title: Right ventricular distension alters monophasic action potential duration during pulmonary arterial occlusion in anaesthetised lambs: evidence for arrhythmogenic right ventricular mechanoelectrical feedback.
abstract: Abnormal loading and distension of the right ventricle may induce arrhythmia through the process of mechanoelectrical feedback. Nonetheless, the electrophysiological effects of right ventricular distension are ill-defined and the mechanisms which underpin mechanoelectrical feedback in the right ventricle are unknown. We examined the effects of changes in right ventricular load (complete occlusion of both caval veins or the main pulmonary artery) in 14 anaesthetised lambs, instrumented with right ventricular surface electrodes and strain gauges for recording monophasic action potential and segment length, and an integrated conductance and micromanometer-tipped catheter for measurement of right ventricular pressure and volume. Caval occlusion did not alter right ventricular segment length and monophasic action potential duration. By contrast, pulmonary arterial occlusion increased the segment length and decreased the monophasic action potential duration at 25, 50 and 70% repolarisation by 29 +/- 6, 22 +/- 4 and 17 +/- 3 ms, respectively (all P < 0.01). Of the 42 pulmonary arterial occlusions, 38 were associated with early afterdepolarisations (EADs) which increased progressively in magnitude as the occlusion was maintained until, in 32, overt arrhythmia was observed. By contrast, none of the four occlusions in which EADs were not observed resulted in arrhythmia. As a result, the proportion of occlusions which resulted in arrhythmia were greater in those associated with EADs than in those which were not (P = 0.002). Right ventricular distension alters the pattern of repolarisation, precipitates early afterdepolarisations and results in a variety of ventricular arrhythmia, including ventricular tachycardia.
authors.affiliation: The National Heart and Lung Institute, Imperial College of Science, Technology and Medicine and The Institute of Child Health, London, UK.
authors.forename: G
authors.initials: G
authors.lastname: Greve
authors.forename: M J
authors.initials: MJ
authors.lastname: Lab
authors.forename: R
authors.initials: R
authors.lastname: Chen
authors.forename: D
authors.initials: D
authors.lastname: Barron
authors.forename: P A
authors.initials: PA
authors.lastname: White
authors.forename: A N
authors.initials: AN
authors.lastname: Redington
authors.forename: D J
authors.initials: DJ
authors.lastname: Penny
mesh_terms: D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D025461:Feedback, Physiological; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D011651:Pulmonary Artery / Q000502:physiology*; D012756:Sheep; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*; D016276:Ventricular Function; D017725:Ventricular Pressure