Abstract
Inflammation and dyslipidemia are central to the pathogenesis of atherosclerotic cardiovascular disease (ASCVD). While lipid-lowering therapies are the cornerstone of ASCVD prevention and treatment, there are other emerging targets, including inflammation (which has been dubbed the 'residual inflammatory risk'), that can be addressed after LDL cholesterol thresholds have been reached. Research over the past 20 years has identified C-reactive protein (CRP) as a key marker of inflammation with atherosclerosis. The association of more sensitive measures of CRP (high- sensitivity C-reactive protein [hsCRP]) with ASCVD risk in epidemiological studies has also led to its incorporation as a risk enhancer in primary prevention guidelines and its incorporation into risk stratification tools. While there are no formal recommendations related to measurement of hsCRP in secondary prevention, consideration should be given to an individualized approach that addresses inflammatory risk in those with major adverse cardiovascular events, despite maximal lipid-lowering therapy and well-controlled LDL cholesterol levels. The aim of this review is to discuss the role of inflammation in ASCVD, the use of hsCRP as a tool to assess residual inflammatory risk to target upstream pathways such as glucose intolerance and obesity, and to consider use of additional anti-inflammatory medications for ASCVD risk reduction. The authors provide clinical context around when to measure hsCRP in clinical practice and how to address residual inflammatory risk in ASCVD.