Key result
Pulmonary homografts were associated with a significantly lower risk of reintervention or structural valve deterioration compared with bioprostheses (adjusted HR 0.27; 95% CI 0.13-0.55; P<0.001).
Why the study?
Uncertainty remains on whether homografts or bioprostheses are superior for pulmonary valve replacement after tetralogy of Fallot repair.
Does pulmonary valve replacement with homograft reduce the composite of reintervention and structural valve deterioration compared to bioprosthesis in patients with previous tetralogy of Fallot repair?
Cohort (n=209)
No
Does pulmonary valve replacement with homograft reduce the composite of reintervention and structural valve deterioration compared to bioprosthesis in patients with previous tetralogy of Fallot repair?
Hazard Ratio: 0.27 (95% CI 0.13–0.55)
Absolute Event Rate: 81.6% vs 43.4%
p-value: p=<0.001
Pulmonary homografts are associated with a significantly lower risk of reintervention or structural valve degeneration compared to bioprostheses in patients with repaired Tetralogy of Fallot.
Homografts were associated with lower gradients and reintervention risk than bioprostheses; leaves open optimal choice pending prospective confirmation.
Background Tetralogy of Fallot repair results in late occurrence of pulmonary regurgitation, which requires pulmonary valve replacement in a large proportion of patients. Both homografts and bioprostheses are used for pulmonary valve replacement as uncertainty remains on which prosthesis should be considered superior. We performed a long‐term imaging and clinical comparison between these 2 strategies. Methods and Results We compared echocardiographic and clinical follow‐up data of 209 patients with previous tetralogy of Fallot repair who underwent pulmonary valve replacement with homograft (n=75) or bioprosthesis (n=134) between 1995 and 2018 at a tertiary hospital. The primary end point was the composite of pulmonary valve replacement reintervention and structural valve deterioration, defined as a transpulmonary pressure decrease ≥50 mm Hg or pulmonary regurgitation degree of ≥2. Mixed linear model and Cox regression model were used for comparisons. Echocardiographic follow‐up duration was longer in the homograft group (8 [interquartile range, 4–12] versus 4 [interquartile range, 3–6] years; P <0.001). At the latest echocardiographic follow‐up, homografts showed a significantly lower transpulmonary systolic pressure decrease (16 [interquartile range, 12–25] mm Hg) when compared with bioprostheses (28 [interquartile range, 18–41] mm Hg; mixed model P <0.001) and a similar degree of pulmonary regurgitation (degree 0‐4) (1 [interquartile range, 0–2] versus 2 [interquartile range, 0–2]; mixed model P =0.19). At 9 years, freedom from structural valve deterioration and reintervention was 81.6% (95% CI , 71.5%–91.6%) versus 43.4% (95% CI , 23.6%–63.2%) in the homograft and bioprosthesis groups, respectively (adjusted hazard ratio, 0.27; 95% CI , 0.13–0.55; P <0.001). Conclusions When compared with bioprostheses, pulmonary homografts were associated lower transvalvular gradient during follow‐up and were associated with a significantly lower risk of reintervention or structural valve degeneration.
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A 2019 study conducted a cohort in Tetralogy of Fallot (n=209). Pulmonary homograft vs. Bioprosthesis was evaluated on Composite of pulmonary valve replacement reintervention and structural valve deterioration (adjusted HR 0.27, 95% CI 0.13-0.55, p=<0.001). Pulmonary homografts were associated with a significantly lower risk of reintervention or structural valve deterioration compared with bioprostheses (adjusted HR 0.27; 95% CI 0.13-0.55; P<0.001).
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