PX-18 Protects Human Saphenous Vein Endothelial Cells under Arterial Blood Pressure.

Background: Arterial blood pressure-induced shear stress causes endothelial cell apoptosis and inflammation in vein grafts after coronary artery bypass grafting. As the inflammatory protein type IIA secretory phospholipase A (sPLA-IIA) has been shown to progress atherosclerosis, we hypothesized a role for sPLA-IIA herein.

Methods: The effects of PX-18, an inhibitor of both sPLA-IIA and apoptosis, on residual endothelium and the presence of sPLA-IIA were studied in human saphenous vein segments (n = 6) perfused at arterial blood pressure with autologous blood for 6 hrs.

Arterial Blood Pressure Induces Transient C4b-Binding Protein in Human Saphenous Vein Grafts.

Background: Complement is an important mediator in arterial blood pressure-induced vein graft failure. Previously, we noted activation of cell protective mechanisms in human saphenous veins too. Here we have analyzed whether C4b-binding protein (C4bp), an endogenous complement inhibitor, is present in the vein wall.

Ten-year patterns in blood product utilization during cardiothoracic surgery with cardiopulmonary bypass in a tertiary hospital.

Background: This retrospective analysis describes blood conservation strategies and overall consumption of red blood cells (RBCs), fresh-frozen plasma (FFP), and platelet (PLT) concentrates during nonaortic cardiac surgery with cardiopulmonary bypass (CPB) in a tertiary hospital over a 10-year period.

Study Design And Methods: Study variables of 6026 patients that underwent cardiac surgery between 2002 and 2011 were incorporated in the database and included hemoglobin (Hb), lowest temperature, CPB duration, 24-hour blood loss, fluid balance, and overall transfusion requirements.

Results: Between 2002 and 2011, the lowest intraoperative Hb levels and temperature increased from 8.

C1-esterase inhibitor protects against early vein graft remodeling under arterial blood pressure.

Objectives: Arterial pressure induced vein graft injury can result in endothelial loss, accelerated atherosclerosis and vein graft failure. Inflammation, including complement activation, is assumed to play a pivotal role herein. Here, we analyzed the effects of C1-esterase inhibitor (C1inh) on early vein graft remodeling.

Degeneration and atherosclerosis inducing increased deposition of type IIA secretory phospholipase A2, C-reactive protein and complement in aortic valves cause neutrophilic granulocyte influx.

Background And Aim Of The Study: Recent studies have indicated that atherosclerosis-like changes are involved in the pathogenesis of aortic valve stenosis. Increased blood and valve tissue levels of C-reactive protein (CRP) have been reported in patients with aortic valve disease, although the different pathological conditions involved were not analyzed. The study aim was to monitor the deposition of CRP, its activator sPLA2-IIA and its effector complement, and the subsequent influx of neutrophilic granulocytes in degenerative and atherosclerotic aortic valves.