Coronary inflammation: Identification, clinical impact and possible therapeutical solutions

Coronary inflammation is now widely recognized as a key driver of atherosclerotic plaque initiation, progression, and destabilization. Histopathological studies and advanced imaging have demonstrated the central role of local inflammation, including extensive macrophage infiltration, cytokine activation, and perivascular adipose tissue, in promoting plaque vulnerability and acute coronary syndromes. Among systemic biomarkers, high-sensitivity C-reactive protein remains the most widely used, although its limited specificity underscores the need for more targeted inflammatory markers such as interleukin-6. Invasive intracoronary imaging with optical coherence tomography can visualize macrophage accumulation and quantify local inflammatory burden. Hybrid molecular imaging with OCT-NIRF, novel PET tracers and peri-coronary adipose tissue attenuation can provide emerging opportunities to further characterize vascular inflammation and residual risk. Anti-inflammatory therapies represent a major opportunity to improve outcomes beyond lipid lowering. Among patients with coronary artery disease, the use of colchicine has demonstrated significant risk reduction in adverse events, though with mixed results. Important randomized trials are underway to investigate the efficacy of novel monoclonal antibodies targeting interleukin pathways. In addition, GLP-1 receptor agonists, SGLT2 inhibitors, and PCSK9 inhibitors have been described to exhibit favourable vascular anti-inflammatory effects in experimental and in-vivo studies. In this comprehensive review, we provide an updated reappraisal of the available evidence unravelling how accurate identification of high-risk patients through multimodal imaging and biomarker profiling, combined with selective anti-inflammatory therapy, can represent a promising strategy for further reducing residual cardiovascular risk.