Early Peak Systolic Velocity and Trend Variation Predict Stent Patency in Chronic Mesenteric Ischemia and Propose a Post-intervention Surveillance Algorithm.

OBJECTIVE

Stenting of the superior mesenteric artery (SMA) and celiac artery is the more prevalent treatment for symptomatic chronic mesenteric ischemia (CMI). The SVS recommends duplex ultrasound for post-stenting surveillance. This study aimed to determine whether early postoperative peak systolic velocity (PSV) and subsequent PSV progression predict primary patency (PP) loss after SMA stenting.

METHODS

Single-center retrospective analysis of 179 patients (240 vessels: 165 SMA, 75 celiac) treated between 2003 and 2020 with ≥2 years of follow-up. Early PSV was defined as duplex velocity within 3 months post-stenting. PSV progression was categorized as <100 cm/s or ≥100 cm/s absolute increase and <50% or ≥50% relative increase from baseline. Cox proportional hazards and time-dependent ROC analyses assessed associations between PSV and PP.

RESULTS

Higher early PSV was a strong independent predictor of PP loss. Each 10 cm/s increase in early SMA-PSV conferred a 5% higher risk of PP loss (HR 1.05; P < 0.001); similar trends were observed in celiac stents (HR 1.06, P 0.064). Progressive PSV increase over time was also predictive: a ≥100 cm/s rise tripled the risk of stent failure (HR 3.26; P 0.001), and a ≥50% rise yielded comparable risk (HR 3.58; P < 0.001). Progressive increase of SMA-PSV by 10 cm/s increased the risk of PP loss by 5% (HR: 1.05; P 0.008). ROC analysis at 24 months showed limited discriminative power for isolated velocity thresholds (AUC 0.66), underscoring the superior predictive value of PSV trends.

CONCLUSION

Both elevated early PSV and progressive increases over time are strong, reproducible predictors of mesenteric stent failure. Every 10 cm/s rise in SMA PSV corresponds to a 4-5% increased risk of PP loss, while a ≥100 cm/s or ≥50% PSV rise triples failure risk. These findings establish PSV progression as a clinically meaningful marker of restenosis and propose a retrospective, hypothesis-generating surveillance framework.