation threshold in the canine ventricle.

Cited by 56 publications

References 9 publications

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Vulnerability of the mildly ischemic ventricle to cathodal, anodal, and bipolar stimulation.

Inhibition in the human heart.

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