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Excimer laser coronary angioplasty (ELCA) plays an important role in modifying plaque composition, yet its impact on neointimal tissue (NIT) in in-stent restenosis lesions has remained unclear. While integrated backscatter intravascular ultrasound (IB-IVUS) can characterize plaque composition in de novo lesions, its ability to reflect tissue characteristics in NIT is limited due to the distinct structural and acoustic properties of neointimal tissue. This study aimed to investigate the effects of ELCA on NIT using IB-IVUS. We examined 49 in-stent lesions in 49 patients. IB-IVUS analysis focused on a 10 mm segment centered on the minimum lumen area (MLA), with data collected every 1 mm. Color maps were generated based on IB-IVUS backscatter values and included the following classifications: Red (typically calcification in de novo lesions), Yellow (dense fibrosis), Green (fibrosis), Blue (lipid pool), and Purple (lipid pool with attenuation). These classifications are based on tissue characteristics as defined in de novo settings and may differ in in-stent neointimal tissue. We compared Color-Ave (average color-coded area across 11 cross-sections, mm) and %Color-Ave (relative to neointimal tissue area), before and after ELCA. IB-related values, including mean (Ave-IB) and variance (Variance-IB), were automatically obtained. Following ELCA, Purple-Ave and %Purple-Ave significantly decreased (from 0.95±1.28 mm to 0.77±1.13 mm, and from 13.5±12.8% to 11.2±11.1%, both p=0.002). %Green-Ave increased significantly (from 53.6±14.1% to 55.5±12.7%, p=0.016), although Green-Ave remained unchanged. No significant changes were observed in Red-, Yellow-, and Blue-code areas. Similar trends were observed in MLA- and volume-based analyses. Ave-IB increased (p=0.028), while Variance-IB decreased (p=0.005). Changes in IB-related values were associated with their pre-ELCA levels. ELCA appears to ablate tissue with high IB-related values, leading to reduced tissue heterogeneity, even in NIT where tissue characterization by IB-IVUS is inherently limited.
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http://dx.doi.org/10.1007/s00380-025-02563-1 | DOI Listing |
FASEB J
September 2025
State Key Laboratory of Discovery and Utilization of Functional Components in Traditional Chinese Medicine, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Restenosis following endovascular intervention in lower extremity arterial disease contributes to significant morbidity and mortality. This study investigates the role of formylpeptide receptor 2 (FPR2) in neointimal hyperplasia and evaluates the therapeutic potential of the selective FPR2 agonist BMS-986235 in mitigating restenosis. FPR2 expression was significantly reduced in the popliteal and anterior tibial arteries of male amputees with restenosis compared to healthy controls.
View Article and Find Full Text PDFCureus
August 2025
Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, USA.
Background and aims The alpha-galactosidase (αGal) epitope and the associated anti-Gal antibodies, along with the non-human sialic acid N-glycolylneuraminic acid (Neu5Gc) and its corresponding anti-Neu5Gc antibodies, represent critical obstacles in the field of xenotransplantation. We present an evaluation of serological and histopathological data from patients who experienced immunological rejection after receiving decellularized xenografts. This study aims to analyze the long-term immune responses that occur following the implantation of these grafts, providing insights into the mechanisms driving rejection and their potential impact on transplant outcomes.
View Article and Find Full Text PDFCell Mol Life Sci
August 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Mole
Endothelial regeneration is critical for maintaining vascular homeostasis and inhibiting neointimal formation during vascular repair following injury. While extracellular matrix (ECM) stiffness of the vascular wall is known to influence vascular endothelial cell (EC) behavior, its role in post-injury endothelial regeneration remains poorly understood. Here, we demonstrate a dynamic change in vascular wall stiffness post-injury, with an initial transient decrease within 5 days, followed by a subsequent increase.
View Article and Find Full Text PDFIEEE Trans Mol Biol Multiscale Commun
March 2025
Department of Pathology and Anatomical Sciences and Department of Biomedical Engineering, University at Buffalo, Buffalo, NY 14203 USA.
Cardiovascular diseases (CVDs) and pathologies are often driven by changes in molecular signaling and communication, as well as in cellular and tissue components, particularly those involving the extracellular matrix (ECM), cytoskeleton, and immune response. The fine-wire vascular injury model is commonly used to study neointimal hyperplasia and vessel stiffening, but it is not typically considered a model for CVDs. However, applying this model to study CVDs in conjunction with established processes could offer valuable insights.
View Article and Find Full Text PDFTheranostics
August 2025
College of Pharmacy, Chongqing Medical University, Chongqing, 400016, China.
Suppressing the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), key pathological features of vascular neointimal hyperplasia (NIH), is an effective strategy for treating vascular insufficiency disorders caused by intimal remodeling. Increasing evidence suggests that Yes-associated protein (YAP) contributes to the abnormal proliferation and migration of VSMCs. However, the mechanisms by which YAP leads to NIH are poorly understood.
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