Numerical simulation of gonadal vein hemodynamics in nutcracker syndrome-associated varicocele: effects of Valsalva maneuver and clinical implications.

Objectives: Nutcracker syndrome (NCS) is a vascular disorder characterized by compression of the left renal vein (LRV), frequently complicated by varicocele in male patients. The Valsalva maneuver is routinely used to provoke venous reflux during ultrasound diagnosis, yet the hemodynamic response of the gonadal vein throughout a complete Valsalva cycle remains poorly characterized. This study aims to quantitatively elucidate the hemodynamic mechanisms by which intra-abdominal pressure elevation-simulated via the Valsalva maneuver-exacerbates gonadal venous reflux in NCS-associated varicocele. Methods: Fifty-seven patients with NCS and concomitant varicocele were consecutively enrolled. Doppler ultrasonography was performed to measure anatomical and hemodynamic parameters, including aortomesenteric angle, LRV diameter, stenotic diameter, peak velocities, and gonadal vein diameter under resting and Valsalva conditions. A representative three-dimensional computational fluid dynamics (CFD) model incorporating the inferior vena cava, LRV, and gonadal vein was reconstructed from contrast-enhanced CT data. A physiologically relevant time-varying pressure boundary condition was applied at the gonadal vein inlet to simulate a complete Valsalva cycle. Pressure, velocity, wall shear stress, and streamline distributions were systematically analyzed. Results: Clinical data revealed significant anatomical compression and hemodynamic abnormalities, with gonadal vein diameter increasing from 3.0 ± 0.94 mm at rest to 3.86 ± 1.07 mm during Valsalva. CFD simulations demonstrated that during the Valsalva plateau phase, pressure at the gonadal vein inlet reached 6,000 Pa, with a pressure gradient of approximately 7,600 Pa across the LRV stenosis. Peak WSS at the stenosis increased 12-fold, exhibiting marked spatial heterogeneity. Velocity at the stenosis reached 2.7 m/s, with pronounced flow separation and disturbed streamlines developing downstream, which reduced the effective flow volume by 50%-60%. Conclusion: The Valsalva maneuver induces a high-pressure-negative-pressure-recompression vicious cycle across the LRV stenosis, with elevated upstream pressure increasing venous congestion risk and downstream negative pressure exacerbating stenotic collapse. The 12-fold WSS elevation far exceeds physiological thresholds, potentially precipitating cumulative endothelial injury. Recirculation zone formation compromises venous return and promotes thrombogenesis. Crucially, these hemodynamic perturbations are not confined to diagnostic maneuvers but are likely mirrored during daily activities that elevate intra-abdominal pressure (e.g., running, jumping), explaining the progressive symptom worsening and activity-related discomfort in NCS patients. These findings provide a hemodynamic rationale for dynamic clinical assessment.