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Multiple reports have raised concerns regarding the high rates of late endocarditis in bovine jugular vein (BJV) grafts used for right ventricular outflow tract reconstruction as conduits
An increased incidence of conduit endocarditis in patients receiving bovine jugular vein grafts compared to cryopreserved homograft for right ventricular outflow reconstruction.
Incidence and outcomes of right-sided endocarditis in patients with congenital heart disease after surgical or transcatheter pulmonary valve implantation.
found that in vitro adherence of bacterial strains to patches of bovine pericardium, BJV, and cryopreserved homograft was similar between materials under both static and simulated flow conditions. These findings were different from those reported by Jalal and colleagues,
who found that static bacterial adherence was greater in BJV tissue (including stent-mounted valves) than in porcine pericardium, and that adherence increased when the leaflets of the valves were traumatized. In a Letter to the Editor in this issue of the Journal, Jalal and colleagues
Both studies are important steps toward the goal of elucidating the mechanisms that cause an increased clinical risk of endocarditis in patients receiving BJV grafts. However, they also illustrate the difficulty of simulating in the laboratory what happens to patients in the clinical setting, especially in the long term. The incidence of endocarditis for patients with BJV seems to be a late-occurring event, with the risk apparently increasing after 7 years from implantation.
Endocarditis is likely a consequence of a complex interplay of multiple factors that include, among other things, material characteristics, bacterial strains, circulating coagulation factors and proteins, patient susceptibility, shear stress, turbulent flow, thrombosis, tissue injury, and time. Simulating this complex interplay in vivo is obviously quite challenging. Bacterial adherence is just one factor. In fact, some studies have shown that in vitro adherence may not correlate as well with the ability of a bacterial strain to cause experimental endocarditis in an in vivo model.
It is clear that more sophisticated in vitro constructs may provide a better insight into the role that different bacterial strains and materials play in the development of endocarditis in real patients. The use of fluorescent-labeled bacteria and flow chambers to simulate shear stress like the ones used by Veloso and colleagues
is a step on the right direction. The use of complex microfluidic devices (laboratory on a chip) that contain different cell lines and tissues to better simulate the interaction between blood and tissue
may be a possible avenue for future experiments. Some authors have developed novel techniques using in vivo intravascular video microscopy to directly visualize bacterial adherence to live tissue.
The closer we get to simulating real in vivo conditions, the closer we will get to elucidating the conundrum of bacterial endocarditis in patients with BJV grafts.
References
Mery C.M.
Guzman-Pruneda F.A.
De Leon L.E.
Zhang W.
Terwelp M.D.
Bocchini C.E.
et al.
Risk factors for development of endocarditis and reintervention in patients undergoing right ventricle to pulmonary artery valved conduit placement.
An increased incidence of conduit endocarditis in patients receiving bovine jugular vein grafts compared to cryopreserved homograft for right ventricular outflow reconstruction.
Incidence and outcomes of right-sided endocarditis in patients with congenital heart disease after surgical or transcatheter pulmonary valve implantation.
We read with great interest the work published by Veloso and colleagues1 that investigated the bacterial adherence to pulmonary valve graft tissues under static and flow conditions. These experiments were achieved using wild bacterial strains of Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus sanguinis and the following valvular substrates: bovine pericardium patch, bovine jugular vein, and cryopreserved homograft. The authors concluded that the surface composition of bovine jugular vein and homograft tissues themselves, bacterial surface proteins, and shear forces per se were not the prime determinants of bacterial adherence.
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