A systematic evaluation of the impact of contralateral stenosis on ipsilateral internal carotid artery hemodynamics using computational fluid dynamics.

Background: Although contralateral internal carotid artery (ICA) stenosis affects ipsilateral velocity measurements, it is unclear how hemodynamics metrics such as cerebral blood flow (CBF), pressure gradient (PG), and wall shear stress (WSS) are impacted. The aim of this study was to leverage patient-specific magnetic resonance imaging-informed computational fluid dynamics (CFD) to quantify the impact of a contralateral ICA stenosis on ipsilateral ICA hemodynamics. Methods: A CFD model of cervical and cerebral arteries was built from imaging data to provide a ground-truth baseline for a patient with asymptomatic ICA stenosis (75% right, 25% left). The contralateral ICA stenosis was systematically altered to different levels (0-100%). Fixed flow waveforms were imposed at the ascending and descending aorta and bilateral subclavian arteries. Intra-cranial vessels were coupled to a 3-element Windkessel model, allowing for variable pressure and flow. Two different models for external carotid outflow behavior were considered: a primary model with fixed flows, and an alternative model with variable flow via a 3-element Windkessel model. Velocity, CBF, PG, and WSS were extracted at each level of left ICA stenosis. Results: Ipsilateral velocities remained unchanged until the contralateral ICA reached ≥50% stenosis. From 75% contralateral stenosis onwards, each 5% increase in stenosis resulted in larger increases in ipsilateral velocities. Ipsilateral PG remained unchanged until the contralateral ICA reached ≥90% stenosis. With contralateral stenoses of 90% and 95% the ipsilateral PG decreased from a ground-truth value of 0.995 to 0.993 and 0.992, respectively. With a contralateral occlusion, the ipsilateral PG decreased to 0.989. WSS remained unchanged from ground-truth (1.43 Pa) until the contralateral ICA reached 90% stenosis (1.67 Pa), 95% stenosis (1.96 Pa), or occlusion (5.69 Pa) at which point significant increases in WSS were observed (P<0.001, for all). Neither ipsilateral nor contralateral CBF changed significantly until the contralateral ICA stenosis reached ≥ 90% stenosis. Conclusions: Contralateral ICA stenosis impacts the ipsilateral ICA hemodynamics and thus may impact the ipsilateral stroke risk. Our data provides a reference for the expected increase in velocities based on contralateral percent stenosis. Percentage of contralateral stenosis should be considered when determining management strategies for ipsilateral ICA stenosis.