CE Mark approval in September 2011 and to date over 100 commercial implants have been performed. The device is composed of a porcine biologic valve attached to a self-expanding nitinol stent designed for simple 2-step implantation and characterized by controlled positioning, self-seating in the native annulus resulting in a negligible paravalvular leak rate. The device was tested in patients at high-risk for mortality with open surgical repair. Methods: Ninety (90) patients (femaleϭ69%) with severe aortic stenosis, a mean age of 83.4 Ϯ 4.1 years, all presenting with NYHA Functional Class III or IV and a mean STS Score of 7.9 Ϯ 4.6 were enrolled in two studies in Germany at 6 centers. Patients are clinically followed at 7 and 30 days, at 6 and 12 months, and annually thereafter out to 5 years post-implant. The device was successfully implanted in 94.4% of patients (nϭ85) with a pacemaker implantation rate of 11.1% (nϭ10). Results: At 12 months the survival rate is 81.1% (nϭ73), the stroke rate is 4.4% (nϭ4), with no further re-intervention required on the implanted device since procedure. Of the returning patients, 87% presented with NYHA Functional Class I/II. The mean gradient at 6 months is 10.3 Ϯ 5.2 mmHg, the mean EOA is 1.5 Ϯ 0.4 cm2 and 77.3% of returning patients suffered no paravalvular leak, 21.2% exhibit mild paravalvular leak (ϩ1) and only 1 patient possesses a moderate paravalvular leak (ϩ2). Conclusions: These data confirm the safety profile at one year of this 2nd Generation TAVI system. We will report the full 12 months results of this multi-center, nonrandomized study of this transapically-placed transcatheter aortic valve at TCT 2012.

Coronary angiography, PCI, and survival to discharge have increased in VT/VF OHCA survivors from event to hospitalization. However, a significant proportion of patients with VT/VF OHCA, especially those without STE, do not undergo coronary angiography and revascularization. Prospective studies are needed to determine whether this limitation has a survival effect.

Objective Lineage negative bone marrow cells (lin− BMCs) are enriched in endothelial progenitor cells (EPCs) and mediate vascular repair. Aging-associated senescence and apoptosis result in reduced number and functionality of lin− BMCs, impairing their pro-repair capacity. The molecular mechanisms underlying lin− BMC senescence and apoptosis are poorly understood. MicroRNAs (miRNAs) regulate many important biological processes. The identification of miRNA-mRNA networks that modulate the health and functionality of lin− BMCs is a critical step in understanding the process of vascular repair. The aim of this study was to characterize the role of miR-146a—Plk2 network in regulating lin− BMC senescence, apoptosis, and their angiogenic capability. Approach and Results Transcriptome analysis in lin− BMCs isolated from young and aged wild type (wt) and apoE−/− mice showed a significant age-associated increase in miR-146a expression. In silico analysis, expression study and Luciferase reporter assay established Plk2 as a direct target of miR-146a. MiR-146a overexpression in young lin− BMCs inhibited Plk2 expression, resulting in increased senescence and apoptosis, via p16Ink4a/p19Arf and p53, respectively, as well as impaired angiogenic capacity in vitro and in vivo. Conversely, suppression of miR-146a in aged lin− BMCs increased Plk2 expression, rejuvenated lin− BMCs, resulting in decreased senescence and apoptosis, leading to improved angiogenesis. Conclusions 1) miR-146a regulates lin− BMC senescence and apoptosis by suppressing Plk2 expression that, in turn, activates p16Ink4a/p19Arf and p53; and 2) modulation of miR-146a or its target Plk2 may represent a potential therapeutic intervention to improve lin− BMC-mediated angiogenesis and vascular repair.