Inflammation and lipid-related determinants in coronary atherosclerosis: mechanisms, biomarkers, and therapeutic implications.

Coronary atherosclerosis is increasingly recognized as a chronic, maladaptive inflammatory disease initiated by arterial retention of apolipoprotein B (apoB)-containing lipoproteins and amplified by innate and adaptive immune responses. Although low-density lipoprotein cholesterol (LDL-C) remains a central causal factor, substantial residual risk persists despite intensive LDL-C lowering, emphasizing the clinical relevance of residual inflammatory risk and additional atherogenic lipid metrics such as apolipoprotein B (apoB), remnant cholesterol, small dense LDL, and lipoprotein(a) [Lp(a)]. Landmark outcome trials validate both paradigms: potent lipid-lowering therapies reduce major adverse cardiovascular events, and targeted anti-inflammatory therapies such as IL-1β inhibition and low-dose colchicine reduce recurrent events without altering LDL-C, establishing inflammation as a modifiable driver of coronary risk. This review integrates mechanistic evidence linking lipids and inflammation across the atherosclerotic continuum-from endothelial activation and leukocyte recruitment to plaque destabilization and thrombosis-while critically appraising biomarkers, imaging approaches, and therapeutic strategies. We propose a practical dual-axis framework integrating residual cholesterol and inflammatory risks to guide combined therapy and highlight future directions including genetics-informed lipid management [notably Lp(a)], inflammation-resolution biology, and precision targeting of upstream inflammatory pathways such as IL-6 signaling.