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. < 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.>.
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http://dx.doi.org/10.1016/j.jccase.2020.11.004 | DOI Listing |
Curr Med Chem
October 2024
Department of Experimental Medicine, Research Institute for Complex Issues of Cardiovascular Diseases, 6 Sosnovy Boulevard, 650002, Kemerovo, Russia.
Background: Citrullination represents a post-translational modification primarily mediated by peptidylarginine deiminase (PADI) 2 and 4 and resulting in the conversion of positively charged peptidylarginine to neutrally charged peptidylcitrulline. Molecular consequences of citrullination include the generation of neoepitopes which provoke the production of autoantibodies implicated in the development of autoimmune diseases. As citrullination initiates, promotes, and is enhanced by aseptic inflammation which plays a pivotal role in atherosclerosis, we proposed that citrullination might accompany the development of atherosclerotic vascular disease.
View Article and Find Full Text PDFCell Death Dis
November 2023
Metabolomics and Cell Biology Platforms, Gustave Roussy Comprehensive Cancer Institute, Villejuif, France.
Autophagy inducers can prevent cardiovascular aging and age-associated diseases including atherosclerosis. Therefore, we hypothesized that autophagy-inducing compounds that act on atherosclerosis-relevant cells might have a protective role in the development of atherosclerosis. Here we identified 3,4-dimethoxychalcone (3,4-DC) as an inducer of autophagy in several cell lines from endothelial, myocardial and myeloid/macrophagic origin, as demonstrated by the aggregation of the autophagosome marker GFP-LC3 in the cytoplasm of cells, as well as the downregulation of its nuclear pool indicative of autophagic flux.
View Article and Find Full Text PDFJ Cardiol Cases
May 2021
Department of Cardiology, Higashi Takarazuka Satoh Hospital, Takarazuka, Japan.
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.
View Article and Find Full Text PDFCardiovasc Res
January 2022
Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Aims: Pathological arterial remodelling including neointimal hyperplasia and atherosclerosis is the main underlying cause for occluding arterial diseases. Cezanne is a novel deubiquitinating enzyme, functioning as a NF-кB negative regulator, and plays a key role in renal inflammatory response and kidney injury induced by ischaemia. Here we attempted to examine its pathological role in vascular smooth muscle cell (VSMC) pathology and arterial remodelling.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2020
Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Recent studies reported that vascular endothelial cells (ECs) secrete NLR family pyrin domain-containing 3 (NLRP3) inflammasome products such as interleukin-1β (IL-1β) via extracellular vesicles (EVs) under various pathological conditions. EVs represent one of the critical mechanisms mediating the cell-to-cell communication between ECs and vascular smooth muscle cells (VSMCs). However, whether or not the inflammasome-dependent EVs directly participate in the regulation of VSMC function remains unknown.
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