Vascular endothelial dysfunction as a mechanism of hearing loss in carotid artery stenosis: a scientific literature review

Abstract Objective This review aimed to examine the potential role of vascular endothelial dysfunction in the development of hearing loss associated with carotid artery stenosis. Methods A narrative literature review was conducted using PubMed, Google Scholar, Web of Science, and Scopus databases. Studies published in English up to January 2026 were identified using predefined search terms related to carotid atherosclerosis, endothelial dysfunction, and hearing loss. A total of 197 records were identified. After screening and eligibility assessment, 25 relevant epidemiological, mechanistic, clinical, and interventional studies were included in the qualitative synthesis. Results The included studies suggest a consistent association between carotid atherosclerosis and sensorineural hearing loss. Increased carotid intima-media thickness and plaque burden were associated with poorer hearing thresholds and a higher risk of both sudden and progressive hearing loss. Mechanistic evidence indicates that endothelial dysfunction—characterized by reduced nitric oxide bioavailability, oxidative stress, and inflammatory activation—may contribute to impaired cochlear microcirculation and ischemic injury. Clinical manifestations range from subclinical auditory decline to sudden sensorineural hearing loss and pulsatile tinnitus. Evidence regarding hearing improvement following carotid revascularization remains limited and is primarily based on small case series. Conclusion Vascular endothelial dysfunction may represent an important mechanism linking carotid artery stenosis to hearing loss. Although current evidence supports an association between vascular disease and auditory impairment, causality has not been definitively established. Recognition of this relationship may support earlier diagnosis and integrated cardiovascular-audiological management, while further prospective and interventional studies are needed to clarify underlying mechanisms and therapeutic implications.