No abstract

BackgroundIt is known that the use of a cardiopulmonary bypass (CPB) during cardiac surgery leads to leukocyte activation and may, among other causes, induce organ dysfunction due to increased leukocyte recruitment into different organs. Leukocyte extravasation occurs in a cascade-like fashion, including capturing, rolling, adhesion, and transmigration. However, the molecular mechanisms of increased leukocyte recruitment caused by CPB are not known. This clinical study was undertaken in order to investigate which steps of the leukocyte recruitment cascade are affected by the systemic inflammation during CPB.MethodsWe investigated the effects of CPB on the different steps of the leukocyte recruitment cascade in whole blood from healthy volunteers (n = 9) and patients undergoing cardiac surgery with the use of cardiopulmonary bypass (n = 7) or in off-pump coronary artery bypass-technique (OPCAB, n = 9) by using flow chamber experiments, transmigration assays, and biochemical analysis.ResultsCPB abrogated selectin-induced slow leukocyte rolling on E-selectin/ICAM-1 and P-selectin/ICAM-1. In contrast, chemokine-induced arrest and transmigration was significantly increased by CPB. Mechanistically, the abolishment of slow leukocyte rolling was due to disturbances in intracellular signaling with reduced phosphorylation of phospholipase C (PLC) γ2, Akt, and p38 MAP kinase. Furthermore, CPB induced an elevated transmigration which was caused by upregulation of Mac-1 on neutrophils.ConclusionThese data suggest that CPB abrogates selectin-mediated slow leukocyte rolling by disturbing intracellular signaling, but that the clinically observed increased leukocyte recruitment caused by CPB is due to increased chemokine-induced arrest and transmigration. A better understanding of the underlying molecular mechanisms causing systemic inflammation after CPB may aid in the development of new therapeutic approaches.

Objective Transcatheter aortic valve implantation (TAVI) has become an alternative to surgical aortic valve replacement (sAVR) in selected high risk patients. While improvement in left ventricular function after TAVI has been demonstrated, little is known about the impact on right ventricular (RV) function. Since postoperative RV dysfunction is linked to adverse outcomes, the authors sought to investigate the effect of TAVI and aortic valve replacement (AVR) on RV function using speckle tracking echocardiography. Design Cross-sectional study in tertiary healthcare setting. Setting 101 patients with severe symptomatic aortic stenosis (age 81611 yrs) who underwent TAVI and 22 patients who underwent sAVR were included. RV function was assessed using 2D longitudinal strain (RV-LS), fractional area change and tricuspid annular plain systolic excursion before and after sAVR and TAVI (median 89 days).

Our data suggest that pulsatile as well as non-pulsatile left ventricular assist devices are equally able to treat chronic heart failure. However pulsatile devices seem to have a greater impact on reversing the changes in plasma renin activity and might thus offer a greater advantage when recovery of left ventricular function is expected.

The initial experience with the Trifecta valve bioprosthesis shows excellent outcomes with favourable early haemodynamics. Further studies with longer follow-up are needed to confirm those preliminary results.