Anti-inflammatory therapies in acute coronary syndromes: is IL-1 blockade a solution?

This editorial refers to ‘The effect of interleukin-1 receptor antagonist therapy on markers of inflammation in non-ST elevation acute coronary syndromes: the MRC-ILA Heart Study’[†][1], by A.C. Morton et al. , on page 377 Elevation of circulating levels of C-reactive protein (CRP) at the time of hospital admission predicts a poor outcome in patients with an acute coronary syndrome (ACS) and is thought to reflect an important inflammatory component in the pathogenesis of this condition.1,2 C-reactive protein is also the preferred systemic inflammatory biomarker for risk stratification in heart disease.3 The link between inflammation and ACS is complex. Atherosclerosis, the primary cause of ACS, is a chronic inflammatory disease of coronary arteries,4 but exacerbations of the inflammatory process within the atherosclerotic plaque may lead to plaque rupture with thrombosis and subsequent myocardial ischaemia.5 Myocardial injury following an ischaemic event is an additional source for a local and systemic inflammatory response; importantly, the intensity of the systemic response is also a predictor of adverse events.6 There are therefore at least three potential sources of inflammation in ACS: (i) the baseline chronic inflammation seen in patients at risk and related to hypercholesterolaemia, diabetes, obesity, and others; (ii) the inflammatory events within the atherosclerotic plaques; and (iii) the systemic inflammatory response to ischaemic myocardial injury ( Figure 1 ). As such it is not surprising that inflammatory biomarkers predict adverse outcomes. Observational data and experimental studies reveal several candidate mediators; the role of each in patients with ACS is, however, unknown. The great majority of clinical studies are limited to associations between biomarker levels and outcomes, without any possibility of determining … [1]: #fn-2