Key result
Zinc deficiency linked to ~15-point lower 1-year amputation-free survival after EVT in CLTI.
Why the study?
The specific impact of zinc deficiency on outcomes in patients with chronic limb-threatening ischemia (CLTI) following endovascular therapy (EVT) remained poorly understood.
Does baseline zinc deficiency (< 60 µg/dL) reduce 1-year amputation-free survival in patients with chronic limb-threatening ischemia undergoing endovascular therapy?
Cohort (n=313)
No
Does baseline zinc deficiency (< 60 µg/dL) reduce 1-year amputation-free survival in patients with chronic limb-threatening ischemia undergoing endovascular therapy?
Baseline zinc deficiency is highly prevalent in patients with chronic limb-threatening ischemia undergoing endovascular therapy, correlates strongly with poor nutritional status (hypoalbuminemia), and serves as a prognostic marker for worse 1-year amputation-free survival.
Background Zinc (Zn) is an essential trace element known to reduce atherosclerotic risk and play a critical role in immune function and wound healing. While its importance is recognized in various cardiovascular conditions, the specific impact of Zn deficiency on outcomes in patients with chronic limb-threatening ischemia (CLTI), the most severe form of peripheral artery disease, remains poorly understood following endovascular therapy (EVT). Purpose This study aimed to investigate the prognostic impact of Zn deficiency on clinical outcomes of CLTI patients with tissue loss following EVT. Methods In this single-center retrospective study, we analyzed 313 consecutive patients with CLTI (mean age: 77.9 ± 9.3 years; male: 58.6%, dialysis: 36.1%) who underwent EVT between April 2023 and January 2026 and had serum Zn levels measured at baseline. Zinc deficiency was defined as a serum Zn level < 60 µg/dL based on the median level. The outcome measure was amputation-free survival. Kaplan-Meier analysis and Cox proportional hazards models were used for statistical analysis. Results Zinc deficiency was present in 144 patients (46.0%). On baseline comparison, patients with Zn deficiency exhibited a significantly higher prevalence of body mass index (BMI) <18.5 kg/m2 (25.9% vs 15.5%), serum albumin level <3.0 g/dL (42.0% vs 11.4%), and WIfI stage 4 (49.3% vs 29.2%), and had a significantly lower prevalence of non-ambulatory status (41.3% vs 62.5%), dyslipidemia (42.4% vs 54.4%), statin therapy (38.9% vs 58.9%), coronary artery disease (29.9% vs 42.0%), and smoking history (33.3% vs 46.2%) compared to those without deficiency (all p < 0.01). Consistent with this, multivariate logistic regression analysis revealed that serum albumin < 3.0 g/dL was the strongest independent predictor of Zn deficiency (odds ratio [OR] 4.08, 95% confidence interval [CI] 2.19–7.60, p < 0.001). Kaplan–Meier analysis demonstrated that patients with Zn deficiency had significantly worse 1-year AFS compared to those without deficiency (77.9% versus 63.3%, log-rank p=0.002). Conclusion The current study revealed that zinc deficiency is prevalent among patients with CLTI and identifies a subgroup with poorer nutritional status. It serves as a robust marker for worse amputation-free survival. Our findings suggest that assessing serum zinc levels could help stratify risk in this high-risk population.
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Ikeuchi et al. (2026) conducted a cohort in Chronic limb-threatening ischemia (CLTI) with tissue loss (n=313). Zinc deficiency (serum Zn < 60 µg/dL) vs. No zinc deficiency (serum Zn ≥ 60 µg/dL) was evaluated on 1-year amputation-free survival (AFS) (p=0.002). Zinc deficiency (<60 µg/dL) was associated with significantly worse 1-year amputation-free survival after endovascular therapy in CLTI patients (63.3% vs 77.9%, p=0.002).
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