In recent years, the extent and quality of the basic science presented at the conferences of the ESC has improved, with the help of its newly established Council on Basic Cardiovascular Science and a large number of Working Groups and sister societies. This is evidenced by 28 invited symposia, five featured research symposia and 18 abstract sessions covering a large variety of areas in which experimental research with strong translational aspects can support progress of cardiovascular medicine (see pages G53-G55 of your programme book).
One specific focus was on new developments in atherosclerosis research. Two symposia are scheduled for the ESC Congress 2007 on this subject. The relation between local haemodynamics and the development of atherosclerosis will be discussed under the provocative title “Atherosclerosis is shear stress!”. I am not sure that after the symposium we will all agree to this proposition, but we will have learned a lot about the effects of the shear stress level and the shear stress pattern on endothelial function and the promotion of atherosclerosis.
In recent years a number of basic and clinical studies have provided evidence that low or turbulent wall shear stress promotes an atherogenic endothelial gene profile. Such flow conditions are also found in arterial regions, which are prone to develop atherosclerotic lesions. However, effects seem to be related to specific cellular set-points of shear stress rather than to the physical effects of absolute shear stress levels. This is evidenced by the finding that typical shear stress levels in rats and mice exceed those of man by a factor of 10-20.
A central mechanism establishing the relation between shear stress and atherosclerosis is the control of gene expression by wall shear stress. In his overview, A. Zakrzewicz will present data from studies showing that the transcription factor Foxo-1, first described in 1999, can be inactivated by shear stress via Akt-mediated phosphorylation. Foxo-1 regulation in turn influences relevant control systems in the endothelium, including the Ang-2/Tie2- and the eNOS-system.
Pictured above right, Compared to static conditions (left) Foxo-1 is excluded from the nucleus after application of shear stress (right, 6 dyn/cm2, 60 min, HUVEC). Chlench et al., FEBS Lett. 2007 Feb 20;581(4):673-80.
A significant role for primary cilia in endothelial cell activation and dysfunction is suggested by R. Krams. His group found that endothelial cilia in the adult aortic arch and common carotid arteries of wild type C57BL/6 and apolipoprotein-E-deficient mice are located at atherosclerotic predilection sites with disturbed flow patterns. Also, experimental induction of flow disturbance led to development of primary cilia, and to atherogenesis. 
Oxidative stress is known to be involved in endothelial dysfunction and subsequent pathophysiological events. In his presentation on “Links between shear stress and oxidant stress”, A. Koller will present new evidence on the involvement of reactive oxygen species in shear stress-related protective and damaging effects.
In several human diseases, such as hyperhomocysteinaemia, diabetes mellitus, and hypertension, there is an increase in serum levels of asymmetrical dimethylarginine (ADMA), which in contrast to L-arginine, cannot support the generation of NO. His group showed that shear stress-induced release of NO is inhibited by augmented levels of ADMA. In contrast, the superoxide-mediated basal vessel tone is increased (Toth J, et al. Hypertension 2007).
The symposium will be concluded by an analysis of the relation between flow patterns and vascular lipid deposition by P.D. Weinberg, bridging to the afternoon symposium on “Lipids. Still relevant in 2007?”, which will have a strong focus on the clinical implications.
Pictured above right, the distribution of primary cilia (green) in the aortic arch of wild type (left) and Apoe−/− (right) mice. Atherosclerotic lesions (red) exhibit a striking relation to the localisation of the primary cilia (Van der Heiden et al. Atherosclerosis; in press doi:10.1016/ j.atherosclerosis. 2007.05.030).
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