Dataset Information

Late peri-stent contrast staining appearance due to rupture of atherogenic neointima following drug-eluting stent.

ABSTRACT: The development of peri-stent contrast staining (PSS) after coronary intervention with implantation of a stent is observed in approximately 1-3% of patients treated with drug-eluting stent. Although the cumulative incidences of late in-stent restenosis and stent thrombosis are significantly higher in lesions with PSS than in those without the finding, the mechanisms for the development of PSS have not yet been fully elucidated. In this report, we describe a case of rapid development of PSS with ulcer formation caused by rupture of atherogenic neointima, which was observed by serial optical coherence tomography examinations over 6 months. Protrusion of the stent-jailed underlying necrotic core toward the lumen by the contracting force might have resulted in formation of atherogenic neointima within the stent. Subsequently, rupture of this necrotic core induced by iatrogenic neointimal injury due to balloon dilation and dissolution of the accumulated necrotic core may have resulted in PSS formation 6 months after the procedure. These findings may be helpful for consideration of etiology and therapeutic strategy for lesions with PSS. <Learning objective: The mechanisms of peri-stent contrast staining (PSS) formation late after drug-eluting stent (DES) implantation are diverse. Rupture of atherogenic neointima with subsequent dissolution of the stent-jailed underlying plaque debris could be one of the mechanisms of rapid PSS formation after implantation of DES. An accurate assessment of lesion morphology within the stent and patient-tailored management can reduce morbidity and mortality in patients who have undergone DES implantation.>.

SUBMITTER: Tamaru H

PROVIDER: S-EPMC8103349 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:AimsUnderstanding endothelial cell repopulation post-stenting and how this modulates in-stent restenosis is critical to improving arterial healing post-stenting. We used a novel murine stent model to investigate endothelial cell repopulation post-stenting, comparing the response of drug-eluting stents with a primary genetic modification to improve endothelial cell function.Methods and resultsEndothelial cell repopulation was assessed en face in stented arteries in ApoE(-/-) mice with endothelial-specific LacZ expression. Stent deployment resulted in near-complete denudation of endothelium, but was followed by endothelial cell repopulation, by cells originating from both bone marrow-derived endothelial progenitor cells and from the adjacent vasculature. Paclitaxel-eluting stents reduced neointima formation (0.423 ± 0.065 vs. 0.240 ± 0.040 mm(2), P = 0.038), but decreased endothelial cell repopulation (238 ± 17 vs. 154 ± 22 nuclei/mm(2), P = 0.018), despite complete strut coverage. To test the effects of selectively improving endothelial cell function, we used transgenic mice with endothelial-specific overexpression of GTP-cyclohydrolase 1 (GCH-Tg) as a model of enhanced endothelial cell function and increased NO production. GCH-Tg ApoE(-/-) mice had less neointima formation compared with ApoE(-/-) littermates (0.52 ± 0.08 vs. 0.26 ± 0.09 mm(2), P = 0.039). In contrast to paclitaxel-eluting stents, reduced neointima formation in GCH-Tg mice was accompanied by increased endothelial cell coverage (156 ± 17 vs. 209 ± 23 nuclei/mm(2), P = 0.043).ConclusionDrug-eluting stents reduce not only neointima formation but also endothelial cell repopulation, independent of strut coverage. In contrast, selective targeting of endothelial cell function is sufficient to improve endothelial cell repopulation and reduce neointima formation. Targeting endothelial cell function is a rational therapeutic strategy to improve vascular healing and decrease neointima formation after stenting.

Project description:AimsIn-stent chronic total occlusion (IS-CTO) represents a unique challenge for percutaneous coronary intervention. Whether the optimal treatment for IS-CTO is angioplasty with paclitaxel-coated balloons (PCBs) or repeat stenting with drug-eluting stents (DESs) is unclear. We aimed to evaluate the long-term clinical outcome of PCB angioplasty and DES repeat stenting for DES IS-CTO.MethodsWe retrospectively included patients with DES IS-CTO who underwent successful PCB angioplasty or DES repeat stenting from January 2016 to December 2019. The primary endpoints were major adverse cardiac events (MACEs), including cardiac death, myocardial infarction, and target lesion revascularization (TLR). Cox proportional hazards model was performed to compare the risk of MACEs between PCB angioplasty and DES repeat stenting, and to further explore the prognostic factors of patients with DES IS-CTO.ResultsA total of 214 patients with DES IS-CTO were enrolled: 78 patients (36.4%) treated with PCB and 136 patients (63.6%) treated with DES respectively. The median follow-up was 1160 days, and MACEs were observed in 28.2% of patients with PCB angioplasty versus 26.5% of patients with DES repeat stenting (P = 0.784), mainly driven by TLR (21.8% vs. 19.9%, P = 0.735). There was no significant difference in the risk of MACEs between the PCB group and the DES group (hazard ratio [HR] 1.25, 95% confidence interval [CI] 0.64-2.46, P = 0.512). Multivariate Cox analysis revealed that chronic kidney disease and ≥ 3 stent layers in the lesion were independent predictors of MACEs, while switching to another antiproliferative drug was an independent protective factor (all P < 0.05).ConclusionsPCB angioplasty was an effective alternative treatment strategy for DES IS-CTO, which had similar long-term outcomes to DES repeat stenting in contemporary practice, but both were accompanied by a high rate of long-term MACEs. Improving the poor prognosis of patients with DES IS-CTO remains a challenge.

Dataset Information

Late peri-stent contrast staining appearance due to rupture of atherogenic neointima following drug-eluting stent.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets