The incidence, natural history, and predictive factors for tissue protrusion after drug‐eluting stent implantation

Abstract

Objectives and background: Although tissue protrusion (TP) between the stent struts after stent implantation has been implicate as a potential factor of stent failure, the incidence, natural history, and predictive factor of TP after stent implantation remains unclear. This prospective study evaluated the fate of TP after drug-eluting stent (DES) deployment using optical coherence tomography (OCT).Method and result: This study analyzed TP for 42 lesions after DES in which three serial OCTs, including preprocedure, postprocedure, and 1-month after the procedure were performed. TP was classified into the five groups: (a) persistent, (b) progressive, (c) healed, (d) regressive, and (e) late-acquired. Immediately after the procedure, 100 TPs in 37 lesions (88%) were identified. Of those, 53 (53%) were persistent, 3 (3%) were progressive, 20 (20%) were healed, and 24 (24%) were regressed at 1-month follow-up. Seven TPs in five patients (13%) were observed only at 1-month follow-up (late-acquired). Conclusion:In lesions with late-acquired TP, calcified nodule was identified as an underlying plaque morphology on preprocedural OCT. A serial OCT analysis found TP occurred not only immediately after DES implantation, but also 1-month after DES implantation.

Comparative Clinical Implications of Calcified versus Non-Calcified Tissue Protrusion After Coronary Stent Implantation

“…Specifically, lesions featuring a calcified nodule, absent a calcified sheet, experienced protrusions of fragmented calcified particles through stent struts. 9 , 24 …”

“…Additionally, it is documented that the majority of TPs, typically resolvable during follow-up, eventually facilitate a more expansive lumen post-PCI. 5 , 17 The subsequent neointimal proliferation within 6–8 months post-DES insertion commonly leads to the disappearance of most TPs, 17 , 24 , 41 potentially elucidating the fewer adverse outcomes in non-calcified TP scenarios. Moreover, TP-afflicted patients might necessitate intensified secondary preventive measures (eg, statins, β-blockers, and angiotensin-converting enzyme inhibitors) to optimize long-term prognoses.…”

“…Specifically, lesions featuring a calcified nodule, absent a calcified sheet, experienced protrusions of fragmented calcified particles through stent struts. 9,24 Predictors of TP TP's emergence has been linked to various determinants including age, body mass index, statin usage, plaque rupture, intracoronary thrombus presence, elevated lipid content, thin-cap fibroatheroma, extensive plaque burden, positive 5942 vascular remodeling, substantial plaque volume, and extended stent implantation durations. [2][3][4]25 This study identified calcified nodules as a conducive factor for calcified TP, while STEMI served as an inhibitory element.…”