Spontaneous delayed expansion of self-expanding stents in stenotic arteries in Takayasu arteritis

PURPOSE: Despite frequent use of self-expanding stents (SES) in treating obstructive arterial lesions in Takayasu arteritis (TA), spontaneous delayed stent expansion (SDSE) in TA remains unstudied. This study aimed primarily to document and quantify SDSE and secondarily to determine factors that might be associated with this process. METHODS: Consecutive TA patients with obstructive arterial lesions undergoing routine percutaneous intervention involving SES use (sized 1 : 1 with normal vessel diameter but dilated only to 4 mm/5 mm) were recruited prospectively. Final stent diameters obtained were measured at 1 cm intervals along the length of the stent using fluoroscopic images and an indwelling marker catheter. At angiographic follow-up, stent diameters were measured again in identical fashion. Interval change in stent diameter at each point was averaged for each stent. In a small sub-study, intravascular ultrasound was used at follow-up to obtain potential mechanistic insights. RESULTS: Seventeen TA patients (age 33 ± 13 years, 15 female) had 22 arterial obstructive lesions (16 occlusions and 18 subclavian) treated with 1 SES each. Follow-up obtained in all patients after 8.7 ± 3.8 months (range: 3-18 months) showed interval increase in mean stent diameter of 1.6 ± 0.5 mm, range 0.7-2.8 mm (P < .001); 36% of stents achieved 100% of the nominal diameter at follow-up, while 90% of stents achieved ≥90%. The degree of SDSE did not correlate with the segment of artery stented or with TA disease activity at baseline. Intravascular ultrasound in 4 lesions showed that SDSE was associated with positive medial-adventitial remodelling and that neointimal hyperplasia occurs concurrently, causing in-stent luminal narrowing. CONCLUSION: SDSE, to diameters equal or close to nominal, occurs in all stenotic TA lesions treated with SES. The degree of SDSE does not correlate with the segment of artery stented or with TA disease activity at baseline. Preliminary results suggest that the mechanism by which SDSE is accommodated by the arterial wall is by positive medial-adventitial remodelling.