OBJECTIVES Currently, Contegra® grafts (processed bovine jugular vein conduits) are widely used for reconstructive surgery of the right ventricular outflow tract in patients with congenital heart disease (CHD). We analysed explanted Contegra conduits from 2 institutions histologically to get a possible hint at the underlying pathomechanisms of degenerative alterations and to find histological correlations of graft failure. Additionally, we compared the explants with a non-implanted processed graft and a native jugular vein obtained from a young bull. METHODS The explanted Contegra grafts were gathered during reoperations of 13 patients (male: n = 9, 69.2%; female: n = 4, 30.8%). After standardized histological preparation, samples were stained with dyes haematoxylin and eosin and Elastica van Gieson. Additionally, X-ray pictures revealed the extent of calcification and chelaplex (III)-descaling agent was used to decalcify selected explants. RESULTS Processing of the native jugular vein leads to tissue loosening and a loss of elastic fibres. For graft failure after implantation, 2 pathomechanisms were identified: original graft alteration as well as intimal hyperplasia. Elastica degeneration and rearrangement with interfibrillary matrix structures were the main developments observed within the graft itself. Intimal hyperplasia was characterized by fibrous tissue apposition, calcification and heterotopic ossification. CONCLUSIONS Regression of the elastic fibre network leads to rigidification of the conduit. In Contegra grafts, atherosclerosis-like changes can be considered the leading cause of graft stenosis and insufficiency. We conclude that both observed mechanisms lead to early reoperation in CHD patients.

OBJECTIVES We aim to investigate the impact of cardiac fibrosis and collagens on right ventricular failure (RVF) and acute kidney injury (AKI) in patients receiving continuous flow left ventricular assist devices. METHODS Heart tissues from 34 patients were obtained from continuous flow left ventricular assist device insertion sites and corresponding clinical data were collected. The participants were divided into 2 groups according to the extent of the cardiac fibrosis or collagens. RESULTS Overall, 18 patients developed RVF with 14 receiving right ventricular assist device (RVAD), and 22 patients developed AKI with 12 needing new-onset renal replacement therapy. Higher collagen I (Col1) was significantly associated with increased incidences of RVF (76.5% vs 29.4%, P = 0.015), RVAD support (64.7% vs 17.6%, P = 0.013) and stage 3 AKI (58.8% vs 17.6%, P = 0.032), and patients with higher Col1 were more prone to renal replacement therapy (52.9% vs 17.6%, P = 0.071). Receiver operating characteristic curves showed that Col1 had good predictive effects on RVF [area under the curve (AUC) = 0.806, P = 0.002], RVAD support (AUC = 0.789, P = 0.005), stage 3 AKI (AUC = 0.740, P = 0.020) and renal replacement therapy (AUC = 0.731, P = 0.028) after continuous-flow left ventricular assist device. Moreover, patients with higher Col1 had significantly longer postoperative duration of mechanical ventilation, duration of intensive care unit stay and hospital length of stay (all P < 0.05). Cardiac fibrosis, collagen III (Col3) and Col1/Col3 shared similar results or trends with Col1. CONCLUSIONS Cardiac fibrosis and related collagens in the apical left ventricular tissue are associated with increased risks of RVF, RVAD use and worse renal function. Further study is warranted owing to the small sample size.