9-year clinical follow-up of patients with ST-segment elevation myocardial infarction with Genous or TAXUS Liberté stents

Abstract

ObjectivesThis matched-cohort retrospective study investigated the long-term (9-year) safety and efficacy outcomes of patients with ST-segment elevation myocardial infarction (STEMI) and primary percutaneous coronary intervention (pPCI) with Genous (n = 102) versus TAXUS Liberté (n = 101) stents in 2006–2008.BackgroundIn the era of off-label use of drug-eluting stents for pPCI in patients with STEMI, the use of first-generation Genous stents (endothelial progenitor cell capture stents that have a passive coating and accelerate re-endothelialization) was proposed.MethodsThe primary endpoint was 9-year major adverse cardiac and cerebrovascular events (MACCE), including all-cause death, re-infarction, target vessel revascularization (TVR), and stroke. The secondary endpoints were the separate primary endpoint events at pre-defined time-points (in-hospital, 6 months, and yearly) and stent thrombosis. Time-dependent 9-year composite MACCE, all-cause death, and TVR were compared using Kaplan-Meier estimates and multivariate Cox regression models.ResultsPropensity score analysis confirmed the comparability of the groups. Patients in the Genous and TAXUS groups had 7 and 1 acute definitive stent thrombosis events, respectively (p<0.001). There was a trend towards higher in-hospital MACCE in the Genous group (10.8%) versus the TAXUS group (4.0%). Kaplan-Meier analysis showed that 9-year MACCE was significantly worse in the Genous than in the TAXUS group. The in-hospital, 6-month, 1-year, and 9-year mortality rates were 7.8%, 8.8%, 9.8%, and 23.5% in the Genous group and 2.0%, 3.0%, 4.0%, and 16.8% in the TAXUS group.ConclusionsHigher peri-procedural, in-hospital, and short-term mortality led to worse outcomes for first-generation Genous stents versus TAXUS Liberté stents for pPCI in STEMI. TAXUS Liberté stents had more favorable 9-year clinical outcomes.

Coronary stent CD31-mimetic coating favours endothelialization and reduces local inflammation and neointimal development in vivo

“…The Genous ® stent, functionalized with anti-CD34 antibodies, was intended to capture circulating CD34 + endothelial progenitor cells, 21 but it showed a higher risk of restenosis compared to DES. 22 – 24 The addition of an abluminal bioabsorbable polymer-eluting sirolimus (Combo ® stent) 25 , 26 reverted the restenosis risk, but the endothelial coverage is actually lower than with DES. 27 This is presumably due to the low frequency of circulating progenitor ECs (0.2% of nucleated blood elements) in coronary patients.…”

Intraprocedural endothelial cell seeding of arterial stents via biotin/avidin targeting mitigates in-stent restenosis

“…Protocols involving stent surface modification to expedite the post-deployment capture and proliferation of circulating endothelial progenitor cells (EPC) have also been explored [17][18][19][20][21]. To date, no major clinical success of either pre-or post-deployment stent endothelialization has been demonstrated [22,23] apparently due to failure to establish integral EC/EPC coverage, which is paramount for aborting platelet attachment to the struts and preventing inflammatory cell recruitment.…”

Surface grafting of Fc-binding peptides as a simple platform to immobilize and identify antibodies that selectively capture circulating endothelial progenitor cells

“…Although previous human clinical trials have demonstrated a better early endothelialization on these stents compared with drug-eluting stents, 12,13 other long-term studies have confirmed the formation of late neointimal hyperplasia and restenosis. [14][15][16] This late in-stent restenosis could be due to poor ECFC selectivity by CD34 antibodies, as there are other circulating progenitor cells (CD34 + ) that could be captured on the surface. 17 Certain CD34 + cells might differentiate into immune cells that mediate inflammatory responses and disturb the signaling and activation pathways of smooth muscle cells (SMCs), leading to intimal hyperplasia.…”