Inflammation as a Modifiable Driver of Ischemic Heart Disease: Mechanisms, Clinical Risks, and Evolving Therapeutic Options

Abstract

This review explores the pivotal role of inflammation in the pathophysiology of ischemic heart disease (IHD), particularly following acute myocardial infarction (AMI). Since the mid-20th century, the inflammatory response has been increasingly linked to cardiovascular events, with biomarkers such as C-reactive protein (CRP) gaining prominence for their prognostic value. Recent clinical trials, including CANTOS and COLCOT, underscore the potential of targeting inflammation to mitigate residual cardiovascular risk, revealing that anti-inflammatory therapies can reduce major adverse cardiac events (MACE) independently of traditional lipid-lowering strategies. We examine the mechanisms by which inflammation contributes to atherosclerosis and the interplay with risk factors, emphasizing the complexity of inflammatory pathways and their systemic implications. Additionally, we discuss both established and novel pharmacological interventions, including low-dose aspirin, statins, canakinumab, colchicine, and emerging agents like Ziltivekimab, assessing their efficacy and safety profiles. The review highlights the necessity for personalized treatment approaches to optimize outcomes in diverse patient populations, particularly among elderly individuals who may benefit from tailored anti-inflammatory strategies. As inflammation remains a significant, albeit underexplored, contributor to IHD, this article advocates for its recognition as a key therapeutic target in contemporary cardiovascular care.