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There is solid evidence that atherosclerosis is an inflammatory disease, and that inflammation represents an important component of atherosclerotic cardiovascular disease (CVD). Subclinical inflammation is considered to be involved in all stages of the atherosclerotic process, from the initiation of fatty streaks to the development of plaque instability and rupture, causing myocardial ischaemia and infarction. Unravelling the function of cytokines as inflammatory messengers provided a mechanism by which risk factors for atherosclerosis can alter arterial biology, and produce a milieu that favours atherothrombotic events. Translation of these findings has enabled both novel mechanistic insights and practical clinical advances in the form of biomarkers and potential therapeutic instruments to lower inflammation and thereby CVD. For example, multiple studies showed a significant contribution of inflammatory biomarkers, such as C-reactive protein (CRP), secretory phospholipase A2 (sPLA2), and lipoproteinassociated phospholipase A2 (Lp-PLA2), to coronary risk prediction. To this effect, JUPITER (Justification for the Use of Statin in Prevention: An Intervention Trial Evaluating Rosuvastatin) was the first large-scale inflammatory biomarker-guided clinical trial. JUPITER evaluated whether subjects with increased subclinical inflammation might benefit from the anti-inflammatory effects of statins. Within the trial 17 802 subjects with elevated CRP levels >2 mg/L (median, 4.2 mg/L) and normal LDL cholesterol levels <130 mg/dL were randomly allocated either to rosuvastatin or to placebo. Besides the decrease in LDL cholesterol, rosuvastatin caused a steep decline in CRP levels and a 44% reduction in cardiovascular event rate. Yet, JUPITER could not discriminate the lipid-lowering effect from the anti-inflammatory effect of the statin, and thereby was never translated into clinical routine.

Linking the sympathetic nervous system to the inflammasome: towards new therapeutics for atherosclerotic cardiovascular disease