Inflammation and cardiovascular disease – Part II: Anti-inflammatory therapy in cardiovascular disease

Inflammation plays a central role in the pathogenesis of atherosclerotic cardiovascular diseases (ASCVDs), contributing to plaque progression, instability, and thrombosis. Chronic systemic inflammation exacerbates endothelial dysfunction, promotes oxidative stress, and accelerates atherogenesis, necessitating targeted interventions. This review explores established and emerging strategies for modulating inflammation to improve cardiovascular outcomes. Statin therapy remains foundational, with trials, such as JUPITER, demonstrating significant reductions in cardiovascular events through high-sensitivity C-reactive protein modulation, independent of low-density lipoprotein lowering. Non-statin lipid-lowering therapies, including proprotein convertase subtilisin/kexin type 9 inhibitors, ezetimibe, and bempedoic acid, have shown additional anti-inflammatory benefits and further reduce inflammation-driven cardiovascular risk. In addition, triglyceride-lowering agents targeting apolipoprotein C-III and angiopoietin-like protein pathways offer promising avenues for reducing metabolic inflammation and residual ASCVD risk. Anti-inflammatory pharmacotherapy has gained traction, with trials such as canakinumab anti-inflammatory thrombosis outcomes study, colchicine cardiovascular outcomes trial, and low-dose colchicine underscoring the efficacy of canakinumab and colchicine in reducing cardiovascular events. Emerging interleukin (IL) pathways (e.g., IL-17, IL-33, and IL-36) and novel therapeutic targets (e.g., cluster of differentiation 47 inhibitors, serum/glucocorticoid-regulated kinase 1 modulation, and P-selectin blockade) present future opportunities for precision cardiovascular medicine. However, residual inflammatory risk persists despite optimal lipid control, highlighting the need for a multimodal approach integrating lipid-lowering, anti-inflammatory, and targeted immunomodulatory therapies. The expanding role of inflammation in ASCVD suggests a paradigm shift toward inflammation-guided treatment strategies. Further research is warranted to refine patient selection, personalize therapy, and optimize long-term outcomes for inflammation-driven cardiovascular disease.