03 Sep 2006

Inflammatory basis of plaque rupture Symposium

Dr. Christopher Jackson

Topics: Acute Coronary Syndromes (ACS)
Session number: 932000
Session title: Inflammatory basis of plaque rupture Symposium
Authors: Jackson, C. Briston, United Kingdom

Dr. Erling Falk ( Denmark ) described how it has become clear that highly localised areas of intense inflammation exist in vulnerable plaques.

Macrophages within these regions express proteins that contribute to breakdown of the fibrous cap, potentially leading to plaque rupture: amongst these are metalloproteinase enzymes, shown in elegant work reported by Dr Peter Libby (USA) to be responsible for collagenolysis in plaques in vivo. Genomic and proteomic analyses of these macrophages are beginning to identify specific molecular targets, helping us to understand how and why plaques rupture and indicating new avenues for therapeutic intervention.

The large Athero-Express human carotid endarterectomy tissue bank is being probed for differentially expressed proteins, work described by Dr Dominic de Kleijn ( Singapore ). Genomic analysis of human tissues has revealed a novel potential regulator of foam cell function, TWIST1, as outlined by Dr Mat Daemen (The Netherlands). Conclusion There is a strong correlation between plaque inflammation and plaque rupture, but it is too early yet to say which is chicken and which is egg. Nonetheless, interrogation of the inflammatory cells at these sites has the potential to generate new therapeutic targets.

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.