## 4 Discussion  
In this prospective study, we demonstrated a significant association between vertebral artery stiffness and idiopathic subjective tinnitus, providing new evidence for a potential vascular contribution to tinnitus pathophysiology. Both vertebral artery stiffness index (VAS) and pulsatility index (PI) were markedly elevated in tinnitus patients compared to healthy controls. Importantly, we observed that these vascular abnormalities were lateralized and correlated with the side of tinnitus symptoms, suggesting a localized hemodynamic component. Our findings are consistent with previous studies suggesting the role of vascular dysfunction and microcirculatory impairment in tinnitus development. [PERSON] et al. demonstrated increased carotid artery stiffness in patients with idiopathic tinnitus, emphasizing the role of systemic arterial stiffness in auditory dysfunction [16]. However, our study is among the first to specifically evaluate the vertebral arteries, which have a more direct contribution to cochlear and brainstem perfusion. In addition, [PERSON] et al. reported a positive relationship between systemic arterial stiffness parameters, including pulse wave velocity, and the presence of tinnitus [17]. While pulse wave velocity provides valuable systemic information, it does not fully capture localized vascular abnormalities in the vertebral system that directly influence cochlear perfusion. In contrast, our use of Doppler ultrasonography enabled regional assessment of vertebral artery stiffness, offering greater specificity for tinnitus-related microvascular changes. Several mechanistic explanations may account for the observed association between increased vertebral artery stiffness and tinnitus. Increased arterial stiffness leads to elevated pulsatile pressure, impaired vascular compliance, and reduced capacity for flow regulation. In the cochlea, such hemodynamic disturbances may result in hypoxia, oxidative stress, and direct injury to the highly vascularized stria vascularis, spiral ganglion cells, and outer hair cells, thereby contributing to tinnitus generation. [PERSON] et al. have previously emphasized that arterial stiffness is closely linked to microvascular brain injury through similar mechanisms [20]. The cochlea was known to be highly sensitive to changes in microvascular perfusion, and such alterations had been proposed as contributing factors in the development of tinnitus [23; 24; 25]. Atherosclerosis was previously identified as one of the key contributors to cochlear microcirculatory impairment, particularly in patients presenting with tinnitus [26; 27]. [PERSON] et al. and [PERSON] et al. described the progression of atherosclerotic lesions in hyperlipidemic animal models and highlighted their impact on various microvascular beds, including those relevant for hearing [28; 29], as well as a higher prevalence of tinnitus among individuals with ischemic cerebrovascular conditions [30]. Our findings of significantly elevated total cholesterol, LDL, and triglyceride levels in the tinnitus group were consistent with earlier reports highlighting the role of dyslipidemia and systemic vascular dysfunction in auditory pathologies. Furthermore, tinnitus symptoms \begin{table}
\begin{tabular}{l l l l l} \hline  & **Left** & **Right** & **Bilateral** & **\(p\) Value** \\ \hline Vert. Art. Stiff Left & 3.27 \(\pm\) 0.79 & 2.57 \(\pm\) 0.76 & 2.2 \(\pm\) 0.45 & 0.058 \\ Vert. Art. Stiff Right & 2.7 \(\pm\) 0.66 & 3.62 \(\pm\) 0.87 & 2.76 \(\pm\) 0.01 & 0.010 \\ Vert Art. RI Left & 0.93 \(\pm\) 0.15 & 0.97 \(\pm\) 0.29 & 0.64 \(\pm\) 0.32 & 0.543 \\ Vert Art. RI Right & 0.84 \(\pm\) 0.19 & 1.08 \(\pm\) 0.19 & 0.69 \(\pm\) 0.4 & 0.579 \\ Vert Art. PI Left & 2.74 \(\pm\) 1.58 & 2.41 \(\pm\) 1.34 & 2.2 \(\pm\) 0.45 & 0.024 \\ Vert Art. PI Right & 2.6 \(\pm\) 1.5 & 2.7 \(\pm\) 0.95 & 2.21 \(\pm\) 0.22 & 0.016 \\ \hline \end{tabular}
\end{table} 
Table 3: Vertebal artery vascular parameters and the side of tinnitus.