The Relationship between Hemodynamics and Intracranial Carotid Artery Calcification: A Pilot Computational Study
P.J. Celie (TU Delft - Mechanical Engineering)
F.F. Fontana – Mentor (TU Delft - Mechanical Engineering)
A.C. Akyildiz – Mentor (TU Delft - Mechanical Engineering)
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Abstract
Background: Intracranial carotid artery calcification (ICAC) is associated with an increased risk of stroke, dementia, and cognitive decline. While disturbed hemodynamics have been linked to vascular pathologies such as atherosclerosis, a potential association with the development of ICAC has not yet been extensively studied. This pilot computational study investigated whether local hemodynamic parameters are associated with areas prone to developing calcification in the intracranial internal carotid artery (ICA).
Methods: Computed tomography angiography (CTA) data from the Erasmus Stroke Study database were used to reconstruct pre-calcification luminal geometries of intracranial carotid arteries. Twenty-three arteries with a stenosis degree ≥ 70% were initially selected. Eight representative arteries were chosen for lumen reconstruction, comparable to the stenosed subset in terms of size and calcium burden. Reconstructions were performed using contour rescaling, interpolation, and contour-copying techniques. Computational fluid dynamics simulations were conducted in reconstructed healthy lumen models using FEBio. Time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), and relative residence time (RRT) were calculated and mapped onto two-dimensional vessel representations. Hemodynamic parameters were compared between calcium-containing and calcium-free regions, as well as across anatomical ICA segments (C2–C6).
Results: Simulations of six reconstructed arteries successfully converged to a solution. In these arteries, calcifications were predominantly located in the cavernous (C4) and clinoid (C5) segments, while no calcifications were observed in the petrous segment (C2). Calcium-containing regions demonstrated a higher median TAWSS of 2.76 (IQR 2.48–3.34) Pa, compared to a median of 1.98 (IQR 1.23–2.63) Pa in calcium-free regions, corresponding to a 39.6% increase. In contrast, OSI and RRT were generally lower in calcium-containing regions. Calcium-containing regions had a median RRT of 0.43 (IQR 0.36–0.48), compared to a median RRT of 0.57 (IQR 0.45–0.88) in calcium-free regions. The median OSI was 0.74 × 10⁻³ (IQR 0.48–0.011 × 10⁻³) in calcium-containing regions, while a value of 0.96 × 10⁻³ (IQR 0.72–1.1 × 10⁻³) was found in calcium-free regions. Segmental analysis showed that TAWSS increased towards the distal ICA segments, whereas RRT decreased downstream. OSI values remained consistently low throughout the arteries.
Conclusions: This pilot study presents a pipeline to extract hemodynamic data from healthy ICA surrogates derived from commonly available CTA images of patients with ICAC. The exploratory findings differed from classical atheroprone hemodynamic patterns characterized by low TAWSS, high OSI, and high RRT. These contradictory findings warrant further investigation. Larger studies with patient-specific boundary conditions are needed to clarify the potential relationship between hemodynamics and ICAC.