Why do Human Femoral Stents Fail? First In-man Pathology and Multimodality Imaging of Acute and Chronic Femoral Stenting in Human

Abstract

Introduction: Lower extremity peripheral arterial disease (PAD) is a major cause of morbidity. Endovascular therapy remains the gold standard to treat PAD1. While pathology of coronary stenting has been well studied2, pathology of lower extremity femoral stenting remains poorly understood. The objective was to comprehensively evaluate the pathology of acute and chronic femoral stenting in symptomatic atherosclerotic patients and to understand the causes of stent failures (SF) using multi-modality imaging including micro-computed tomography (microCT). Methods: Twelve stents were obtained from 10 patients with history of PAD (mean age 74 ± 9.3; 7 male and three female); all the stented arteries underwent radiography, microCT and histologic assessment. Dissected arteries were embedded in Spurr and sawed at 3-5 mm intervals and Exact slides were prepared at 60 to 100 mm and a total of 78 sections examined following co-registration with microCT. Results are reported as median and interquartile (25 to 75th percentile, IQR). Results: Duration was 150 days (30 - 365, IQR), diameter was 5.90 mm (5.44 - 7.16, IQR) and stented length was 39.5 mm (27 - 107.5, IQR). Two of 12 stents were drug-eluting stents, 10 of 12 were bare-metal stents. Half of them were overlapping stents. Indications for stenting were intermittent claudication (40%), chronic limb ischemia (50%), and acute limb ischemia (10%). Morphometric analysis of the histologic sections showed stent success [(defined as < 75% cross sectional area narrowing and absence a thrombus (>30% narrowing from thrombus)] in 4 of 12 stents with 31.0% stenosis (22.16 - 35.0, IQR). The causes of SF in the remaining 8 were: stent-thrombosis (Figure 1), 3; in-stent restenosis, 2; and chronic total occlusions, 3, with 91.5% stenosis (78.3 - 100, IQR). Histologic malapposition3 occurred in 8 of the 12 stented lesions. Underlying nodular calcification (NC) was observed in half of the lesions, medial calcifications observed in 67% of cases with the median arch of calcification of 63° (0-283, IQR). Intimal calcification was observed in 11/12 cases, degree of calcification was 126° (38 - 248, IQR). The duration of implantation was divided into short-term (≤90 days) and long-term (>90 days) stenting. The extent of medial calcification was significantly different in short-term vs. long-term stenting [126° (18.0 - 195.8) vs 0 (0 - 2.25) respectively, p=0.003]. Malapposition (Figure 2) was observed more frequently in the short-term vs. long-term groups [50.0% (25.0 - 87.5) vs 0% (0-11.9) respectively, p=0.02]. Stent fractures were observed in 3 stents (3/11, 27.7%) and all of them were associated with SF. Also, SF had a higher medial injury score4: 2 (1 - 3, IQR) vs 1 (1 - 2, IQR), p=0.04. Conclusion: This descriptive histologic study is the first series of explanted human femoral stents, removed at surgery (n=10) and autopsy (n=2). Medial calcification and malapposition play an important role in long-term stent patency. Excessive injury and stent fracture also contributes to SF. Use of microCT in this study illustrates the advantages of high-resolution CT to detect SF, especially stent fractures. This study also enlightens the necessity to evaluate any explanted material in the future5.Figure 2Multi-modality imaging showing stent malapposition.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Disclosure: Sho Torii receives research grants from SUNRISE lab. Renu Virmani and Aloke V. Finn have received institutional research support from Abbott Vascular, Boston Scientific, Cook Medical, Cardiovascular Systems, Inc., Medtronic, and Terumo Corporation; Renu Virmani is a consultant for 480 Biomedical, Abbott Vascular, Medtronic, and W.L. Gore. Other authors report no conflicts of interest.