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Abstract
Ischemic stroke remains one of the leading causes of mortality and long-term disability worldwide. Increasing evidence suggests that disturbances in calcium–phosphorus homeostasis and lipid metabolism contribute to vascular calcification, endothelial dysfunction, and progression of atherosclerosis. However recent studies highlight the “vascular-bone axis” as a critical factor in stroke pathogenesis, where dysregulation of mineral homeostasis—specifically calcium and phosphorus—promotes medial arterial calcification and increases arterial stiffness. This process, coupled with dyslipidemia, accelerates the formation of unstable carotid plaques and impairs compensatory hemodynamic mechanisms. Furthermore, Vitamin D deficiency has been linked to impaired nitric oxide bioavailability and heightened neuro-inflammation, potentially exacerbating the severity of ischemic brain injury. Despite these insights, the synergistic predictive value of integrated biochemical and duplex-derived hemodynamic parameters in acute stroke management remains poorly defined.