Abstract
Intimal hyperplasia (IH) is a major risk for inferior vena cava (IVC) filter retrieval failures and potentially fatal vascular trauma to the IVC or caudal vena cava (CVC) wall post-retrieval. However, demonstrating neointimal formation in humans presents challenges due to the difficulty in obtaining quantitative pathological evidence from the IVC. Here, it was hypothesized that the mismatch between the diameter of the CVC and the filter would correlate with increased IH. Radial force (RF) exerted by filter struts at various CVC diameters was tested in vitro. In vivo, Bama miniature swine were randomly fitted with IVC filters of 32 mm-20 mm diameter, and a three-dimensional digital subtraction angiography model was used to determine the oversizing ratio (OR). After dwelling times of 2, 3, and 4 weeks, the macroscopic CVC wall and intima in the areas adjacent to IVC filter struts were observed. The proliferation and thickness of IH and presentations of vascular smooth muscle cells (VSMCs) were evaluated. Masson trichrome staining was used to determine the production of collagen fiber. The RFs of the IVC filter consistently increased with the OR, suggesting a correlation coefficient (R(2) = 0.74, p < 0.001). Notable response in the CVC wall after filter placement, characterized by vessel wall injury, VSMCs dedifferentiation, proliferation, and extracellular matrix secretion, which tended to increase and change over time. Increased ORs and dwelling time correlated linearly with greater IH thickness (adjusted R(2) = 0.456, p < 0.001). Moreover, restricted cubic splines (RCS) analysis revealed that ORs had a non-linear relationship with the IH thickness after adjusting for the IVC filter dwelling time (nonlinear p = 0.047, p < 0.001). A linear correlation was also noted between increased ORs and dwelling time with the collagen area fraction (adjusted R(2) = 0.860, p < 0.001). Furthermore, RCS indicated a consistently higher risk of increased collagen fiber content when the OR exceeded 100.75% (nonlinear p = 0.047, p < 0.001). IH developed in response to CVC injury, VSMCs proliferation, and secretion of the extracellular matrix collagen fiber. RFs increased with increased ORs. Increased ORs and dwelling time correlate linearly with greater IH thickness and increased production of collagen fiber.