title: Effects of chronic, rapid right atrial pacing on cardiac hemodynamics and myofibrillar ATPase activity in piglets.
abstract: OBJECTIVE
  To determine whether chronic, rapid right atrial pacing in newborn neonatal piglets has any effects on cardiac hemodynamics, and whether these changes are associated with intrinsic alterations in cardiac contractile potential as shown by cardiac myofibrillar calcium ATPase activity.
  
  
  BACKGROUND
  Although many studies have examined aspects of heart function in models of supraventricular tachycardia, far less is known about its effects in neonatal animals. It is thought that rapid pacing induces a dilated cardiomyopathy in immature pigs.
  
  
  METHODS
  Two-week-old piglets underwent rapid right atrial pacing (250 beats/min) for 10 days, and their cardiac hemodynamic response was monitored. To obtain subcellular mechanistic information regarding systolic dysfunction, cardiac myofibrils were isolated and calcium adenosine triphosphatase activity was measured.
  
  
  RESULTS
  Control piglets had a heart rate of 185 beats/min at the end of the experimental period. Pulmonary artery flow, pulmonary artery flow index and left ventricular end-diastolic diameter were unchanged as a function of rapid, chronic right atrial pacing. Aortic pressure decreased in the paced piglets. Left atrial pressure increased approximately threefold in the paced animals. Left ventricular end-systolic diameter was also significantly higher after pacing, but left ventricular end-diastolic diameter was unchanged. Left ventricular shortening fraction was depressed approximately 50%. Myofibrillar calcium adenosine triphosphatase activity was significantly depressed as a function of pacing.
  
  
  CONCLUSIONS
  Neonatal piglets undergoing chronic supraventricular tachycardia exhibit systolic dysfunction in the absence of dilation. The depression in contractile protein calcium adenosine triphosphatase activity provides information at a subcellular level regarding the mechanism responsible for this cardiomyopathy.
authors.affiliation: Department of Pediatrics, University of Manitoba, Winnipeg.
authors.forename: Niels G
authors.initials: NG
authors.lastname: Giddins
authors.forename: Kim
authors.initials: K
authors.lastname: Duncan
authors.forename: Rabindranath
authors.initials: R
authors.lastname: Persad
authors.forename: James S C
authors.initials: JS
authors.lastname: Gilchrist
authors.forename: Grant N
authors.initials: GN
authors.lastname: Pierce
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004195:Disease Models, Animal; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D011336:Probability; D012016:Reference Values; D012680:Sensitivity and Specificity; D013552:Swine; D013617:Tachycardia, Supraventricular / Q000628:therapy*
chemical_list: D000251:Adenosine Triphosphatases; D009218:Myosins