| 1. |
- Jensen, Lisette Okkels, et al.
(author)
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Intravascular ultrasound assessment of minimum lumen area and intimal hyperplasia in in-stent restenosis after drug-eluting or bare-metal stent implantation. The Nordic Intravascular Ultrasound Study (NIVUS)
- 2017
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In: Cardiovascular Revascularization Medicine. - : Elsevier BV. - 1553-8389. ; 18:8, s. 577-582
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Journal article (peer-reviewed)abstract
- Introduction: Drug-eluting stents (DES) reduce the risk of restenosis after percutaneous coronary intervention. The aim of the study was to evaluate, by intravascular ultrasound (IVUS), the minimum lumen area site in the stented segment and the distribution of intimal hyperplasia in patients presenting with a DES or bare-metal stent (BMS) in-stent restenosis. Methods: The “Nordic Intravascular Ultrasound Study (NIVUS)” study was conducted in Nordic and Baltic countries as a prospective multicenter registry. Two hundred nine patients (DES n = 121 and BMS n = 88) with in-stent restenosis were enrolled. Results: At the minimum lumen area site in the stented segment, the stent area (5.8 ± 2.2 mm2 vs. 7.6 ± 2.4 mm2, p < 0.001) and intimal hyperplasia area (2.6 ± 2.0 mm2 vs. 5.0 ± 2.2 mm2, p < 0.001) were significantly lower in patients treated with DES compared to BMS. The percentage of stents that did not have a minimum stent area of at least 5.0 mm2 (under expansion) was higher in DES (58.7% vs. 37.7%, p = 0.008) compared to BMS. Intimal hyperplasia covered 55.4 ± 33.3% of the stent length in the DES compared to 90.7 ± 17.4% in the BMS group, p < 0.001. Focal in-stent restenosis was more often seen in DES treated patients compared to BMS treated patients (DES n = 84 (59.9%) vs. BMS n = 15 (17.0%), p < 0.001). Conclusion: Stent underexpansion was more often seen in DES than BMS in-stent restenosis. DES more often had focal in-stent restenosis with less intimal hyperplasia.
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| 2. |
- Kosonen, Joonas P., et al.
(author)
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Injury-related cell death and proteoglycan loss in articular cartilage : Numerical model combining necrosis, reactive oxygen species, and inflammatory cytokines
- 2023
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In: PLoS Computational Biology. - : Public Library of Science (PLoS). - 1553-734X .- 1553-7358. ; 19:1
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Journal article (peer-reviewed)abstract
- Osteoarthritis (OA) is a common musculoskeletal disease that leads to deterioration of articular cartilage, joint pain, and decreased quality of life. When OA develops after a joint injury, it is designated as post-traumatic OA (PTOA). The etiology of PTOA remains poorly understood, but it is known that proteoglycan (PG) loss, cell dysfunction, and cell death in cartilage are among the first signs of the disease. These processes, influenced by biomechanical and inflammatory stimuli, disturb the normal cell-regulated balance between tissue synthesis and degeneration. Previous computational mechanobiological models have not explicitly incorporated the cell-mediated degradation mechanisms triggered by an injury that eventually can lead to tissue-level compositional changes. Here, we developed a 2-D mechanobiological finite element model to predict necrosis, apoptosis following excessive production of reactive oxygen species (ROS), and inflammatory cytokine (interleukin-1)-driven apoptosis in cartilage explant. The resulting PG loss over 30 days was simulated. Biomechanically triggered PG degeneration, associated with cell necrosis, excessive ROS production, and cell apoptosis, was predicted to be localized near a lesion, while interleukin-1 diffusion-driven PG degeneration was manifested more globally. Interestingly, the model also showed proteolytic activity and PG biosynthesis closer to the levels of healthy tissue when pro-inflammatory cytokines were rapidly inhibited or cleared from the culture medium, leading to partial recovery of PG content. The numerical predictions of cell death and PG loss were supported by previous experimental findings. Furthermore, the simulated ROS and inflammation mechanisms had longer-lasting effects (over 3 days) on the PG content than localized necrosis. The mechanobiological model presented here may serve as a numerical tool for assessing early cartilage degeneration mechanisms and the efficacy of interventions to mitigate PTOA progression.
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| 3. |
- Kosonen, Petteri, et al.
(author)
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Intravascular ultrasound assessed incomplete stent apposition and stent fracture in stent thrombosis after bare metal versus drug-eluting stent treatment the Nordic Intravascular Ultrasound Study (NIVUS)
- 2013
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In: International Journal of Cardiology. - : Elsevier BV. - 0167-5273. ; 168:2, s. 1010-1016
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Journal article (peer-reviewed)abstract
- Background: This prospective multicenter registry used intravascular ultrasound (IVUS) in patients with definite stent thrombosis (ST) to compare rates of incomplete stent apposition (ISA), stent fracture and stent expansion in patients treated with drug-eluting (DES) versus bare metal (BMS) stents. ST is a rare, but potential life threatening event after coronary stent implantation. The etiology seems to be multifactorial. Methods: 124 patients with definite ST were assessed by IVUS during the acute ST event. The study was conducted in 15 high-volume percutaneous coronary intervention -centers in the Nordic-Baltic countries. Results: In early or late ST there were no differences in ISA between DES and BMS. In very late ST, ISA was a more frequent finding in DES than in BMS (52% vs. 16%; p=0.005) and the maximum ISA area was larger in DES compared to BMS(1.1 +/- 2.3 mm(2) vs. 0.1 +/- 0.5 mm(2); p=0.004). Further, ISA was more prevalent in sirolimus-eluting than in paclitaxel-eluting stents (58% vs. 37%; p-0.02). Stent fractures were found both in DES (16%) and BMS (24%); p=0.28, and not related to time of stent thrombosis occurrence. For stents with nominal diameters >= 2.75 mm, 38% of the DES and 22% of the BMS had a minimum stent area of less than 5 mm(2); p=0.14. Conclusions: Very late stent thrombosis was more prevalent and associated with more extensive ISA in DES than in BMS treated patients. Stent fracture was a common finding in ST after DES and BMS implantation. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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