The changing face of atherosclerotic plaque inflammation

In August 2014, the Journal of Internal Medicine organized a symposium to discuss vascular inflammation as a pathogenic mechanism underlying the development of acute ischaemic cardiovascular events. This concept has gained considerable support from experimental studies over the last two decades, but the question whether these processes represent possible targets for clinical intervention remains to be finally resolved. Analyses from large genomewide association studies consortia have identified three major networks associated with coronary artery disease: lipid metabolism, inflammation and repair, and immune cell trafficking [1]. These observations were well in line with the idea that atherosclerosis is the result of inflammatory and immune responses to lipoprotein lipids accumulated in the arterial wall. Additional support has come from epidemiological studies of associations between HLA type, lipoprotein autoantibodies, inflammatory biomarkers, immune cell subsets and cardiovascular disease (CVD), but results has not been as clear and straightforward as in the experimental studies [2]. Moreover, the first large randomized clinical trials directly targeting plaque inflammation by inhibition of lipoprotein-associated phospholipase A2 failed to reduce the incidence of cardiovascular events [3, 4]. Accordingly, although there is persuasive evidence that plaque inflammation plays a key role in the development of acute cardiovascular events, it remains to be revealed how this knowledge can be used to improve patient risk prediction and treatment.