Termination of refractory ventricular tachycardia by a combination of intravenous sotalol and overdrive ventricular pacing

Llewellyn, Michael J.; Ramsdale, David R.

doi:10.1002/clc.4960100709

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…The bradycardia‐dependence of EAD emergence and APD lengthening during oxidative stress may have clinical relevance in at least two respects: (1) anti‐tachycardia pacing (also known as overdrive pacing or entrainment), which has been routinely used by electrophysiologists to terminate refractory ventricular tachycardia in human patients (Llewellyn & Ramsdale, ) or mammalian models (Furukawa et al . ; Arnar et al .…”

Section: Discussionmentioning

confidence: 99%

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension

Nguyen

Sovari

Pezhouman

et al. 2016

The Journal of Physiology

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Key pointsr Hypertension is a risk factor for sudden cardiac death caused by ventricular tachycardia and fibrillation.r Whether hypertension in its early stage is associated with an increased risk of ventricular tachyarrhythmias is not known.r Based on experiments performed at the cellular and whole heart levels, we show that, even early in chronic hypertension, the hypertrophied and fibrotic ventricles of spontaneously hypertensive rats aged 5 to 6 months have already developed increased stress-induced arrhythmogenicity, and this increased susceptibility to ventricular arrhythmias is primarily a result of tissue remodelling rather than cellular electrophysiological changes.r Our findings highlight the need for early hypertension treatment to minimize myocardial fibrosis, ventricular hypertrophy, and arrhythmias.Abstract Hypertension is a risk factor for sudden cardiac death caused by ventricular tachycardia and fibrillation (VT/VF). We hypothesized that, in early hypertension, the susceptibility to stress-induced VT/VF increases. We compared the susceptibility of 5-to 6-month-old male spontaneously hypertensive rats (SHR) and age/sex-matched normotensive rats (NR) to VT/VF during challenge with oxidative stress (H 2 O 2 ; 0.15 mmol l −1 ). We found that only SHR hearts exhibited left ventricular fibrosis and hypertrophy. H 2 O 2 promoted VT in all 30 SHR but none of the NR hearts. In 33% of SHR cases, focal VT degenerated to VF within 3 s. Simultaneous voltage-calcium optical mapping of Langendorff-perfused SHR hearts revealed that H 2 O 2 -induced VT/VF arose spontaneously from focal activations at the base and mid left ventricular epicardium. Microelectrode recording of SHR hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activity. However, despite the increased susceptibility of SHR hearts to VT/VF, patch clamped isolated SHR ventricular myocytes developed EADs and triggered activity to the same extent as NR ventricular myocytes, except with larger EAD amplitude. During the early stages of hypertension, when challenged with oxidative stress, SHR hearts showed an increased ventricular arrhythmogenicity that stems primarily from tissue remodelling (hypertrophy, fibrosis) rather than cellular electrophysiological changes. Our findings highlight the need for early hypertension treatment to minimize myocardial fibrosis, ventricular hypertrophy, and arrhythmias. NR, normotensive rats; PA peak vel, pulmonary artery peak velocity; (P)CL, (pacing) cycle length; PW, posterior wall; P-ECG, pseudo-electrocardiogram; RV, right ventricle; RWT, relative wall thickness; SHR, spontaneously hypertensive rats; SHHF, spontaneously hypertensive heart failure; SBP, systolic blood pressure; VT/VF, ventricular tachycardia and fibrillation.

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Section: Discussionmentioning

confidence: 99%

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension

Nguyen

Sovari

Pezhouman

et al. 2016

The Journal of Physiology

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“…It has been shown to terminate sustained ventricular tachycardia (VT) in 70% of cases, which was significantly better than the results achieved with lidocaine. 2 It may also prove to be useful in the termination and suppression of refractory VT 3 and VT associated with acute myocardial infarction (MI), 3,4 and to facilitate defibrillation of ventricular fibrillation. 5 Intravenous racemic sotalol terminates about 70% of cases of atrioventricular nodal reentrant and atrioventricular reciprocating tachycardias [6][7][8][9] It is not as effective as adenosine or verapamil, 10 but it may be useful for patients with recurrent or refractory supraventricular tachycardias (SVTs), particularly when calcium-channel blockers are contraindicated.…”

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confidence: 99%

Meta‐analysis of the Risk of Torsades de Pointes in Patients Treated with Intravenous Racemic Sotalol

Marill

Runge

2001

Academic Emergency Medicine

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Abstract. Objective: Intravenous (IV) racemic sotalol is useful for the treatment of multiple tachydysrhythmias. The authors hypothesized that the risk of torsades de pointes (TdP) in patients treated with a single IV infusion of sotalol is lower than the 2-4% risk associated with chronic oral sotalol therapy. Methods: A MEDLINE search under the subject heading ''sotalol'' was made of all publications involving humans written in English or German from 1966 to October 1, 2000. A meta-analysis of all original reports including patients who were given a single infusion of at least 1.5 mg/kg or 100 mg of IV sotalol over 30 minutes or less was performed. Potential variables predictive of TdP were assessed. The primary outcome was the observation of TdP associated with IV sotalol infusion. Secondary measurements included hypotension, bradycardia, and worsening of congestive heart failure. All excluded studies and case reports were also examined for evidence of TdP associated with IV sotalol treatment. Results: The search included 1,005 publications. There were 37 reports in which 962 patients received IV sotalol and met the inclusion criteria. There was one report of self-terminating TdP lasting 10 seconds among the 962 patients included in the study. There was no report of TdP associated with only IV racemic sotalol administration in any of the excluded studies. If it is assumed that the risk of TdP is homogeneous in the population of patients treated with IV sotalol, then based on the 962 included patients, the rate of TdP is 0.1% (95% CI = 0.003% to 0.6%). Conclusions: The overall risk of TdP in patients treated with a single infusion of IV sotalol is low compared with that in patients given chronic oral sotalol therapy.

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Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachycardia

et al. 1990

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Termination of refractory ventricular tachycardia by a combination of intravenous sotalol and overdrive ventricular pacing

Cited by 4 publications

References 5 publications

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension

Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension

Meta‐analysis of the Risk of Torsades de Pointes in Patients Treated with Intravenous Racemic Sotalol

Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachycardia

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