Effect of Hinge Motion on Stent Edge-Related Restenosis After Right Coronary Artery Treatment in the Current Drug-Eluting Stent Era

Background: Stent edge-related restenosis (SER) remains a potential limitation of drug-eluting stent (DES). Hinge motion at the stent edge could lead to mechanical stress and contribute to incidents of SER. We investigated the effect of hinge motion on SER after implantation of current-generation DES in the right coronary artery (RCA), where excessive vessel movement is commonly observed. Methods and Results: Of 647 consecutive lesions in the RCA treated with second-generation or later DESs, 426 with follow-up angiography were included in this study. Intravascular imaging analysis was performed for 584 stent edges and reference segments. Binary restenosis occurred in 42 lesions (9.9%), and 55% were SERs. The hinge angle was significantly larger in the SER group than in the other restenosis or the no-restenosis group (17.9 degrees vs. 11.6 degrees and 10.6 degrees, respectively; P<0.001). Lesions with an excessive hinge angle (>11.5 degrees) had an increased rate of target lesion revascularization (19.1% vs. 7.2%; P<0.001) during the median follow-up period of 1,578 days. In per-edge analysis, hinge angle and residual plaque burden were independent predictors of SER. The coexistence of excessive hinge motion and residual plaque burden had a synergistic effect on stenotic progression in quantitative angiographic analysis (P-interaction<0.001) at follow-up angiography. Conclusions: Substantial stress determined by angulation at a stent edge and its interaction with residual plaque can be considered as one plausible mechanism for SER.

Automated summary

This study investigated the impact of hinge motion on stent edge-related restenosis (SER) in the right coronary artery (RCA) after implantation of current-generation drug-eluting stents (DES). The results indicated that hinge angle and residual plaque burden were independent predictors of SER, with a synergistic effect observed when excessive hinge motion and residual plaque burden coexisted. These findings suggest that mechanical stress at stent edges and its interaction with residual plaque may contribute to SER progression.