Optimal surgical management of severe tricuspid regurgitation in cardiac transplant patients.

BACKGROUND: Severe tricuspid regurgitation (TR) with signs of right-sided heart failure is rare after orthotopic heart transplantation (OHT). In some instances, this condition will require surgical correction using reconstructive surgery or prosthetic valve replacement. Repair techniques of atrioventricular valves are now well described. However, the results of the different surgical procedures in this setting have not been widely reported and may depend on the type of valvular dysfunction and lesions present. Herein we report our experience in a group of patients requiring surgical correction of symptomatic severe TR after OHT.
METHODS: We reviewed our transplant experience during the period from July 1992 to July 1999 (n = 138 cardiac transplants). Eight patients (5.8%) developed symptomatic severe TR requiring surgical correction after a mean duration of 21 months after OHT. Patients were divided into 2 groups based on the mechanism of regurgitation using Carpentier's functional classification. In Group 1 (n = 4), the mechanism of tricuspid regurgitation was Carpentier's Type I, secondary to annular dilation. In Group 2 (n = 4) the mechanism of TR was leaflet prolapse (Type II), due to chordal rupture after biopsy injury. Initially, tricuspid valve integrity was surgically restored in all 8 patients with either valve repair (n = 6) or replacement (n = 2). In Group 1, 2 patients underwent valve repair using a ring annuloplasty and 2 patients underwent valve replacement with a bioprosthetic valve (n = 1) or pulmonary allograft (n = 1). In Group 2, all patients underwent valve repair using a variety of techniques in combination with tricuspid annuloplasty.
RESULTS: During the follow-up period, 3 of the 6 (50%) primary repairs (1 patient in Group 1 and 2 in Group 2) failed and required replacement with a bioprosthesis at 8 days, 14 days and 4 years, respectively. The pulmonary allograft failed secondary to valvular stenosis and was replaced with a bioprosthesis after 10 months. Overall, no failures occurred in any of the 5 bioprosthetic valves placed at the primary operation (n = 1) or after failed tricuspid repair/pulmonary allograft (n = 4), after a mean follow-up of 55 months.
CONCLUSIONS: TR requiring surgical correction after OHT is a rare condition and requires a tailored surgical strategy. This strategy should take into account the mechanism of valve dysfunction and specific valvular lesions. In patients with Type I dysfunction secondary to annular dilation, valve repair with a remodeling annuloplasty should be performed; however, in the presence of any residual TR on transesophageal echocardiography (TEE) at the completion of cardiopulmonary bypass (CPB), a valve replacement with a bioprosthesis is warranted during the same procedure. In patients with Type II dysfunction with leaflet prolapse and biopsy-induced chordal injury, a bioprosthetic valve replacement seems a reliable surgical option.