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http://dx.doi.org/10.1016/j.hrthm.2021.09.017 | DOI Listing |
Heart Rhythm
May 2022
Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, California.
Eur Heart J Case Rep
December 2019
Department of Cardiology, Huaihe Hospital, Henan University College of Medicine, Kaifeng, Henan 475000, China.
Cardiovasc Res
February 2012
UCLA Cardiovascular Research Laboratory, Division of Cardiology, Department of Medicine, Los Angeles, CA, USA.
Aims: Fibrosis is known to promote cardiac arrhythmias by disrupting myocardial structure. Given recent evidence that myofibroblasts form gap junctions with myocytes at least in co-cultures, we investigated whether myofibroblast-myocyte coupling can promote arrhythmia triggers, such as early afterdepolarizations (EADs), by directly influencing myocyte electrophysiology.
Methods And Results: Using the dynamic voltage clamp technique, patch-clamped adult rabbit ventricular myocytes were electrotonically coupled to one or multiple virtual fibroblasts or myofibroblasts programmed with eight combinations of capacitance, membrane resistance, resting membrane potential, and gap junction coupling resistance, spanning physiologically realistic ranges.
Aberrant ventricular conduction is a rare phenomenon as compared with the more frequently occurring antrioventricular conduction disturbances. It leads to widening of the QRS complex, which is either due to a complete or functional block in one of the bundle branches or a block within the intramyocardial conduction system itself. Mechanisms that are potentially involved in the genesis of aberrant ventricular conduction are sudden shortening of cycle length (tachycardia-dependent phase III), antegrade block with retrograde concealed conduction, or bradycardia-dependent block (enhanced phase IV).
View Article and Find Full Text PDFJ Appl Physiol (1985)
March 2002
Cardiovascular Research Programme, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada M5G 1X8.
Complete heart block (CHB) provides a useful substrate for study of bradycardia-dependent ventricular arrhythmias and cardiac function. Existing CHB animal models are limited by surgical recovery time and reliance on intrinsic escape rhythms. We describe a novel closed-chest rabbit model of CHB involving transcatheter radiofrequency (RF) atrioventricular (AV) node ablation and ventricular rate control with chronic transvenous pacing.
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