title: Direct imaging of the tricuspid valve annular motions by fiberoptic cardioscopy in dogs. I. Does De Vega's annuloplasty preserve the annular motions?
abstract: Applying the technology of direct imaging by fiberoptic cardioscopy, physiologic and pathophysiologic motions of the tricuspid valve anulus were studied in 10 anesthetized normal dogs (control group) and in 9 dogs that had chronic tricuspid regurgitation (TR group). The heart was perfused with transparent modified Tyrode's solution by working heart method, and the anuli, outlined by sutured beads, were observed and recorded on a high-speed video system in real time. Tricuspid valve annular area was calculated at 14 points during the cardiac cycle. The control group was studied in the normal condition, and the tricuspid regurgitation group was studied during four interventions: nontricuspid annuloplasty group and three tricuspid annuloplasty groups with reducing tricuspid valve annular area to 80%, 65%, and 50% of that of the non-tricuspid annuloplasty group by De Vega's procedure. Tricuspid valve annular area in the control group increased by 7% during atrial systole and was reduced by 34% mainly during ventricular systole, in which the free wall annular area and the septal annular area narrowed by an equal 34%. Chronic tricuspid regurgitation lessened tricuspid valve annular area narrowing to 20% in percent reduction (p < 0.01). In the TR group the decrease in tricuspid valve annular area narrowing was attributed mainly to lessened narrowing of the free wall anulus (percent reduction of tricuspid valve annular area, 19%; p < 0.01). The amplitudes in tricuspid valve annular area narrowing were unchanged in the tricuspid annuloplasty groups even when tricuspid valve annular area, was reduced to 50% by De Vega's tricuspid annuloplasty (percent reduction of tricuspid valve annular area, 16%; not significant). These findings suggest that De Vega's tricuspid annuloplasty is a reasonable method that does preserve the physiologic annular motions in the opening and closing mechanism of the tricuspid valve.
authors.affiliation: Department of Surgery, Saga Medical School, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Minato
authors.forename: T
authors.initials: T
authors.lastname: Itoh
mesh_terms: D000818:Animals; D006348:Cardiac Surgical Procedures / Q000379:methods; D016022:Case-Control Studies; D004285:Dogs; D004724:Endoscopy / Q000379:methods; D005336:Fiber Optic Technology; D014261:Tricuspid Valve / Q000502:physiology* / Q000503:physiopathology / Q000601:surgery; D014262:Tricuspid Valve Insufficiency / Q000503:physiopathology* / Q000601:surgery