Prof. Lina Badimon,
The session was devoted to the analysis of how biological studies are translated into the uncovering of pathophysiological mechanisms that provide, or will provide, clinical understanding of disease onset and progression, as well as possible pathways of treatment, specifically in the area of the endothelium. “Classical histopathology has provided the basis for uncovering the mechanisms of atherosclerotic plaque formation” said Dr M. Daemen (Maastrict,NL). He believes that pathology is yet a useful tool for “the translation of animal results to human tissue, to perform critical observations without interpretation, to deduct from observations and to provide novel insights and concepts”. Based on the reported differences between murine and human atherosclerotic lesions, the importance of avoiding direct translation from mice atherosclerosis to human disease was highlighted. Dr Daemen presented interesting preliminary data on molecular imaging with specifically labelled markers of disease (i.e. alpha2-antiplasmin for detecting fibrin) as an innovative aspect of new research in the pathology field. Endothelial function was the target of the major part of the session. Dr. S. Tadei (Pisa, IT) described endothelial cell function modulators and the effects of cardiovascular risk factors on the endothelium. Endothelial pathology should be classified into “endothelial dysfunction (reduced vascular reactivity), endothelial activation (acquisition of inflammatory activity) and endothelial injury/repair (anatomical disruption/ regeneration) to better understand associated syndromes” said Dr Tadei. The important role of asymmetric dimethylarginine (ADMA) was discussed. ADMA is an endogenous inhibitor of endothelial nitric oxide synthase (eNOS); therefore, increased ADMA levels contribute to the development of endothelial dysfunction. Indeed ADMA has been proposed as a prospective marker of coronary artery disease and an association of ADMA levels with cardiovascular events and all cause mortality reported. Additionally, Dr Tadei reported on original work on endothelial cell dependent vasodilatation changes with aging and hypertension. He concluded that although a lot of information has been generated “the different aspects of endothelial dysfunction are not yet related to a specific clinical significance”. Further research is needed to establish the exact relationship between the different types of endothelial alterations and the development of cardiovascular disease. The role of environmental influences on endothelial function was analyzed by Dr W. Koening (Ulm, DE). Leaving out lipids and obesity as well known factors, he concentrated on describing how smoking, periodontitis/infection and air pollution (very small particulate material) have been shown to be clear inducers of endothelial dysfunction. Interestingly, periodontal disease, a widespread chronic inflammatory gingival disease affecting over 40% of Europeans aged 35-44, has a significant effect impairing endothelial function. Whether the effects are due to low chronic inflammation or to the gum bacterial infection is not yet clear. Endothelial progenitor cell dysfunction and its relationship with outcomes is a topic that commandeers a lot of interest. Dr N. Werner (Bonn,DE) analyzed the state of the art and highlighted that one of the problems in this rapidly changing field lies in the definition of EPCs. These cells are difficult to identify and difficult to measure and depending on certain surface marker positivity, exhibit different biological roles and regeneration capacity. Dr Werner presented original data on the characterization of EPCs and discussed the encouraging results of a pooled analysis of 4 longitudinal studies in high risk individuals showing that a reduced circulating endothelial progenitor cell count helps identify more patients at higher risk of MACE over the short term. He concluded with a critical but positive evaluation of the field, which still needs significant investment in research to fully uncover its full potential.
From arterial biology to pathophysiology
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