title: How does intermittent pacing modify the response to rapid ventricular pacing in experimental heart failure?
abstract: Rapid ventricular pacing is widely accepted as a useful model to produce heart failure. The heart failure is associated with reduced myocardial energy stores and absence of cardiac hypertrophy. In this study, it was hypothesized that a modification of the protocol to intermittent pacing would permit time for partial recovery of myocardial energetics leading to improved cardiac function and development of hypertrophy. Eight dogs underwent conventional continuous right ventricular pacing to a biologic endpoint of severe heart failure (group 1). Another eight dogs underwent an intermittent pacing protocol over 7 weeks, consisting of 48-hour pacing alternating with 24-hour sinus rhythm (group 2) so as to produce the same total exposure to continuous pacing as in group 1. Six additional normal dogs were used as control animals for tissue metabolic data. Although both paced groups had similar directional changes in hemodynamic, neurohormonal, and echocardiographic variables, the absolute increases in pulmonary capillary wedge and right atrial pressures in group 2 (13 +/- 8 and 3 +/- 4 mmHg, respectively) were less marked than in group 1 (29 +/- 5 and 12 +/- 4 mmHg, respectively; both P = .002). Group 2 also had a more modest rise in plasma atrial natriuretic peptide and norepinephrine concentrations. There was no significant increase, however, in left ventricular mass in either group, and myocardial adenosine 5'-triphosphate levels were reduced to a similar extent compared to the control animals. Intermittent pacing produces a less advanced syndrome of heart failure than continuous pacing. Furthermore, the data suggest that reduced energy stores are not the predominant mechanism for impaired cardiac function, although they may contribute to the failure to hypertrophy in this model.
authors.affiliation: Department of Medicine, St. Michael's Hospital, University of Toronto, Ontario, Canada.
authors.forename: G W
authors.initials: GW
authors.lastname: Moe
authors.forename: R J
authors.initials: RJ
authors.lastname: Howard
authors.forename: E A
authors.initials: EA
authors.lastname: Grima
authors.forename: P W
authors.initials: PW
authors.lastname: Armstrong
mesh_terms: D000818:Animals; D016275:Atrial Function; D009320:Atrial Natriuretic Factor / Q000097:blood; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004195:Disease Models, Animal; D004285:Dogs; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000097:blood; D011669:Pulmonary Wedge Pressure; D013997:Time Factors
chemical_list: D009419:Nerve Tissue Proteins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor