Abstract
Inflammation plays an integral role in the pathogenesis of atherosclerosis and cardiovascular (CV) disease. Clinical trials have evaluated whether anti-inflammatory therapies can reduce major adverse cardiovascular events (MACE), including myocardial infarction and stroke. Broad-spectrum agents have not demonstrated benefit in lowering CV risk. Colchicine is approved for reducing MACE in high-risk patients, but recent studies are neutral. Canakinumab reduces MACE, but FDA approval was denied based on an unfavorable risk-benefit ratio. Data on ziltivekimab, an investigational agent, for reducing MACE are not yet available. Therapies for hypertension, dyslipidemia, and type 2 diabetes mellitus modestly reduce anti-inflammatory biomarkers, but these effects likely play a limited role in their overall cardioprotection. Current guidelines emphasize identifying patients with chronic inflammation for risk stratification and initiating or intensifying treatment for hypertension, dyslipidemia, and other CV risk factors. Targeted therapies that can markedly reduce inflammation are needed to achieve clinically relevant reductions in CV morbidity and mortality.