## 1 Introduction  
Laryngotracheal stenosis (LTS) [1] is characterized by the narrowing of the airway between the larynx and trachea which can occur in the supraglottic, glottic, subglottic, and tracheal regions. It is commonly associated with voice changes or loss, hoarseness, and stridor. LTS can result from prolonged medical intubation, laryngeal trauma, granulomatous with polyangiitis, or may be idiopathic in nature. The symptoms vary based on the location and severity of the stenosis, but frequently include a breathy, strained voice and increased respiratory effort [2, 3]. Narrowing that occurs specifically in the subglottic region is referred to as subglottic stenosis (SGS). In this distinctive disorder, the stenosis is below the true vocal folds and the shape and vibratory properties of the vocal folds themselves remain largely unaffected. Yet, despite anatomically normal vocal folds, breathing difficulty, shortness of breath, hoarseness, and dysphonia are common debilitating symptoms associated with even mild to moderate grades of SGS [4; 5; 6]. The precise underlying mechanism of how SGS impacts voice production still remains incompletely understood. The Myer-Cotton scale is clinically used to classify the severity of SGS based on the narrowing of the subglottic area into four grades: I (0% to 50%), II (51% to 70%), III (71% to 99%), and IV (100% obstruction) [7; 8]. While lower-grade SGS (Grade I and II) may require minimal or no treatment, higher-grade SGS (Grade III and IV) often necessitates laryngotracheal resection with reconstruction to restore airway patency and improve voice-related quality of life. Outcomes are generally good with patients experiencing improved breathing and voice. Regular follow-up is important to monitor for potential recurrence [9; 10; 11; 12]. Prior studies have attempted to elucidate the interplay between SGS and phonation. [PERSON] and [PERSON] [13] employed a two-dimensional computational fluid dynamics model to simulate the effects of SGS on vocal fold vibration and voice production. They found that increased airway resistance was the primary factor explaining the minimal effects of SGS up to 60% obstruction, while noticeable changes in voice production occurred at 90% obstruction and beyond. Building on this work, our recent study [14] employed a high-fidelity three-dimensional idealized fluid-structure-acoustic interaction model, confirming that minimal effects persisted up to 75% obstruction, while significant alterations in glottal flow and pressure were evident at 90% and beyond. Additionally, we identified the ratio of the glottis outlet area to the SGS narrowed area as a critical determinant of degree of impact on phonation. Most recently, [PERSON] et al. [15] validated these computational predictions through an experimental study using a self-oscillating synthetic vocal fold model in conjunction with a subglottic stenosis. Consistent with the simulations, their results demonstrated negligible influence below 80-90% obstruction but significant deviations in aerodynamic, acoustic, and vibratory responses beyond that threshold. Despite advancements in computational and experimental studies of subglottic stenosis (SGS), several limitations remain. Past studies [13; 14; 15] have employed idealized or simplified vocal fold geometries, often relying on two-dimensional models that fail to accurately capture the true three-dimensional nature of fluid-structure interactions. While synthetic vocal fold designs offer valuable insights, they typically lack the precise material properties and layered microstructure of actual human vocal folds. Additionally, neglecting the complex aerodynamic interactions between the glottis, subglottic region, and trachea, as well as the realistic asymmetries of the vocal tract and irregular obstructions, may impact the accuracy of voice production simulations compared to previously studied symmetric idealized airway models [16].