Is the amount of glow predicting the fire? Residual inflammatory risk after percutaneous coronary intervention

This editorial refers to ‘Residual inflammatory risk and the impact on clinical outcomes in patients after percutaneous coronary interventions’, by D.N. Kalkman et al., doi:10.1093/eurheartj/ehy633. Initially considered a mere cholesterol storage disorder, atherogenesis is now seen as a complex immunometabolic process, where immune cells and their soluble mediators interact with metabolic triggers and mediators. Thereby, an orchestrated interplay of genetic, epigenetic, environmental, and endogenous factors induce a proatherogenic soil that perpetuates itself within the intimal layer. Importantly, accumulation of oxidized LDL particles in the subintimal layer promotes recruitment and differentiation of activated macrophages into lipid-laden foam cells, leading to the growth of atherosclerotic plaques.1 The immunopathogenesis of stable atherosclerotic disease has been extensively investigated, including its molecular pathways. However, our understanding of acute events in patients due to coronary plaque destabilization with subsequent acute coronary syndromes (ACS) remains incomplete. This might be in part due to the challenge of investigating the relevant time window at the clinical level as well as the shortage of pre-clinical models that reflect plaque rupture.2 These limitations can be partially overcome by studying ACS patients upon hospital admission and during primary percutaneous coronary interventions (PCIs). This setting has enabled the investigatation of the role of immune cells and their mediators in a relevant clinical context.