Evaluating Changes in Pulsatile Flow With Endovascular Stents in an In Vitro Blood Vessel Model: Potential Implications for the Future Management of Neurovascular Compression Syndromes

Background: Neurovascular compression syndromes (NVCS), encompassing conditions such as trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia, significantly impair patient quality of life through abnormal vascular compression and micro-pulsation of vasculature on cranial nerves at the Obersteiner-Redlich zone. The modulation of pulsatile flow dynamics via endovascular stents presents a novel research frontier for alleviating these syndromes.

Aim: The primary aim of this investigation was to delineate the impact of various endovascular stents on pulsatile flow within an in vitro model of a blood vessel, thereby elucidating their potential applicability in the therapeutic management of NVCS.

Materials and methods: A simple in vitro analog of a posterior circulation artery was developed, employing an intravenous pump to replicate cardiac-induced blood flow. Within this model, alterations in pulsatile flow were quantitatively assessed following the introduction of three categorically distinct endovascular stents, varying in size. This assessment was facilitated through the employment of both micro-Doppler and Doppler ultrasound methodologies.

Results: The Pipeline 5x35 mm stent (Medtronic, Minneapolis, MN) demonstrated the most significant reductions in peak systolic velocity (Vmax) and pulsatility index (PI), PI especially over the stent, suggesting its potential for drastically altering blood flow dynamics. Similarly, Neuroform Atlas 4.5x30 mm and Neuroform Atlas 4x24 mm stents (Stryker, Kalamazoo, MI) also showed notable decreases in hemodynamic parameters, albeit to different extents. Statistical analysis confirmed that these changes were significantly different from the control (P < 0.0001 for PI and Vmax; P < 0.05 for inter-stent comparisons), except for proximal PI means, which did not significantly differ from the control (P = 0.2777).

Conclusion: These findings affirm the potential of endovascular stents to substantially modulate arterial pulsatility. The observed decrease in pulsatile flow resultant from endovascular stent application has the potential to attenuate ectopic nerve excitation, a hallmark of NVCS. Consequently, this research highlights the prospective utility of endovascular stents in developing minimally invasive therapeutic approaches for NVCS.