Descending aortic bypass for middle aortic syndrome due to Takayasu arteritis: A case report.

Stroke remains one of the most severe epidemiological burdens for the global healthcare system. According to the latest data from the Global Burden of Disease (GBD) 2023 study, in 2023 stroke was the second leading cause of death after ischemic heart disease, claiming 6.79 million lives; disability-adjusted life years (DALYs) lost to stroke reached 157 million (). The GBD 2021 stroke-specific analysis showed that in 2021, 11.9 million new stroke cases were recorded, 93.8 million people were living with the consequences of stroke, and the DALY figure exceeded 160.5 million (). The fact that over 87 percent of the global stroke burden falls on low- and middle-income countries demonstrates that this problem carries not only clinical but also systemic and policy significance (). Yet against this statistical backdrop lies a deep conceptual paradox. According to the results of the second phase of the INTERSTROKE study, approximately 90.7 percent of stroke cases are directly associated with preventable or modifiable risk factors—namely arterial hypertension, dyslipidemia, smoking, diabetes mellitus, and central obesity (). Thus, while the causal factors are largely known and modifiable, the global burden of the disease remains remarkably high. In such a situation, the question may lie not solely in the insufficiency of treatment or diagnostic technologies, but also in how stroke is understood, named, and conceptually situated. The terms “cerebrovascular” and “cardiovascular” have been used in clinical language for over a century, products of the classical nosological model that combines an anatomical organ name with a pathological process. This model emerged in an era when diseases were primarily described through anatomical observation and the logic of localization, and pathogenetic mechanisms had not yet been fully elucidated. However, pathogenetic knowledge subsequently deepened dramatically. Ross () defined atherosclerosis not as a local vascular lesion but as a chronic systemic inflammatory disease, demonstrating that it is not limited to lipid accumulation but is governed by an immune-inflammatory cascade. Furchgott and Zawadzki () discovered the central role of endothelial dysfunction and nitric oxide (NO) in vascular tone regulation, earning the Nobel Prize. Additionally, the independent significance of hemodynamic-rheological factors such as blood viscosity, erythrocyte aggregation, and fibrinogen in stroke pathogenesis has been confirmed by an increasing body of evidence (). Yet despite these fundamental discoveries, terminological frameworks have remained virtually unchanged. As a result, today’s clinical language often foregrounds not where the process begins, but where it manifests. The term “cerebrovascular” exemplifies this: it names the cerebral phenotype of a systemic hemovascular process but does not bring vascular wall pathology, hemodynamic mediation, or blood composition changes to the center of the term. It is worth noting that in cardiology, the term “cardiovascular” has over time moved closer to an etiology-based concept: vascular wall remodeling, thrombolytic therapy, and blood rheology management have become established as core treatment strategies, ensuring that the term itself also operates in alignment with etiological logic. In neurology, however, the term “cerebrovascular” has remained unchanged under the influence of neuro-centered traditions, laying the groundwork for the prolonged dominance of the neuroprotection paradigm. The reclassification of cerebrovascular diseases to the nervous system chapter in ICD-11 was an important institutional step (), yet the terminology itself and its alignment with the pathogenetic hierarchy were not revisited.