Abstract 13344: Variable Factors Influence Restenosis Following Endovascular Therapy in the Superficial Femoral Artery: Comparison Between TASC II A-C and D lesions
Background: Endovascular therapy (EVT) by nitinol stenting is widely performed for femoropopliteal (FP) lesions in patients with peripheral artery disease (PAD). The latest European Society of Cardiology guideline recommends an EVT-first strategy for Trans-Atlantic Intersociety Consensus (TASC II) A-C lesions. However, restenosis following EVT remains as an important issue in FP lesions. We sought to investigate the risk factors for restenosis in FP lesions and compared TASC II A-C with D.
Methods: We studied 3471 limbs from 2742 consecutive patients (73±17 years, female: 31%, critical limb ischemia: 30%) who underwent successful EVT for de novo FP lesions with provisional nitinol stenting from April 2004 to December 2011. Primary outcome measure was restenosis. Predictors for restenosis in TASC II A-C and D lesions were assessed using Cox proportional hazards model.
Results: Diabetes was present in 61% (2118) of patients and 26% (917) were on dialysis. Twenty-six % (895) of limbs had a TASC II D lesion. Overall 5-year primary patency was 52%. TASC II D status was an independent predictor for restenosis (hazard ratio [HR]: 2.25, p < 0.001), as were diabetes mellitus (HR: 1.22, p=0.015), stent use (HR: 0.81, p=0.027), chronic total occlusion (HR: 1.42, p 1.5). Female gender was significantly associated with TASC II D (adjusted HR 0.56, p <0.001), and renal failure with TASC II A-C (adjusted HR 1.43; p <0.001). The adjusted hazard ratio for IVUS use was 0.56 (p <0.001) for TASC II A-C, and 0.80 (p = 0.114) for TASC II D (interaction p = 0.060)
Conclusion: Presence of diabetes, stent use, chronic total occlusion, and poor BTK runoff were shared restenosis predictors between TASC II A-C and D lesions, while renal failure was a predictor only in TASC II A-C lesions and female gender in TASC II D lesions. Restenosis factors differ between TASC II A-C and D lesions.
- © 2013 by American Heart Association, Inc.