Immune-inflammatory response after bioresorbable vascular scaffold implantation in patients with acute myocardial infarction with ST elevation in a long-term perspective
Jazyk angličtina Země Japonsko Médium print-electronic
Typ dokumentu časopisecké články, multicentrická studie
PubMed
30315494
DOI
10.1007/s00380-018-1281-7
PII: 10.1007/s00380-018-1281-7
Knihovny.cz E-zdroje
- Klíčová slova
- Bioresorbable vascular scaffold, Immune–inflammatory reaction, Myocardial infarction, Percutaneous coronary intervention, Thrombosis,
- MeSH
- časové faktory MeSH
- cytokiny metabolismus MeSH
- dospělí MeSH
- everolimus farmakologie MeSH
- imunosupresiva farmakologie MeSH
- infarkt myokardu s elevacemi ST úseků diagnóza imunologie chirurgie MeSH
- koronární angiografie MeSH
- koronární angioplastika přístrojové vybavení metody MeSH
- lidé středního věku MeSH
- lidé MeSH
- následné studie MeSH
- přirozená imunita * MeSH
- protézy - design MeSH
- retrospektivní studie MeSH
- senioři MeSH
- stenty uvolňující léky * MeSH
- tkáňové podpůrné struktury * MeSH
- vstřebatelné implantáty * MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- multicentrická studie MeSH
- Názvy látek
- cytokiny MeSH
- everolimus MeSH
- imunosupresiva MeSH
A higher rate of bioresorbable vascular scaffold (BVS) thrombosis has been observed after device implantation compared to implantation of permanent metallic stents in recently published studies. The mechanism of BVS thrombosis is currently under debate. To assess whether the immune-inflammatory response after BVS implantation is a potential trigger of BVS thrombosis. The PRAGUE-19 study was an academic study that enrolled consecutive patients with ST-segment elevation myocardial infarction (STEMI) with the intention to implant a BVS. A laboratory sub-study included 49 patients with an implanted BVS (of which 38 underwent the complete 2-year follow-up) and 52 patients having an implanted permanent metallic stent as the control group (of which 30 underwent the complete 2-year follow-up). Samples for inflammatory markers [high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)] were taken before BVS or stent implantation, on days 1 and 2 after device implantation and at 1 month and 2 years for a clinical control. The primary combined clinical endpoint of the sub-study (death, reinfarction or target vessel revascularization) occurred in 4.08% of the BVS group and 7.69% of the control group (p = 0.442) during the 2-year follow-up period, with overall mortality of 2.04% in the BVS group and 1.92% in the control group (p = 0.966). Definite BVS thrombosis occurred in one patient in the subacute phase; there was no late or very late thrombosis. Two definite stent thromboses were observed in the control group: one in the subacute phase and the other in the late phase. Baseline inflammatory marker levels did not differ between the groups. Lower levels of IL-6 and hs-CRP were observed in the BVS group compared to the control group (12.02 ± 5.94 vs. 15.21 ± 5.33 pg/ml; p < 0.01; 3952.9 ± 1704.75 ng/ml vs. 4507.49 ± 1190.01 ng/ml; p = 0.037, respectively) on days 1 and 2 (12.01 ± 6.31 vs. 13.85 ± 6.01 pg/ml; p = 0.089; 4447.92 ± 1325.31 ng/ml vs. 4637.03 ± 1290.99 ng/ml; p = 0.255, respectively). No differences in IL-6 or hs-CRP were observed after 1 month or 2 years in the clinical control. Levels of TNF-α did not differ between the groups in the early period after BVS or metallic stent implantation, nor during follow-up. The immune-inflammatory response is lower during the early phase after BVS implantation compared to that after metallic stent implantation, but the responses did not differ in the long term.
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