Neutrophil extracellular trap (NET) formation, or NETosis, is a key innate immune response that contributes to cardiovascular diseases, including vascular inflammation, atherosclerosis, and thrombosis. In the cardiovascular system, neutrophils encounter mechanical cues such as shear stress, matrix stiffness, and cyclic stretch that influence their activation and NET release. This review examines emerging evidence linking altered mechanotransduction to dysregulated NETosis in vascular aging and cardiovascular pathology. We also highlight intracellular signalling pathways by which neutrophils sense and respond to mechanical stress. Understanding how biomechanical cues regulate NETosis may uncover novel therapeutic opportunities to control inflammation in cardiovascular disease without compromising host defence.