Inflammation in Coronary Atherosclerosis: Insights into Pathogenesis and Therapeutic Potential of Anti-Inflammatory Drugs

Abstract

Atherosclerosis is a lipid-driven immune-inflammatory disease that affects the arteries, leading to multifocal plaque development. The inflammatory process involves the activation of immune cells and various inflammatory pathways. Anti-inflammatory drugs have been shown to be effective in reducing cardiovascular events in individuals with coronary disease. However, their use is still limited due to concerns about long-term follow-up, cost-effectiveness, adverse effects, and the identification of the ideal patient profile to obtain maximum benefits. This review aims to improve the understanding of inflammation in coronary atherosclerosis and explore potential therapeutic interventions, encompassing both traditional and non-traditional anti-inflammatory approaches. By addressing these concepts, we seek to contribute to the advancement of knowledge about this type of treatment for coronary artery disease.

Keywords: anti-inflammatories; coronary artery disease; myocardial ischemia.

Figure 1

Pathophysiology of atherosclerosis associated with drug therapy and its stages—the formation of atheromatous plaque initially depends on the accumulation of lipids in the intima of the vessels; therefore, antilipemic therapy contributes to the reduction or cessation of this stimulus. However, after oxidation and the phagocytosis of these molecules by macrophages, an intense inflammatory cascade occurs, causing a cycle of the recruitment of inflammatory cells and the release of cytokines, culminating in tissue damage, allowing therapeutic targets to be used in anti-inflammatory therapy. Finally, when the plaque ruptures, there is the possibility of using thrombolytics to minimize the repercussions on the blood flow caused by the obstruction resulting from the consequent formation of thrombi.