Sustained safety and clinical performance of a drug-eluting absorbable metal scaffold up to 24 months: pooled outcomes of BIOSOLVE-II and BIOSOLVE-III.

AIMS: We aimed to assess the safety and performance of the DREAMS 2G scaffold up to 24 months post implant. METHODS AND RESULTS: The present study population comprises a total of 184 patients with 189 lesions who were enrolled in the prospective, multicentre BIOSOLVE-II and BIOSOLVE-III trials. Clinical follow-up was scheduled at one, six, 12, 24 and 36 months. The present report includes pooled follow-up data at six months and BIOSOLVE-II data at 24 months. Patients were 65.5±10.8 years old, and lesions were 12.5±5.1 mm long with reference diameters of 2.7±0.4 mm. Procedural success was obtained in 97.8%. At six months, the composite clinical endpoint target lesion failure was 3.3% (95% CI: 1.2-7.1), based on two cardiac deaths (1.1%, one unknown and one not device-related), one target vessel myocardial infarction (0.6%), and three clinically driven target lesion revascularisations (1.7%). For BIOSOLVE-II at 24 months, the target lesion failure rate was 5.9% (95% CI: 2.4-11.8), based on two cardiac deaths (1.7%), one target vessel myocardial infarction (0.9%) and four target lesion revascularisations (3.4%). There was no definite or probable scaffold thrombosis. CONCLUSIONS: The present analysis provides additional evidence on the safety of a drug-eluting absorbable metal scaffold with promising clinical outcomes up to 24 months and absence of definite or probable scaffold thrombosis.

Final results of the HEALING IIB trial to evaluate a bio-engineered CD34 antibody coated stent (Genous™Stent) designed to promote vascular healing by capture of circulating endothelial progenitor cells in CAD patients.

OBJECTIVE: To assess the safety and efficacy of the Genous™ endothelial progenitor cell (EPC) capturing stent in conjunction with HmG-CoA-reductase inhibitors (statins) to stimulate EPC recruitment, in the treatment of patients with de novo coronary artery lesions. METHODS AND RESULTS: The HEALING IIB study was a multi-center, prospective trial, including 100 patients. The primary efficacy endpoint was late luminal loss by QCA at 6-month follow-up (FU). Although statin therapy increased relative EPC levels by 5.6-fold, the angiographic outcome at 6 month FU was not improved in patients with an overall in-stent late luminal loss of 0.76±0.50 mm. The composite major adverse cardiac events (MACE) rate was 9.4%, whereas 6.3% clinically justified target lesion revascularizations (TLRs) were observed. 2 Patients died within the first 30 days after stent implantation due to angiographically verified in-stent thrombosis. At 12 month FU, MACE and TLR increased to 15.6% and 11.5% respectively and stabilized until 24 month FU. 18 Month angiographic FU showed a significant decrease in late luminal loss (0.67±0.54, 11.8% reduction or 10% by matched serial analysis, P=0.001). CONCLUSION: The HEALING IIB study suggests that statin therapy in combination with the EPC capture stent does not contribute to a reduction of in-stent restenosis formation for the treatment of de novo coronary artery disease. Although concomitant statin therapy was able to stimulate EPC recruitment, it did not improve the angiographic outcome of the bio-engineered EPC capture stent. Remarkably, angiographic late loss was significantly reduced between 6 and 18 months.

Procedural, 30-day and one year outcome following CoreValve or Edwards transcatheter aortic valve implantation: results of the Belgian national registry.

We report clinical outcomes following transcatheter aortic valve implantation (TAVI), using the CoreValve revalving system (18 Fr transfemoral or subclavian) or the Edwards Sapien valve (22 Fr transfemoral or 24 Fr transapical) as part of a Belgian prospective non-randomized multicentre registry. All 15 Belgian centres performing TAVI participated to this registry (seven exclusively Edwards Sapien, eight exclusively CoreValve). All consecutive high-risk symptomatic patients with severe aortic stenosis were evaluated by a heart team and screened for eligibility for TAVI. Three hundred and twenty-eight patients underwent TAVI with CoreValve (n = 141; eight subclavian and 133 transfemoral) or Edwards Sapien (n = 187; 99 transfemoral and 88 transapical) up to April 2010. Procedural success was 97%. One-month survival was 88% for the Edwards and 89% for the CoreValve treated patients. One-month mortality was both related to cardiac and non-cardiac reasons. Overall one-year survival was 78% in the CoreValve transfemoral treated patients, 100% in the CoreValve subclavian treated patients, 82% in the Edwards transfemoral treated patients and 63% in the Edwards transapical treated patients. This mid-term mortality was mainly related to age-related, non-cardiac complications.

Augmentation of wall shear stress inhibits neointimal hyperplasia after stent implantation: inhibition through reduction of inflammation?

BACKGROUND: Low wall shear stress (WSS) increases neointimal hyperplasia (NH) in vein grafts and stents. We studied the causal relationship between WSS and NH formation in stents by locally increasing WSS with a flow divider (Anti-Restenotic Diffuser, Endoart SA) placed in the center of the stent. METHODS AND RESULTS: In 9 rabbits fed a high-cholesterol diet for 2 months to induce endothelial dysfunction, 18 stents were implanted in the right and left external iliac arteries (1 stent per vessel). Lumen diameters were measured by quantitative angiography before and after implantation and at 4-week follow-up, at which time, macrophage accumulation and interruption of the internal elastic lamina was determined. Cross sections of stent segments within the ARED (S+ARED), outside the ARED (S[minus]ARED), and in corresponding segments of the contralateral control stent (SCTRL) were analyzed. Changes in WSS induced by the ARED placement were derived by computational fluid dynamics. Computational fluid dynamics analysis demonstrated that WSS increased from 0.38 to 0.82 N/m2 in the S+ARED immediately after ARED placement. This augmentation of shear stress was accompanied by (1) lower mean late luminal loss by quantitative angiography ([minus]0.23+/-0.22 versus [minus]0.58+/-0.30 mm, P=0.02), (2) reduction in NH (1.48+/-0.58, 2.46+/-1.25, and 2.36+/-1.13 mm2, P<0.01, respectively, for S+ARED, S[minus]ARED, and SCTRL), and (3) a reduced inflammation score and a reduced injury score. Increments in shear stress did not change the relationship between injury score and NH or between inflammation score and NH. CONCLUSIONS: The newly developed ARED flow divider significantly increases WSS, and this local increment in WSS is accompanied by a local reduction in NH and a local reduction in inflammation and injury. The present study is therefore the first to provide direct evidence for an important modulating role of shear stress in in-stent neointimal hyperplasia.