Capture Stent Research Articles

Abstract 2520: Drug-Eluting Stents for the Treatment of Chronic Total Occlusion: A Comparison with Sirolimus, Paclitaxel, Zotarolimus, EPC Capture and Everolimus-Eluting Stent: Multicenter Registry in Asia

The aim of this study is to compare the safety and efficacy of Sirolimus (SES), Paclitaxel (PES), Zotarolimus (ZES), EPC capture (ECS) and Everolimus-eluting stent (EES) on the outcome of patients with chronic total occlusion (CTO). A prospective analysis of 1149 patients with 1183 CTOs (396 SES, 526 PES, 177 ZES, 41 ECS, 43 EES) in five high volume Asian centers after successful recanalization of CTO was performed. The study endpoints were 30 days and 9 months major adverse cardiac events (MACE), 9 months angiographic restenosis and target lesion revascularization (TLR). See table for clinical results. The use of drug-eluting stents in patients with CTO was safe with low acute complication. Patients treated with SES and EES showed lesser rate of restenosis compared with other drug-eluting stents.

Abstract 5998: Final Results of the HEALING 2B Trial to Evaluate a Bioengineered CD34 Antibody Coated Stent (Genous ™ Stent) Designed to Promote Vascular Healing by Capture of Circulating Endothelial Progenitor Cells in CAD Patients

Background: In contrast to a cytotoxic or cytostatic pharmacotherapy, promoting the vascular healing response by capturing and sequestering circulating endothelial progenitor cells (EPC) to the stent surface by a CD34 antibody coating (Genous ™ stent) may accelerate stent reendo-thelialization and prevent restenosis formation, as well as stent thrombosis (ST) Methods: The HEALING IIB study was a multi-center, prospective trial designed to assess the safety and efficacy of the Genous ™ bio-engineered stent in conjunction with HmG CoA reductase inhibitors (statins) to stimulate EPC recruitment, in the treatment of patients with de novo coronary artery lesions (n=100 pts). The primary safety endpoint was major adverse cardiac events (MACE) at 30 days, whereas the primary efficacy endpoint was late luminal loss by QCA at 6 months follow-up. Results: At interim analysis of the first 45 patients that completed the 6-month angiographic follow-up, the composite MACE rate was 11.1%, whereas 6.6% clinically justified target lesion revascularizations were observed. 2 Patients died within the first 30 days after stent implantation due to angiographically verified stent thrombosis. Low circulating EPC titers were previously associated with a poor response to the EPC capture stent with TLR events and high late loss. Therefore, patients were pre-treated with Atorvastatin 80 mg qd prior to the PCI in order to augment EPC levels. Statin therapy stimulated the levels of committed EPCs by +294%, but failed to increase the titer of CD34+cells (+25%). Although statin pretreatment stimulated EPC levels, the angiographic outcome of the EPC capture stent was not improved in these patients: in-stent late luminal loss was 0.77±0.46 mm. We anticipate to complete analysis of the 6 month angiographic follow-up of all 100 patients by the time of the AHA2008. Conclusions: The HEALING-IIB study suggests that the EPC capture coronary stent in combination with statin therapy does not sufficiently impede stent restenosis formation for the treatment of de novo coronary artery disease. Although concomitant statin therapy was able to stimulate EPC recruitment, it failed to stimulate CD34+ stem cell levels and did not improve the angiographic outcome of the bioengineered EPC capture stent.

Percutaneous coronary intervention utilizing a new endothelial progenitor cells antibody‐coated stent: A prospective single‐center registry in high‐risk patients

To prospectively evaluate the outcome with circulating endothelial progenitor cell (EPC) capture stent implantation in a cohort of consecutive patients with high-risk angiographic and/or clinical features. Genous R-stent is a stainless steel coronary stent covered with antibodies specific to EPC's surface antigens, designed to promote the formation of a confluent functional endothelial layer over the device; conceivably, this may prevent both stent thrombosis and restenosis. From November 2005 to March 2007, 80 patients received 93 EPC capture stents at Campus Bio-Medico, University of Rome. Patients had two or more of the following high-risk features: diabetes mellitus (33%), unstable coronary syndromes (73%), left ventricular dysfunction (8%), multivessel intervention (9%), B2/C lesions (56%). Acute success was achieved in 79/80 patients (98%), without Q-wave myocardial infarction (MI), in-hospital death or emergency bypass surgery; no patient had acute or subacute stent thrombosis. Follow-up was available in 78 patients (mean 14 +/- 4 months): noncardiac death occurred in one patient, acute MI in one patient; no patient required bypass surgery; 10 patients (13%) underwent percutaneous target lesion revascularization (TLR); three patients (4%) had reintervention on a nontarget vessel. Kaplan-Meyer life-table analysis showed event-free survival of 86% and TLR-free survival of 90% at one and a half year follow-up. The cell capture stent is safe and effective, with satisfactory immediate results and mid-term outcome, without evidence of stent thrombosis. Whether those devices represent a viable alternative to currently available drug-eluting or bare metal stents will need to be evaluated in larger randomized studies.

Use of endothelial progenitor cell capture stent (Genous Bio-Engineered R Stent) during primary percutaneous coronary intervention in acute myocardial infarction: Intermediate- to long-term clinical follow-up

We assessed the use of the endothelial progenitor cell (EPC) capture stent in primary percutaneous intervention in ST-elevation myocardial infarction (STEMI). One hundred and twenty patients with acute STEMI without cardiogenic shock received 129 EPC capture stents. Procedural success was achieved in 95% of patients. Dual antiplatelet therapy was given for a month and statin therapy started immediately after the procedure. The study end points are major adverse cardiac events inhospital and at 30 days, 6 months, and 1 year. Hypertension was present in 47.5% and diabetes mellitus in 30% of the patients. The left anterior descending artery was the treated artery in 54% of the patients. Mean lesion length was 17.4 +/- 7.15 mm with mean reference vessel diameter of 3.18 +/- 0.6 mm. Platelet glycoprotein IIb/IIIa inhibitor was used in 14% of patients and 58% had thrombosuction before stent implantation. Ninety-five percent of patients achieved Thrombolysis in Myocardial Infarction 3 flow with cumulative major adverse cardiac event rate at 1.6% inhospital, 4.2% at 30 days, 5.8% at 6 months, and 9.2% at 1 year. There was 1 patient each with acute and subacute stent thrombosis but no incidence of late stent thrombosis. Using EPC capture stent during primary percutaneous coronary intervention for STEMI is feasible and safe.

Accelerated vascular repair following percutaneous coronary intervention by capture of endothelial progenitor cells promotes regression of neointimal growth at long term follow-up: final results of the Healing II trial using an endothelial progenitor cell capturing stent (Genous R stent)™

The study sought to define the long-term angiographic and clinical outcome of a bio-engineered stent, able to sequester endothelial progenitor cells (EPC) to the stent to promote the post-stenting vascular repair response. The HEALING-II was a multicentre, prospective registry, including 63 patients treated with the implantation of a Genous EPC capture stent. Serial quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS) analysis was performed at 6 and 18 month. The 18 month composite MACE rate was 7.9%, whereas 6.3% clinically justified target lesion revascularisations were observed. Although patients received one month of clopidogrel, no (sub)acute or late angiographic stent thrombosis occurred. At 6 month follow-up, in-stent late luminal loss was 0.78+/-0.39 mm and percent in-stent volume obstruction was 22.9+/-13.7% (mean+/-sd). Serial angiographic and IVUS analyses were available in 30 event-free patients at post-procedure, 6 months and 18 months. From 6 months to 18 months follow-up, a significant late regression of neointimal hyperplasia was observed on QCA (late luminal loss 0.59+/-0.31, 24.4% reduction or 16.9% by matched serial analysis) and IVUS (percent in-stent volume obstruction 20.3+/-14.3%, 11.4% reduction or 9.6% by matched serial analysis). The relative increase in circulating EPC titers at long-term follow-up correlated with neointimal compaction in individual patients, suggestive of an EPC-mediated vascular repair response. The HEALING II study suggests that the EPC capture stent, aimed to stimulate the coronary vascular repair response, significantly promotes late regression of neointimal hyperplasia up to 18 months after stent implantation.

Abstract 3438: Comparison of Endothelial Progenitor Cell Capture Stent with Bare Metal Stent In Patients Undergoing Primary Percutaneous Coronary Intervention for Acute Myocardial Infarction

Background: The endothelial progenitor cell (EPC) capture bio-engineered stent (Genous ® stent, OrbusNeich) was designed to attract circulating EPCs and promote rapid endothelization. The aim of this study was to compare clinical outcomes between patients with ST-segment elevation myocardial infarction (STEMI) who received this stent versus those who received Liberte (Boston Scientific) bare metal stents. Methodology: Three hundred and forty two patients who presented to our centers with STEMI without cardiogenic shock and underwent primary PCI with either EPC Capture-or bare metal stent implantation were enrolled in this study. All patients received dual anti-platelet therapy for a month; and statin therapy was initiated soon after PCI. The study endpoints were major adverse cardiac events (MACE) at 30 days, 6 months and 1 year. Results: A total of 164 EPC Capture stents and 178 BMS were implanted. Baseline patient characteristics were comparable in the 2 groups. The mean lesion length in the 2 groups were 20.4.0 ± 5.1 and 22.8 ± 7.6mm, and the mean reference vessel diameter 3.14 ± 0.65 and 2.70 ± 1.14 mm respectively. At 6 months, the results were: Conclusion: There was no significant difference in MACE at 6 month between EPC Capture-and bare metal stents in patients with STEMI who underwent primary PCI. The 1-year data will be presented at the meeting.

Circulating endothelial progenitor cells predict angiographic and intravascular ultrasound outcome following percutaneous coronary interventions in the HEALING-II trial: evaluation of an endothelial progenitor cell capturing stent.

In contrast to the cytostatic and cytotoxic pharmacotherapy of drug eluting stents, approaches to stimulate the arterial healing response by accelerating re-endothelialisation may be an attractive alternative to prevent post-stenting neointimal formation and thrombosis. The study sought to evaluate whether stainless steel stents able to sequester endothelial progenitor cells (EPCs) to the stent surface to promote the endogenous arterial healing, can prevent in-stent restenosis and stent thrombosis. The HEALING-II study was a multicentre, prospective registry study, including 63 patients treated with the implantation of a Genous EPC capture stent. The primary safety endpoint was Major Adverse Cardiac Events (MACE) at 30 days, whereas the primary efficacy endpoint was percent in-stent volume obstruction at 6 months by intravascular ultrasound (IVUS). The 9 month composite MACE rate was 7.9%, whereas 6.3% clinically justified target lesion revascularisations were observed. Although patients received one month of clopidogrel, no angiographic stent thrombosis occurred. In-stent late luminal loss was 0.78+/-0.39 mm and percent in-stent volume obstruction was 22.9+/-13.7% (mean+/-sd). Patients with normal EPC titers at 6 months FU responded favourably to the EPC capturing stent (late luminal loss 0.53+/-0.06) as opposed to patients with low EPC titers (late luminal loss 1.01+/-0.07). These low circulating EPC titers were generally associated with the lack of HMG-Co-A reductase inhibitors ('statins') at the time of stent implantation and diabetes mellitus. The HEALING-II study suggests that the EPC capture coronary stents are safe and effective for the treatment of de novo coronary artery disease in patients with normal EPC levels.

Endothelial Progenitor Cells, Neointimal Hyperplasia, and Hemodialysis Vascular Access Dysfunction

Vascular stenosis as a result of neointimal hyperplasia is a major clinical problem that has an impact on multiple and diverse disciplines, including cardiology (coronary restenosis), cardiothoracic and vascular surgery (saphenous vein and polytetrafluoroethylene [PTFE] graft failure), neurology (carotid stenosis), nephrology (dialysis access dysfunction), and transplant medicine (chronic allograft rejection in hearts and kidneys). The traditional response to injury hypothesis on the pathogenesis of neointimal hyperplasia focuses on the migration of medial smooth muscle cells from the media into the intima.1 Recently, there has been a great deal of excitement about the role of circulating smooth muscle progenitor cells in the pathogenesis of neointimal hyperplasia. These cells have been identified in a variety of experimental models of vascular injury,2 and interventions that reduce the number of these cells can attenuate neointimal hyperplasia. In marked contrast to the deleterious effects of smooth muscle progenitor cells on neointimal hyperplasia, circulating endothelial progenitor cells (EPCs) are believed to play an important role in vascular repair and in the inhibition of neointimal hyperplasia.3 See p 12 In this issue of Circulation , Rotmans and colleagues have attempted to achieve the “holy grail” for a vascular access procedure: rapid and complete endothelialization.4 Their experiments are based on a newly developed technique that can coat the surface of stent and graft material with antibodies against CD34 (Orbus Medical Technologies). CD34 is a marker for hematopoietic stem cells, and previous research has demonstrated that coronary stents coated with anti-CD34 have a significant increase in endothelialization as early as 1 hour after deployment because of the binding of circulating CD34+ cells, which then differentiate into endothelial cells.5 Placement of anti-CD34–coated grafts in an arteriovenous model of PTFE graft stenosis by Rotmans et al resulted in almost complete endothelialization of the grafts (both …

Endothelial Progenitor Cell Capture by Stents Coated With Antibody Against CD34: The HEALING-FIM (Healthy Endothelial Accelerated Lining Inhibits Neointimal Growth-First In Man) Registry

This study was designed to evaluate whether rapid endothelialization of stainless steel stents with a functional endothelium prevents stent thrombosis and reduces the restenotic process. A "pro-healing" approach for prevention of post-stenting restenosis is theoretically favored over the use of cytotoxic or cytostatic local pharmacologic therapies. It is believed that the central role of the vascular endothelium is to maintain quiescence of the underlying media and adventitia. Sixteen patients with de novo coronary artery disease were successfully treated with implantation of endothelial progenitor cell (EPC) capture stents. Complete procedural and angiographic success was achieved in all 16 patients. The nine-month composite major adverse cardiac and cerebrovascular events (MACCE) rate was 6.3% as a result of a symptom-driven target vessel revascularization in a single patient. There were no other MACCE despite only one month of clopidogrel treatment. At six-month follow-up, mean angiographic late luminal loss was 0.63 +/- 0.52 mm, and percent stent volume obstruction by intravascular ultrasound analysis was 27.2 +/- 20.9%. This first human clinical investigation of this technology demonstrates that the EPC capture coronary stent is safe and feasible for the treatment of de novo coronary artery disease. Further developments in this technology are warranted to evaluate the efficacy of this device for the treatment of coronary artery disease.