04 Sep 2006

Vasa vasorum, Atherosclerotic plaque, Acute Coronary Syndrome

Prof. Gerard Pasterkamp

Topics: Acute Coronary Syndromes (ACS)
Session number: 930000
Session title: Vasa vasorum and the Atherosclerotic plaque: is there a causal link?
Authors: Pasterkamp, G. Utrecht, NL

At this symposium four speakers discussed the potential role of intra plaque vessel growth in atherosclerosis progression.

The first speaker J. Waltenberger (Maastricht, NL) kicked off with a challenging concept. He postulated that plaque angiogenesis may induce plaque progression but it may also stabilise plaques. The idea was that VEGF inhibits apoptosis and stabilises endothelial integrity thereby also stabilising the vascular structure. Cox-2 inhibitors downregulate VEGF expression and increases the incidence of plaque rupture. The latter would support the idea that VEGF may have a plaque stabilising effect.

The next speaker was Dr E Arbustini (Pisa, Italy). She was the first to point to the potential role of the erythrocyte membranes as potential contributors to atheromatous core formation. This is an intriguing concept since it indicates that intraplaque haemorrhage can accelerate atheroma formation. Dr Arbustini presented more pathological evidence supporting the concept that large atheroma may represent erythrocyte graveyards.

The third speaker was Dr A D Blann (Birmingham, GB). He summarised data that showed a potential association between angiopoietins , their receptor Tie-2 and plaque neovascularisation. Data on plaque progression or phenotype in relation with these angiopoietins is lacking, but serological data support the hypothesis that angiopoietins may play a role in plaque neovascularisation and subsequent cardiovascular events.

The last speaker was Dr K S Moulton (Boston, US). She summarised her data on animal models in studies on plaque angiogenesis. She mentioned that compounds affecting plaque neovascularisation mainly sort effect late in the atherosclerotic process. In early phases of atherosclerosis growth factors like VEGF may be present but without subsequent neovascularisation. Dr Moulton also presented very interesting data on the mechanisms she studied in her animal models in relation to neovessel formation. Conclusion The link between vaso vasorum and plaque formation and destabilisation is becoming evident. Inhibition of plaque neovascularisation may be an interesting approach to prevent intraplaque bleeding and subsequent atheroma formation and plaque progression.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.