Factors predisposing to ventricular proarrhythmia during antiarrhythmic drug therapy for atrial fibrillation in patients with structurally normal heart

Lin, Chin Yu; Lo, Li Wei; Chen, Yun Yu; Chong, Eric; Chang, Shih Lin; Chao, Tze Fan; Hu, Yu Feng; Tuan, Ta Chuan; Liao, Jo Nan; Chang, Yao‐Ting; Chien, Kuo–Liong; Chiou, Chuen Wang; Chen, Shih Ann

doi:10.1016/j.hrthm.2015.04.018

Cited by 14 publications

(4 citation statements)

References 29 publications

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“…Dofetilide is a selective I Kr blocker (Jurkiewicz & Sanguinetti, 1993;Mounsey & DiMarco, 2000), which prolongs APD 90 , and therefore increases the EW. Quinidine, procainamide and flecainide exhibit more complex pharmacological profiles that include I Na -blocking effects and, as a result, a slowing of conduction, along with inhibition of the repolarizing K + currents that contributes to the prolonged APD 90 (Glaaser & Clancy, 2006;Lin et al, 2015). These drugs, therefore, might induce variable changes in cardiac EW, suggesting diverse effects on arrhythmic vulnerability.…”

Section: Excitation Wavelength and Vulnerability To Arrhythmiamentioning

confidence: 99%

“…Antiarrhythmic drugs used for the control of cardiac rhythm in atrial fibrillation can unexpectedly induce ventricular tachyarrhythmia, thereby increasing the risk for sudden cardiac death (Frommeyer & Eckardt, 2016;Lin et al, 2015;Prystowsky, 1996). The arrhythmia is typically triggered by a premature ectopic beat superimposed on the T wave of the preceding ventricular contraction (Ruberman et al, 1981), which provokes complex electrical derangements in cardiac cells.…”

Section: Introductionmentioning

confidence: 99%

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Antiarrhythmic drug effects on premature beats are partly determined by prior cardiac activation frequency in perfused guinea‐pig heart

Osadchii

2020

Experimental Physiology

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Antiarrhythmic drugs used to treat atrial fibrillation can occasionally induce ventricular tachyarrhythmia, which is typically precipitated by a premature ectopic beat through a mechanism related, in part, to the shortening of the excitation wavelength (EW). The arrhythmia is likely to occur when a drug induces a reduction, rather than an increase, in the EW of ectopic beats. In this study, I examined whether the arrhythmic drug profile is shaped by the increased cardiac activation rate before ectopic excitation. Ventricular monophasic action potential durations, conduction times and EW values were assessed during programmed stimulations applied at long (S 1 -S 1 [basic drive cycle length] = 550 ms) and short (S 1 -S 1 = 200 ms) cycle lengths in perfused guinea-pig hearts. The premature activations were induced with extrastimulus application immediately upon termination of the refractory period. With dofetilide, a class III antiarrhythmic agent, a prolongation in action potential duration and the resulting increase in the EW obtained at S 1 -S 1 = 550 ms were significantly attenuated at S 1 -S 1 = 200 ms, in both the regular (S 1 ) and the premature (S 2 ) beats. With class I antiarrhythmic agents (quinidine, procainamide and flecainide), fast S 1 -S 1 pacing was found to attenuate the drug-induced increase in action potential duration, while amplifying drug-induced conduction slowing, in both S 1 and S 2 beats. As a result, although the EW was increased (quinidine and procainamide) or not changed (flecainide) at the long S 1 -S 1 intervals, it was invariably reduced by these agents at the short S 1 -S 1 intervals. These findings indicate that the increased heart rate before ectopic activation shapes the arrhythmic profiles by facilitating drug-induced EW reduction. K E Y W O R D Santiarrhythmic agents, excitation wavelength, premature beats How to cite this article: Osadchii OE. Antiarrhythmic drug effects on premature beats are partly determined by prior cardiac activation frequency in perfused guinea-pig heart.

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Section: Excitation Wavelength and Vulnerability To Arrhythmiamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antiarrhythmic drug effects on premature beats are partly determined by prior cardiac activation frequency in perfused guinea‐pig heart

Osadchii

2020

Experimental Physiology

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“…First, drug-related proarrhythmia is a possible mechanism. [ 12 ] However, previously ineffective antiarrhythmic drugs without demonstrated proarrhythmic effects were prescribed post ablation in our study, which is against this possibility. Second, Patel et al [ 6 ] hypothesized that the modulation of adjacent autonomic ganglia by AF ablation developed new-onset OT PVC.…”

Section: Discussionmentioning

confidence: 78%

New-onset ventricular arrhythmias post radiofrequency catheter ablation for atrial fibrillation

Yao

et al. 2016

Medicine

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As a new complication, new-onset ventricular arrhythmias (VAs) post atrial fibrillation (AF) ablation have not been well defined. This prospective study aimed to describe the details of new-onset VAs post AF ablation in a large study cohort.One thousand fifty-three consecutive patients who underwent the first radiofrequency catheter ablation for AF were enrolled. All patients had no evidence of pre-ablation VAs. New-onset VAs were defined as new-onset ventricular tachycardia (VT) or premature ventricular contractions (PVC) ≥1000/24 h within 1 month post ablation.There were 46 patients (4.4%) who had 62 different new-onset VAs, among whom 42 were PVC alone, and 4 were PVC coexisting with nonsustained VT. Multivariate analysis showed that increased serum leukocyte counts ≥50% post ablation were independently associated with new-onset VAs (OR: 1.9; 95% CI: 1.0–3.5; P = 0.043). The median number of PVC was 3161 (1001–27,407) times/24 h. Outflow tract VAs were recorded in 35 (76.1%) patients. No significant differences were found in origin of VAs (P = 0.187). VAs disappeared without any treatment in 6 patients (13.0%). No VAs-related adverse cardiac event occurred.The study revealed a noticeable prevalence but relatively benign prognosis of new-onset VAs post AF ablation. Increased serum leukocyte counts ≥50% post ablation appeared to be associated with new-onset VAs, implying that inflammatory response caused by ablation might be the mechanism.

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“…12,17 Flecainide and propafenone are effective antiarrhythmics that should be combined with an AV nodal blocking agent. 85,86 Sotalol can be effective as a solitary agent. 87 Synchronized cardioversion may not be effective in the absence of antiarrhythmic therapy, particularly in the setting of an automatic focal atrial tachycardia, as atrial tachycardia may resume.…”

Section: Supraventricular Arrhythmia In the Absence Of Structural Heamentioning

confidence: 99%

Management of tachyarrhythmias in pregnancy – A review

Kugamoorthy

Spears

2020

Obstet Med

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Factors predisposing to ventricular proarrhythmia during antiarrhythmic drug therapy for atrial fibrillation in patients with structurally normal heart

Cited by 14 publications

References 29 publications

Antiarrhythmic drug effects on premature beats are partly determined by prior cardiac activation frequency in perfused guinea‐pig heart

Antiarrhythmic drug effects on premature beats are partly determined by prior cardiac activation frequency in perfused guinea‐pig heart

New-onset ventricular arrhythmias post radiofrequency catheter ablation for atrial fibrillation

Management of tachyarrhythmias in pregnancy – A review

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