Predictors of target lesion restenosis after endovascular therapy for lower-extremity atherosclerotic peripheral artery disease: a real-world single center cohort.

BACKGROUND

Lower-extremity peripheral artery disease often requires endovascular therapy. Target-lesion restenosis (TLRS) remains frequent, but current risk stratification is limited.

METHODS

We retrospectively analyzed 1,005 lesions from 917 patients undergoing endovascular therapy for lower-extremity atherosclerotic disease at a single center (2019-2024) with scheduled surveillance (approximately 6, 12, and 24 months) and administrative censoring at 36 months. The primary endpoint was time to first TLRS ≥ 50%, adjudicated by duplex ultrasound (peak systolic velocity ratio criteria) or CTA/DSA when available. Lesion‑level Fine-Gray competing‑risk models (death as a competing event) with patient‑level clustering were used. A prespecified Core model (clinical, anatomic, procedural/device covariates and C‑reactive protein) was compared with an Extended model additionally including the Atherogenic Index of Plasma (AIP) and log‑transformed Systemic Immune-Inflammation Index (SII). Models were internally validated by 1,000 bootstrap resamples and assessed at the 24‑month horizon using the C‑index, calibration, Brier score, integrated discrimination improvement (IDI), net reclassification improvement (NRI), and decision‑curve analysis.

RESULTS

Among 917 patients (1,005 lesions), mean age was 75.2 ± 11.7 years and 68.6% were male. At 24 months, cumulative incidences were 31.4% for TLRS, 14.9% for clinically driven target‑lesion revascularization, and 12.3% for death. In multivariable analyses, GLASS stage III, lesion length ≥ 150 mm, residual stenosis > 20%, chronic kidney disease, and Rutherford class 4-6 predicted higher TLRS risk, whereas good distal runoff was protective. In the Extended model, AIP and SII remained independent predictors and improved the optimism‑corrected 24‑month C‑index from 0.68 to 0.73 (Δ0.05, p = 0.002), reduced the Brier score (0.19 to 0.17), yielded positive IDI and NRI, and preserved good calibration. Exploratory analyses suggested lower TLRS risk with cilostazol and low‑dose rivaroxaban plus aspirin.

CONCLUSIONS

AIP and SII improved lesion-level prediction of TLRS beyond conventional covariates. The Extended model may support risk-tiered surveillance after endovascular therapy; external validation is warranted.