Assessment of Hypercoagulability After Orthopedic Trauma Surgery Using Coagulation Biomarkers and TEG/ROTEM.

Aortic diseases primarily include atherosclerosis, abdominal aortic aneurysm (AAA), and aortic dissection (AD), all of which represent major causes of cardiovascular-related mortality. Despite their distinct clinical manifestations, these conditions share common pathophysiological features, including chronic low-grade inflammation, progressive degradation of the vascular wall, and dysregulation of the local immune microenvironment (). In recent years, accumulating evidence has demonstrated that macrophages are not only among the predominant immune cell populations within the inflamed aorta but also serve as central regulatory hubs linking multiple key pathological processes, including lipid metabolism dysregulation, extracellular matrix remodeling, vascular smooth muscle cell injury, and immune homeostasis imbalance (, ). The second population comprises tissue-resident macrophages (RTMs), which are primarily derived from embryonic yolk sac and fetal liver progenitors. These cells are maintained long-term through local self-renewal and contribute to vascular homeostasis by clearing apoptotic cells, preserving immune equilibrium within the vessel wall, and modulating the adventitial microenvironment (). Recent studies have further demonstrated that Lyve1+ RTMs can secrete Sparcl1 to inhibit aberrant lymphangiogenesis and tertiary lymphoid structure formation, thereby attenuating AAA progression and highlighting their vasculoprotective functions (). The third population consists of macrophages associated with the intima of the aorta (MacAIR), which are predominantly localized in regions of disturbed blood flow. These cells are characterized by the expression of signature markers including Mmp12, F11r, and Asb2. They participate in fibrin clearance, regulation of coagulation-related processes, and early foam cell formation, thereby playing an important role in the initiation of atherosclerosis ().