Introduction: Neutrophils are the most prevalent leukocyte population in the circulation. Neutrophils are multifunctional cells that have broad capabilities in a wide range of infectious and non-infectious disease conditions. In addition to their defensive function against infections, neutrophils have demonstrated an important role in the pathophysiology of cardiovascular (CV) diseases such as myocardial infarction and heart failure as our research team has discussed in several published papers. Neutrophils are also implicated in acute cardiac fibrosis after MI, as necrosis is associated with inflammation and fibrosis, but they release NETs that contribute to chronic cardiac fibrosis and remodeling after MI. Neutrophils are known to release neutrophil extracellular traps (NETs) which are web-like structures composed of DNA filaments coated with histones and granule proteins. This phenomenon has recently garnered significant attention because the excessive release of NETs induces inflammation and host tissue damage that goes beyond their antimicrobial functions. In the context of coronary artery disease (CAD), NETs have been shown to play a pivotal role. Specifically, higher levels of circulating NET markers such as MPO-DNA, nDNA, and cit-H3, as well as platelet activation markers like soluble P-selectin, have been reported to confer an increased risk of major cardiovascular events (MACEs) after MI. Recent evidence indicates that uncontrolled and excessive formation of neutrophil extracellular traps (NETs) within the vasculature may contribute to the development of pathological thrombotic disorders. Specifically, it has been confirmed that coronary thrombi are enriched with a significant amount of NETs, which act as a scaffold for platelets, red blood cells, and fibrin. Inhibition of NET formation may represent a potential strategy for reducing thrombogenicity, thereby offering promising therapeutic options. Consequently, NETs have emerged as a promising area of research for targeted therapies. However, further investigations are necessary to comprehensively elucidate all of the diverse functions of NETs and their clinical significance.