The role of inflammation in atherothrombosis: implications for clinical practice

Abstract

Inflammation plays a key role in atherothrombosis: in the development of plaques, plaque rupture and thrombus formation. Various biochemical substances have been shown to be involved in the inflammatory process, some with pro-inflammatory activity and others with anti-inflammatory activity. Increased expression of many inflammatory mediators (e.g. C-reactive protein, CD40 ligand, P-selectin and IL-6) has been shown to correlate with increased risk of atherothrombotic events. One possible strategy for primary and secondary prevention is likely to focus on minimizing the inflammatory response and tipping the balance in favour of anti-inflammatory mediators and, therefore, plaque stability.