Dr Wies from Munich set the stage by giving an excellent overview of the crucial role of immune response in atherosclerosis. The essentials were:
1) inflammation has a prosnostic impact independent of classical risk factors,
2) vascular inflammation and endothelial dysfunction are the hallmarks of atherosclerosis,
3) vascular inflammation precedes plaque growth,
4) inate immune response via toll-like receptors is important for initiators and progression of atherosclerosis,
5) Dendritic cells are crucial immune cells triggering subintimal inflammations,
6) infection modulates vascular inflammation (and thereby structural vascular changes) by inducing auto-immune regulatory responses (antigenic mimicry), and
7) microbials may condition as opposed to directly infecting the vasculature.
Dr Willoughby from Woodville focused attention on the role of platelets in vascular inflammation. The essentials were:
1) activated platelets have an important role in the pathogenesis of cardiovascular disease
2) platelets interact directly with inflammatory cells (monocytes),
3) platelets contain, respond to and secrete various inflammatory mediators, most importantly P-selectin, RANTES and CD40L,
4) thus inflammatory responses can activate platelets which stimulate inflammation contributing to atherosclerosis.
Dr Crea, from Rome, introduced the symposium into the clinical arena by discussing the widespread inflammation in acute coronary syndromes (ACS). The essentials were:
1) multifocal unstable coronary lesions appear in ACS,
2) widespread vascular inflammation is associated with multifocal instability,
3) the level of inflammation in the acute state as indicated by hsCRP levels has an important influence on long term prognosis. Therefore, the distinction between inflammatory and non-inflammatory ACS is important.
The issue of prognostic impact of endothelial dysfunction and systemic inflammation was discussed by Dr Fichtlscherer from Frankfurt. The essentials were:
1) the endothelium is an important target for vascular inflammation resulting in impaired endothelial function (EF),
2) EF can be assessed invasively and non-invasively (i.e. response to acetylcholine),
3) endothelial dysfunction can be related to a multitude of mediators including vaccinations, TNFα (in CHF), CRP and PlGF, while others can act as counterplayers (i.e. Flt-1 receptor and VEGF-1 receptor),
4) endothelial function can be used as a predictor of both acute and chronic coronary syndromes.
Finally Dr Libby from Boston discussed strategies to modulate inflammation in atherosclerosis. Essential were:
1) anti-inflammatory strategy where statins are the only drugs known to effectively reduce vascular inflammation, thus statin dosage should be targeted both to LDL and hsCRP levels,
2) promoting endogenous anti-inflammatory strategy. Known substances include COX2- produced PGEg and Adiponectin (exercise, weight control, life style modification).
1) anti-inflammatory strategy where statins are the only drugs known to effectively reduce vascular inflammation, thus statin dosage should be targeted both to LDL and hsCRP levels, 2) promoting endogenous anti-inflammatory strategy. Known substances include COX2- produced PGEg and Adiponectin (exercise, weight control, life style modification).