Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

Furukawa, Tetsushi; Rozanski, John J.; Moroe, Kazuo; Gosselin, Arthur J.; Lister, John

doi:10.1016/0002-8703(89)90582-6

Cited by 48 publications

(13 citation statements)

References 24 publications

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“…The therapeutic effects of procainamide are often offset by adverse electrical changes which either reduce its clinical efficacy or even translate to drug‐induced arrhythmia. In 50–70% of patients with organic heart disease, intravenous procainamide infusion fails to prevent the induction of VT by programmed stimulation, or even facilitates it . This refers to the increased number of trials with inducible arrhythmia, to the conversion of non‐sustained to sustained VT, or to arrhythmia induction with a fewer extrastimuli.…”

Section: Arrhythmogenic Responses To Antiarrhythmic Drugsmentioning

confidence: 99%

“…The arrhythmogenic responses to procainamide have been ascribed to drug‐induced conduction slowing, an effect that contributes to the increased excitable gap within the re‐entrant circuit, and hence sustains arrhythmia . Nevertheless, the same mechanism may be employed to explain the antiarrhythmic effect of this agent.…”

Section: Arrhythmogenic Responses To Antiarrhythmic Drugsmentioning

confidence: 99%

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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: Arrhythmogenic Responses To Antiarrhythmic Drugsmentioning

confidence: 99%

Section: Arrhythmogenic Responses To Antiarrhythmic Drugsmentioning

confidence: 99%

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Osadchii

2017

Acta Physiologica

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“…However, more comprehensive analyses were performed when multiple pacings were used. The changes In response to pharmacological therapy, responders had 15 or less beats of inducible nonsustained ventric- 6 390±84 500±217 .079 Longest NSVT (beats) 6 15.8±20.7 4.5±4 .25…”

Section: Left Ventricular Ejection Fractionmentioning

confidence: 99%

Antiarrhythmic effects of selective prolongation of refractoriness. Electrophysiologic actions of sematilide HCl in humans.

et al. 1993

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The electrophysiologic profile of sematilide is consistent with selective block of outward potassium currents and associated isolated lengthening of the ventricular effective refractory period and APD; sematilide demonstrates a significant degree of reverse frequency-dependence of the ventricular APD and effective refractory period; and suppression of ventricular tachycardia inducibility by sematilide appears to be correlated with increases in the right ventricular effective refractory period.

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“…The arrhythmogenic potential of procainamide was also demonstrated in some experimental studies . Increased electrical instability in the presence of procainamide was attributed to drug‐induced conduction slowing, which would increase the excitable gap within the re‐entrant circuit and therefore promote arrhythmia . Nevertheless, the same mechanism may be employed to explain anti‐arrhythmic effect of procainamide.…”

Section: Discussionmentioning

confidence: 94%

“…Furukawa et al. showed that intravenous procainamide prevents VT induction by programmed stimulation in only 24% of patients with healed myocardial infarction while producing no protective effects in others. There was no difference in plasma concentrations of procainamide (about 7 mg/L) between the ‘responders’ and ‘nonresponders’ groups .…”

Section: Discussionmentioning

confidence: 99%

Procainamide and lidocaine produce dissimilar changes in ventricular repolarization and arrhythmogenicity in guinea‐pig

Osadchii

2013

Fundamemntal Clinical Pharma

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Procainamide is class Ia Na(+) channel blocker that may prolong ventricular repolarization secondary to inhibition of IK r , the rapid component of the delayed rectifier K(+) current. In contrast to selective IN a blockers such as lidocaine, procainamide was shown to produce arrhythmogenic effects in the clinical setting. This study examined whether pro-arrhythmic responses to procainamide may be accounted for by drug-induced repolarization abnormalities including impaired electrical restitution kinetics, spatial gradients in action potential duration (APD), and activation-to-repolarization coupling. In perfused guinea-pig hearts, procainamide was found to prolong the QT interval on ECG and left ventricular (LV) epicardial monophasic APD, increased the maximum slope of electrical restitution, enhanced transepicardial APD variability, and eliminated the inverse correlation between the local APD and activation time values determined at distinct epicardial recording sites prior to drug infusion. In contrast, lidocaine had no effect on electrical restitution, the degree of transepicardial repolarization heterogeneities, and activation-to-repolarization coupling. Spontaneous episodes of monomorphic ventricular tachycardia were observed in 57% of procainamide-treated heart preparations. No arrhythmia was induced by lidocaine. In summary, this study suggests that abnormal changes in repolarization may contribute to pro-arrhythmic effects of procainamide.

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Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

Cited by 48 publications

References 24 publications

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

Antiarrhythmic effects of selective prolongation of refractoriness. Electrophysiologic actions of sematilide HCl in humans.

Procainamide and lidocaine produce dissimilar changes in ventricular repolarization and arrhythmogenicity in guinea‐pig

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