Abstract 14539: Impact of Tricuspid Regurgitation on Chronic Hepatic and Cardiac Function After Pulmonary Valve Replacement With Repaired Tetralogy of Fallot.

Introduction: Tricuspid regurgitation (TR) is a common long-term complication in patients with repaired tetralogy of Fallot (TOF). However, tricuspid valve repair associated to pulmonary valve replacement (PVR) in adults with repaired TOF, is still debated. Hypothesis: We hypothesized tricuspid regurgitation after PVR may affect hepatic and cardiac function. Methods: We performed a retrospective review of patients (n=59) after TOF repair who underwent first PVR with tricuspid valve repair (n=11, Group T) or without tricuspid valve repair (n=48, Group P). Preoperative and postoperative serial echocardiograms and cardiac magnetic resonance (CMR) imaging were assessed for TR, pulmonary regurgitation (PR), right ventricular size and function. Laboratory value were also examined. PR and TR were scored as 0 (none), 1 (mild), 2 (moderate), and 3 (severe). Results: Mean follow-up duration was 4.6±3.9 years. Mean age at PVR was 30.8±10.3 years. At 1 year after PVR, there were significant reductions in TR (mean 2.1 vs 0.8, p<0.01) in Group T, in right ventricular end-diastolic volume index and in PR fraction in both groups. At latest follow-up (mean 5.7±3.8years), despite the degrees of PR (mean 0.75 vs 0.8) and pulmonary stenosis (peak pressure gradient 23.1mmHg vs 23.3mmHg) were unchanged in both groups, the degree of TR significantly deteriorated compared with the value 1 year after PVR in Group T (mean 0.8 vs 1.6). At latest laboratory value (mean 5.2±3.5 years), γ-glutamyl transferase was significantly higher in Group T (mean 56 vs 25U/L, p=0.01), platelet count (mean 16.3 vs 20.9 X103/μL, p=0.02) and cholinesterase (mean 274 vs 331U/L, p=0.04) were significantly lower in Group T. In addition, plasma BNP level was significantly higher in Group T (mean 62.9 vs 35.8 pg/ml, p=0.03), Conclusions: Early improvement in TR showed gradual return toward preoperative value in mid-term after PVR and tricuspid valve repair even though pulmonary valve function remains normal. This may suggest TR is due to not only functional regurgitation but structural deformity of tricuspid valve. In addition, our data demonstrated TR might contribute to chronic hepatic and cardiac damage. These findings highlighted the importance of TR after PVR in repaired TOF. [ABSTRACT FROM AUTHOR]