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.

Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and may favor atherosclerotic plaque instability.

Objectives: Mast cells (MCs) may play an important role in plaque destabilization and atherosclerotic coronary complications. Here, we have studied the presence of MCs in the intima and media of unstable and stable coronary lesions at different time points after myocardial infarction (MI).

Methods: Coronary arteries were obtained at autopsy from patients with acute MI (up to 5 days old; n=27) and with chronic MI (5-14 days old; n=18), as well as sections from controls without cardiac disease (n=10).

C4b-Binding Protein Deposition is Induced in Diseased Aortic Heart Valves, Coinciding with C3d.

Background And Aim Of The Study: It has been found recently that activated complement is more widespread in diseased aortic valves compared to the endogenous complement inhibitors C1-inhibitor and clusterin. Previously, another endogenous inhibitor of complement, C4b-binding protein (C4BP) has been described in atherosclerotic diseased coronary arteries. The study aim was to analyze C4BP levels in diseased aortic valves.

Prevention of age-induced N(ε)-(carboxymethyl)lysine accumulation in the microvasculature.

Objective: N(ε)-(carboxymethyl)lysine (CML) is one of the major advanced glycation end products in both diabetics and nondiabetics. CML depositions in the microvasculature have recently been linked to the aetiology of acute myocardial infarction and cognitive impairment in Alzheimer's disease, possibly related to local enhancement of inflammation and oxidative processes. We hypothesized that CML deposition in the microvasculature of the heart and brain is age-induced and that it could be inhibited by a diet intervention with docosahexaenoic acid (DHA), an omega-3 fatty acid known for its anti-inflammatory and antioxidative actions.