ARRS 2022 Abstracts


E2101. Assessment of May-Thurner Iliac Venous Compression with 4D Flow MRI
  1. Christine Boone; UC San Diego Health
  2. Albert Hsiao; UC San Diego Health
  3. Sophie You; UC San Diego Health
  4. Pam Taub; UC San Diego Health
  5. Anne Roberts; UC San Diego Health
  6. Joy Liau; UC San Diego Health
Pelvic venous disease can arise from multiple etiologies, including May-Thurner Syndrome, caused by compression of the left common iliac vein (LCIV) between a common iliac artery and the spine. Diagnosis by conventional CT, MRI, and ultrasound can be challenging. We hypothesize that the hemodynamic significance of LCIV compression might be assessed by measuring the relative blood flow in the proximal LCIV and proximal right common iliac vein (RCIV). We use 4D flow MRI to quantify the LCIV and RCIV blood flow and assess whether the LCIV/RCIV flow ratio is decreased in patients with LCIV compression compared to control patients with no vascular anomalies (NVA).

Materials and Methods:
With IRB approval and waiver of informed consent, we retrospectively reviewed clinically indicated abdominopelvic MRI/MRA acquired on a 3 T MRI (GE Healthcare) in 41 patients found to have no vascular abnormalities (NVA, n = 25) or left common iliac vein (LCIV, n = 16) compression. The presence or absence of pelvic collaterals was also tabulated. 4D flow analysis software (Arterys) was used to measure blood flow and velocity in abdominopelvic veins, including at the RCIV and LCIV.

Distinct patterns of blood flow were observed among NVA and LCIV compression patients. Notably, patients with LCIV compression had significantly greater flow in their RCIV compared to NVA patients. Conservation of mass, in the form of flow, was observed in NVA and LCIV compression groups. The LCIV compression group had a reduced LCIV/RCIV flow ratio compared to patients with NVA (mean ± standard error of the mean [SEM] , NVA: 1.0 ± 0.09 vs. LCIV compression: 0.64 ± 0.07, p < 0.01, t-test). Additionally, patients with LCIV compression and pelvic collaterals had significantly decreased LCIV/RCIV ratios relative to NVA patients, whereas patients with LCIV compression without pelvic collaterals did not (mean ± SEM, NVA: 1.0 ± 0.45 vs. LCIV compression with pelvic collaterals: 0.46 ± 0.17, p < 0.01; NVA vs. LCIV compression without pelvic collaterals: 0.80 ±0.30, p > 0.5; one-way ANOVA with Tukey multiple comparisons test).

Abdominopelvic venous 4D flow revealed quantifiable hemodynamic differences between patients with and without LCIV compression. Patients with LCIV compression had increased RCIV blood flow, resulting from diversion of flow away from the site of stenosis or obstruction at the LCIV. Normal control patients had symmetric LCIV and RCIV flow with an LCIV/RCIV flow ratio of 1.0, whereas patients with LCIV compression exhibited reduced LCIV/RCIV ratios, which was even further reduced in those patients with visible pelvic collaterals. Hence, the LCIV/RCIV flow ratio may be a helpful marker to assess the hemodynamic significance of LCIV compression and has potential to guide intervention.