Risk factors for early pulmonary homograft dysfunction in congenital heart disease

Abstract

Pulmonary homografts (PH) are used as a first-line treatment for surgical right ventricular outflow tract (RVOT) reconstruction in patients with congenital heart disease (CHD). Despite a better freedom from reintervention than prosthetic conduits, PH are not spared from failure and cases of early dysfunction are regularly described. The aim of this study was to assess the rate of early PH dysfunction in patients of the Bordeaux University Hospital and to identify associated risk factors. A monocentric retrospective study was conducted in children and adults with CHD and PH implantation for RVOT reconstruction. Clinical and echocardiographic data were collected during follow-up. PH dysfunction was defined as a peak of gradient greater than 50 mmHg and/or as pulmonary regurgitation greater than moderate. Early dysfunction was defined as occurring within two years postoperatively. Primary endpoint was the early PH dysfunction rate at 2 years. The dysfunction-free survival curve was calculated according to the Kaplan-Meier method. A logistic regression with univariate then multivariate analysis was performed to identify risk factors for early dysfunction. Between January 2002 and November 2020, 112 PH were implanted in 110 patients and 11 cases of homograft dysfunction were reported during the follow-up, including 9 cases of early dysfunction. The rate of early dysfunction was 9.4 [3.3–15.1] % and freedom from reintervention was 94.6 [90.0–99.0] % at two years. The only independent risk factor identified by the multivariate analysis was duration of extracorporeal circulation ( P = 0.007) but the length of stay in intensive care unit ( P = 0.088) and the initial maximum pulmonary transvalvular gradient ( P = 0.06) were also close to significance in the multivariate analysis. Although PH provide a durable substitute for RVOT reconstruction, a significant proportion of patients presents early PH dysfunction and requires premature reintervention. An inflammatory mechanism is suspected but dedicated studies should be conducted to validate this hypothesis.