Conţinutul numărului revistei |
Articolul precedent |
Articolul urmator |
1148 7 |
Ultima descărcare din IBN: 2023-06-15 21:27 |
SM ISO690:2012 CIOBANU, Liliana, POPOVICI, Ion, COBEŢ, Valeriu, IVANOV, Victoria, COSTIN, Sava. Evaluarea markerilor inflamaţiei în restenoza intra-stent. In: Curierul Medical, 2012, nr. 5(329), pp. 3-8. ISSN 1875-0666. |
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Curierul Medical | ||||||
Numărul 5(329) / 2012 / ISSN 1875-0666 | ||||||
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Pag. 3-8 | ||||||
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Rezumat | ||||||
In-stent restenosis is a serious complication that usually follows 6 months after angioplasty. It is believed to be a manifestation of negative coronary remodeling. In order to focus on the role of inflammation in this phenomenon we determined the circulating levels of the lipoprotein-associated phospholipase A2 (Lp-PA2) and C reactive proteins (CRP), as well as the content of macrophages in the restenosis tissue pattern. We found that the blood Lp-A2 and CRP levels were significantly elevated in first 72 hours after angioplasty, independently of the restenosis hazard. We also discovered that after 3 to 6 months these markers remained boosted only in patients with restenosis, while the markers notably declined in those without restenosis. Elevation in inflammation markers was associated with a significant increase in the macrophage amount in the luminal part of restenosis tissue, an important source of the synthesis of the Lp-A2, a marker of endothelial inflammation and dysfunction. |
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Cuvinte-cheie in-stent restenosis, inflammation markers |
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Cerif XML Export
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In order to focus on the role of inflammation in this phenomenon we determined the circulating levels of the lipoprotein-associated phospholipase A2 (Lp-PA2) and C reactive proteins (CRP), as well as the content of macrophages in the restenosis tissue pattern. We found that the blood Lp-A2 and CRP levels were significantly elevated in first 72 hours after angioplasty, independently of the restenosis hazard. We also discovered that after 3 to 6 months these markers remained boosted only in patients with restenosis, while the markers notably declined in those without restenosis. 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