Tricuspid valve repair improves early right ventricular and tricuspid valve remodeling in patients with hypoplastic left heart syndrome.

OBJECTIVE: Tricuspid regurgitation is a significant risk factor for reoperation and mortality in patients with hypoplastic left heart syndrome. The effects of tricuspid valve repair on quantitative measures of right ventricle and tricuspid valve remodeling have not been well documented.

METHODS: We reviewed retrospectively the 2-dimensional echocardiograms of 17 tricuspid valve repairs (male, n = 12; female, n = 5; median age, 30 months; age range, 1.5-53 months) performed 1 month before and after tricuspid valve repair between 2005 and 2011. From the apical 4-chamber view, we measured right ventricle end-diastolic area, right ventricle fractional area change, and tricuspid valve leaflet coaptation length. The severity of tricuspid regurgitation was graded qualitatively. A 2-sided paired t test was used to compare changes in tricuspid valve and right ventricle outcomes, and the Wilcoxon signed-rank test was used to compare changes in tricuspid regurgitation grades.

RESULTS: Right ventricle end-diastolic area decreased significantly after tricuspid valve repair from 14.1 ± 5.2 to 11.8 ± 3.9 cm(2) (P = .001), whereas right ventricle fractional area change declined from 44.4% ± 6.4% to 39.7% ± 8.5% (P = .016). The coaptation length of the lateral and septal leaflet improved significantly after tricuspid valve repair (0.4 ± 2.4 mm vs 3.1 ± 2.7 mm, P = .002; 2.0 ± 2.7 vs 3.4 ± 2.0 mm, P = .036; respectively). Furthermore, the tricuspid regurgitation grade improved after tricuspid valve repair (3.1 ± 0.6 to 1.7 ± 0.9, P < .001).

CONCLUSIONS: Tricuspid valve repair improved significantly the tricuspid valve coaptation length and reduced right ventricle volume in children with hypoplastic left heart syndrome. Further follow-up of decreased right ventricle function is required to determine whether this is a temporary phenomenon related to reduced right ventricle preload, permanent right ventricle dysfunction from late repair of the tricuspid valve, or unavoidable sequelae of a right ventricle exposed to systemic vascular resistance.