Elucidating the mechanisms of infective endocarditis in bovine jugular vein conduits: Are we any closer?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 conduits1,2 (Figure 1) or as percutaneously placed stent-mounted valves.3,4 The pathophysiologic mechanisms for these findings remain unclear.
Are plasma proteins key players in the pathogenesis of infective endocarditis?Infective endocarditis (IE) after the implantation of a bovine jugular vein (BJV) graft in the right ventricular outflow tract has recently been described to be more frequent than for other conduits.1 Yet, the exact mechanisms that drive this phenomenon are under discussion. Jalal and colleagues2 were the first to study bacterial adhesion to different tissues in vitro; their clinical bacterial isolates displayed increased adherence to BJV valves, as compared with bovine and porcine pericardium, especially in traumatized valve leaflets.
What matters more in testing bacterial adhesion: Flow conditions or choice of bacterial strain?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.