Direct versus late maxLCBI4mm changes after paclitaxel-coated balloon treatment of lipid-rich plaques

Background Lipid-rich plaques are a frequent cause of adverse cardiovascular events. Paclitaxel-coated balloons (PCB) can be used for focal pre-emptive treatment of lipid-rich plaques (LRPs) in non-culprit coronary lesions. However, the evolution of intracoronary imaging features after PCB-treatment remains inadequately understood. This post-hoc analysis of the DEBuT-LRP study aimed to evaluate direct versus late changes in intracoronary imaging features stratified per treated vessel. Methods In DEBuT-LRP, 20 patients with non-ST-segment elevation acute coronary syndrome underwent PCB treatment of a non-culprit lipid-rich plaque, identified by three-vessel intravascular ultrasound and near-infrared spectroscopy after percutaneous coronary intervention of flow-limiting lesions. PCB inflation was performed under nominal pressure for an inflation duration of at least 60 seconds. LRPs were defined as a maximum lipid-core burden index in a four millimeter segment (maxLCBI4mm) of >325. Intracoronary imaging was repeated immediately post-procedure and at 9-month follow-up. MaxLCBI4mm was analyzed using the Wilcoxon signed-rank test for pairwise changes and Kruskal-Wallis test for inter-vessel differences. Results Complete intracoronary imaging at baseline, directly post-PCB treatment and at 9-month follow-up was available in 14 patients. The median MaxLCBI4mm in treated segments significantly decreased from 461 (IQR 315-536) at baseline to 233 (IQR 124-375) at 9-months (p <0.01), with a significant reduction from directly post-PCB (400 with IQR 286-516) to 9-months (p = 0.01). No significant reduction was observed from baseline to post-PCB (p = 0.57). Stratified analysis per vessel showed a significant reduction in maxLCBI4mm over 9 months in the left circumflex artery (n = 7, p = 0.02), while changes in the left anterior descending artery (n = 4, p = 0.25) and right coronary artery (n = 3, p = 0.50) were not significant. However, inter-vessel comparisons showed no significant differences in maxLCBI4mm reduction across the different coronary arteries (baseline to post-PCB: p = 0.99, baseline to 9 months: p = 0.67, post-PCB to 9 months: p = 0.60). Conclusion Our findings demonstrate that PCB treatment of LRPs leads to a significant reduction in maxLCBI4mm over 9 months, with similar effects across the different coronary arteries. The absence of immediate post-PCB changes suggests a gradual biological response to paclitaxel rather than an immediate lipid modification effect caused by the balloon inflation. This supports the potential of drug-coated balloon therapy in altering plaque composition over time. Future large-scale studies are warranted to confirm these findings, explore predictors of response, and evaluate the clinical implications for long-term cardiovascular risk reduction.