ArticleHeart rhythm2009
Mechanisms of recurrent ventricular fibrillation in a rabbit model of pacing-induced heart failure.
Article in Heart rhythm, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 59 citations in OpenAlex.
- HiPSC-derived cardiomyocyte to model Brugada syndrome: both asymptomatic and symptomatic mutation carriers reveal increased arrhythmogenicity.BMC cardiovascular disorders · 2023Article
- Effects of ondansetron on apamin-sensitive small conductance calcium-activated potassium currents in pacing-induced failing rabbit hearts.Heart rhythm · 2020Article
- Effect of flunarizine on defibrillation outcomes and early refibrillation in a canine model of prolonged ventricular fibrillation.Experimental physiology · 2019Article
- Small-Conductance Calcium-Activated Potassium Current in Normal Rabbit Cardiac Purkinje Cells.Journal of the American Heart Association · 2017Article
- Atrial-selective targeting of arrhythmogenic phase-3 early afterdepolarizations in human myocytes.Journal of molecular and cellular cardiology · 2016Article
- SK channels and ventricular arrhythmias in heart failure.Trends in cardiovascular medicine · 2015Review
- Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.Journal of arrhythmia · 2014Article
- Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation.Circulation research · 2014Article
- Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles.Heart rhythm · 2014Article
- Revisiting K(+) channel-dependent electrical remodeling in the border zone.Journal of cardiovascular electrophysiology · 2013Article
- Apamin-sensitive calcium-activated potassium currents in rabbit ventricles with chronic myocardial infarction.Journal of cardiovascular electrophysiology · 2013Article
- Article
- Heterogeneous upregulation of apamin-sensitive potassium currents in failing human ventricles.Journal of the American Heart Association · 2013Article
- Amiodarone inhibits apamin-sensitive potassium currents.PloS one · 2013Article
- Imaging arrhythmogenic calcium signaling in intact hearts.Pediatric cardiology · 2012Article
- Spontaneous atrial fibrillation initiated by tyramine in canine atria with increased sympathetic nerve sprouting.Journal of cardiovascular electrophysiology · 2012Article
- Intramural optical mapping of V(m) and Ca(i)2+ during long-duration ventricular fibrillation in canine hearts.American journal of physiology. Heart and circulatory physiology · 2012Article
- Spontaneous ventricular fibrillation in right ventricular failure secondary to chronic pulmonary hypertension.Circulation. Arrhythmia and electrophysiology · 2012Article
- Glycolytic inhibition causes spontaneous ventricular fibrillation in aged hearts.American journal of physiology. Heart and circulatory physiology · 2011Article
- Transmural heterogeneity and remodeling of ventricular excitation-contraction coupling in human heart failure.Circulation · 2011Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSuccessful defibrillation may be followed by recurrent spontaneous ventricular fibrillation (VF). The mechanisms of postshock spontaneous VF are unclear.
objectiveThe purpose of this study was to determine the mechanisms of spontaneous VF after initial successful defibrillation in a rabbit model of heart failure (HF).
methodsSimultaneous optical mapping of intracellular calcium (Ca(i)) and membrane potential (Vm) was performed in 12 rabbit hearts with chronic pacing-induced heart failure, in 4 sham-operated hearts, and in 5 normal hearts during fibrillation-defibrillation episodes.
resultsTwenty-eight spontaneous VF episodes were recorded after initial successful defibrillation in 4 failing hearts (SVF group) but not in the remaining 8 failing hearts (no-SVF group) or in the normal or sham-operated hearts. The action potential duration (APD(80)) before pacing-induced VF was 209 +/- 9 ms in the SVF group and 212 +/- 14 ms in the no-SVF group (P = NS). After successful defibrillation, APD(80) shortened to 147 +/- 26 ms in the SVF group and to 176 +/- 14 ms in the no-SVF group (P = .04). However, the duration of Ca(i) after defibrillation was not different between the two groups (246 +/- 21 ms vs 241 +/- 17 ms, P = NS), resulting in elevated Ca(i) during late phase 3 or phase 4 of the action potential. Standard glass microelectrode recording in an additional 5 failing hearts confirmed postshock APD shortening and afterdepolarizations. APD(80) of normal and sham-operated hearts was not shortened after defibrillation.
conclusionHF promotes acute shortening of APD immediately after termination of VF in failing hearts. Persistent Ca(i) elevation during late phase 3 and phase 4 of the shortened action potential result in afterdepolarizations, triggered activity, and spontaneous VF.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.