title: Electrophysiological effect of varied rate and extent of acute in vivo left ventricular load increase.
abstract: OBJECTIVE
  The aim was to determine whether the rate, the magnitude, or both, of increased left ventricular wall stress in vivo has consistent and prominent effects on repolarisation, afterdepolarisations, or arrhythmogenicity.
  
  
  METHODS
  Ten anaesthetised dogs underwent transient proximal aortic occlusion. Wall stress was estimated from pressure-volume data obtained by volume catheter, normalised to preocclusion values, and correlated with simultaneously determined changes in monophasic action potential duration (MAPd). Data were obtained during both fast (greater than 50% rise in wall stress within two beats) and slow occlusions, as well as during innervated and denervated conditions.
  
  
  METHODS
  Adult mongrel dogs (20-25 kg) were used.
  
  
  RESULTS
  Two- to threefold increases in wall stress resulted in less than 5 ms shortening in MAPd and there was little correlation between wall stress and MAPd shortening. The strongest relation between normalised wall stress (EWSnorm) and MAPd was observed under denervated conditions during rapid aortic occlusion (delta MAPd = -2.5 x EWSnorm +2.1, r2 = 0.44, p less than 0.001). Afterdepolarisations were observed in fewer than 10% of occlusions and were not related to the magnitude or rate of loading change. Ventricular ectopy occurred more frequently during rapid than slow occlusions (87% v 56%, p = 0.01), but was unrelated to the level of wall stress increase or the presence of afterdepolarisations.
  
  
  CONCLUSIONS
  Marked acute increases in left ventricular loading in vivo minimally alter repolarisation, and rarely lead to afterdepolarisations. The speed rather than magnitude of load change appears more important in the development of ventricular ectopy. These findings suggest that load induced ventricular ectopy is due to stretch induced automaticity rather than triggered activity or re-entry.
authors.affiliation: Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
authors.forename: H
authors.initials: H
authors.lastname: Calkins
authors.forename: J H
authors.initials: JH
authors.lastname: Levine
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000208:Acute Disease; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D004285:Dogs; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology*