Left ventricular systolic dysfunction induced by XXXX : a novel model for premature ventricular contraction-induced @entity296 .

@entity32 @entity296 @entity82 @entity2634 @entity235 @entity1540 @entity2383
BACKGROUND: @entity1540 ( @entity1540 ) commonly coexist with @entity296 . Recently, @entity1540 have been identified as a possible cause of @entity296 . We developed a @entity2634 -induced @entity296 animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this @entity296 and examine the associated histopathologic abnormalities. METHODS AND RESULTS: Thirteen mongrel @entity235 were implanted with a specially programmed pacemaker capable of simulating @entity1540 . Animals were randomly assigned to either 12 weeks of bigeminal @entity1540 (n = 7) or no @entity1540 (control, n = 6). Continuous 24-hour Holter monitoring corroborated ventricular bigeminy in the @entity2634 group ( @entity2634 , 49.8% versus control, < 0.01%; P<0.0001). After 12 weeks, only the @entity2634 group had @entity296 , with a significant reduction in left ventricular ejection fraction ( @entity2634 , 39.7    5.4% versus control, 60.7    3.8%; P < 0.0001) and an increase in left ventricular end-systolic dimension ( @entity2634 , 33.3    3.5 mm versus control, 23.7    3.6 mm; P < 0.001). Ventricular effective refractory period showed a trend to prolong in the @entity2634 group. @entity2634 -induced @entity296 was resolved within 2 to 4 weeks after discontinuation of @entity1540 . No @entity32 , @entity82 , or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with @entity2634 -induced @entity296 . CONCLUSIONS: This novel @entity2634 animal model demonstrates that frequent @entity1540 alone can induce a reversible form of @entity296 in otherwise structurally normal hearts. @entity2634 -induced @entity296 lacks gross histopathologic and @entity2383 seen in other @entity235 models of @entity296 .
