The idea that inflammatory processes are involved in the pathogenesis of atherosclerotic coronary artery disease is not new,1 but it has attracted renewed focus recently because of combined clinical, epidemiological, pharmacological, and histological observations. Case–control studies have established consistent associations between circulating inflammatory markers, in particular C reactive protein (CRP), and the subsequent risk of cardiovascular events in healthy people2 ,3 and in patients with established coronary heart disease.4 ,5 CRP concentrations are often increased during acute coronary syndromes and higher concentrations predict a worse outcome in patients with unstable angina.6 Indeed, the protective effects of aspirin3 and pravastatin5 are greatest in patients with the highest baseline CRP concentrations, in keeping with the anti-inflammatory properties of both drug classes,7 while angiotensin converting enzyme (ACE) inhibitors also prevent coronary events, probably through anti-inflammatory activity.8 The pivotal roles of monocyte derived macrophages and T lymphocytes as the regulators of matrix degradation, apoptosis, cell replication, and recruitment of circulating cells within the atherosclerotic plaque continue to be elucidated.9