Anti-inflammatory treatment of acute coronary syndromes: the need for precision medicine

This editorial refers to ‘Effect of a single dose of the interleukin-6 receptor antagonist tocilizumab on inflammation and troponin T release in patients with non-ST elevation myocardial infarction: a double-blind, randomized, placebo-controlled phase 2 trial’[†][1], by O. Kleveland et al ., on page 2406. The link between inflammation and acute coronary syndromes (ACS) is complex and not yet fully understood.1 Atherosclerosis is a chronic inflammatory disease on its own, but an flare up of the inflammatory process within the atherosclerotic plaque may lead to plaque rupture and thrombus formation, resulting in myocardial ischaemia and necrosis. The latter is an additional source for a local and systemic inflammatory response accelerating atherosclerosis.2 Furthermore, patients with ACS frequently undergo percutaneous coronary intervention (PCI), which may cause iatrogenic myocardial injury,3 a further source of inflammation.4 Therefore, there are three potential sources of inflammation in ACS, beside the baseline chronic inflammation related to atherosclerosis and to risk factors such as hypercholesterolaemia, diabetes, and obesity: (i) the inflammatory outburst at the site of the culprit plaque; (ii) the primary ischaemic myocardial injury; and (iii) the iatrogenic myocardial injury ( Figure 1 ). Furthermore, patients in whom plaque instability is caused by an inflammatory flare up present hyper-reactivity to other inflammatory stimuli,5 which, in turn, promote plaque instability: inflammation begets inflammation.2 Thus, it is not surprising that a plethora of studies has consistently shown a marked elevation of circulating levels of high sensitivity C-reactive protein (hs-CRP) or of other soluble markers of inflammation at the time of hospital admission. Interestingly, the intensity of this inflammatory surge predicts the short- and long-term outcome.6 Figure 1 Schematic representation of … [1]: #fn-2