Stenting has become more prevalent in recent years as a durable treatment to reestablish venous flow in cases of iliofemoral deep vein thrombosis (DVT). Venous stents have helped alleviate symptoms of both acute DVT and chronic postthrombotic syndrome of the lower extremities, such as pain, edema, and chronic skin changes leading to ulceration.[1] However, despite the development of vein-specific, self-expanding nitinol stents such as the Venovo (BD Interventional), Zilver Vena (Cook Medical), and Abre (Medtronic), achieving long-term venous stent patency remains a complex challenge. The incidence of repeat interventions in patients with iliofemoral venous stents has been reported between 11 and 33.5% of cases due to recurrence of symptoms in the setting of in-stent stenosis, stent compression, and complete occlusion.[2] [3] Patients treated with dedicated venous stents for thrombotic disease have shown significantly lower primary patency rates compared with those stented for nonobstructive stenotic lesions of the iliac vein (70 vs. 93.6% in the VERNACULAR Trial and 70.4 vs. 97.1% in the ABRE Study) at 3 years.[4] [5] This complexity underscores the need for close follow-up and continuous imaging surveillance of these patients who tend to return with in-stent thrombosis and recurrent lower extremity symptoms.

Some degree of endothelialization, remodeling, and narrowing along the stent wall inevitably occurs and is postulated to stabilize by 3 months after stenting.[2] However, progression of this process to hemodynamically significant stenosis >50% or complete thrombosis has been attributed to numerous causes, including inadequate inflow veins from the lower extremity that are necessary to supply blood flow into the stent to keep it open, residual outflow stenosis of the inferior vena cava (IVC) or common iliac vein, noncompliance or failure of anticoagulation, or mechanical malfunction of the stent[6] [7] [8] ([Fig. 1]). While data on the exact mechanism of in-stent stenosis remains unclear, several observations stay at the forefront. Histologic samples from animal models with in-stent stenosis have shown a layer of neointima within the stent as early as 1 week after implantation and intimal thickening with fibrotic changes and smooth muscle proliferation by 8 weeks.[9]