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Inflammation is a fundamental driver of atherosclerotic cardiovascular disease (ASCVD), orchestrating immune activation, endothelial dysfunction, and plaque instability. While lipid-lowering therapies can reduce the burden of ASCVD, persistent inflammation remains a critical determinant of residual cardiovascular risk, highlighting the need for deeper investigation into inflammatory pathways. Key mediators, including interleukin-6, high-sensitivity C-reactive protein, and myeloperoxidase, amplify immune cell infiltration, foam cell formation, and extracellular matrix degradation, exacerbating atherosclerotic progression. Beyond these well-established markers, emerging inflammatory biomarkers, such as cluster of differentiation (CD)47, serum and glucocorticoid-regulated kinase 1 (SGK1), P-selectin, and growth differentiation factor 15 (GDF15), provide novel insights into vascular inflammation and immune dysregulation. CD47 modulates macrophage-mediated immune evasion, allowing apoptotic debris to accumulate within plaques, while SGK1 enhances pro-inflammatory signaling and endothelial dysfunction. P-selectin facilitates leukocyte adhesion and platelet aggregation, contributing to plaque destabilization and thrombotic risk. GDF15, a stress-responsive cytokine, is associated with adverse cardiovascular outcomes, linking metabolic dysfunction to chronic inflammation. Likewise, inflammasome activation, particularly through NACHT, LRR, and PYD domains-containing protein 3 and absent in melanoma 2 pathways, triggers cytokine cascades that perpetuate vascular injury, while clonal hematopoiesis of indeterminate potential promotes myeloid-driven inflammation and atherosclerotic acceleration. The expanding role of these biomarkers underscores the complexity of inflammation in ASCVD and highlights their potential for refining cardiovascular risk assessment and elucidating novel mechanisms underlying plaque progression.