title: Left ventricular mechanical dyssynchrony is load independent at rest and during endotoxaemia in a porcine model.
abstract: OBJECTIVE
  In diseased or injured states, the left ventricle displays higher degrees of mechanical dyssynchrony. We aimed at assessing mechanical dyssynchrony ranges in health related to variation in load as well as during acute endotoxin-induced ventricular injury.
  
  
  METHODS
  In 16 juvenile anaesthetized pigs, a five-segment conductance catheter was placed in the left ventricle as well as a balloon-tipped catheter in the inferior vena cava. Mechanical dyssynchrony during systole, including dyssynchrony time in per cent during systole and internal flow fraction during systole, were measured at rest and during controlled pre-load reduction sequences, as well as during 3 h of endotoxin infusion (0.25 microg kg(-)1 h(-1)).
  
  
  RESULTS
  Systolic dyssynchrony and internal flow fraction did not change during the course of acute beat-to-beat pre-load alteration. Endotoxin-produced acute pulmonary hypertension by left ventricular dyssynchrony measures was not changed during the early peak of pulmonary hypertension. Endotoxin ventricular injury led to progressive increases in systolic mechanical segmental dyssynchrony (7.9 +/- 1.2-13.0 +/- 1.3%) and ventricular systolic internal flow fraction (7.1 +/- 2.4-16.6 +/- 2.8%), respectively for baseline and then at hour 3. There was no localization of dyssynchrony changes to segment or region in the ventricular long axis during endotoxin infusion.
  
  
  CONCLUSIONS
  These results suggest that systolic mechanical dyssynchrony measures may be load independent in health and during acute global ventricular injury by endotoxin. More study is needed to validate ranges in health and disease for parameters of mechanical dyssynchrony.
authors.affiliation: Anesthesia and Intensive Care Medicine, University Hospital of Umeå, Umeå, Sweden. roman.aroch@vll.se
authors.forename: R
authors.initials: R
authors.lastname: A'roch
authors.forename: P
authors.initials: P
authors.lastname: Steendijk
authors.forename: A
authors.initials: A
authors.lastname: Oldner
authors.forename: E
authors.initials: E
authors.lastname: Weitzberg
authors.forename: D
authors.initials: D
authors.lastname: Konrad
authors.forename: G
authors.initials: G
authors.lastname: Johansson
authors.forename: M
authors.initials: M
authors.lastname: Haney
mesh_terms: D000818:Animals; D019446:Endotoxemia / Q000150:complications / Q000382:microbiology / Q000503:physiopathology*; D004926:Escherichia coli; D004927:Escherichia coli Infections / Q000150:complications / Q000382:microbiology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000382:microbiology / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology; D009200:Myocardial Contraction; D010507:Periodicity; D013312:Stress, Physiological; D013318:Stroke Volume; D013552:Swine; D013599:Systole; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*; D016277:Ventricular Function, Left