In a randomized trial of 220 patients, angioplasty with a PCB was noninferior to paclitaxel-eluting stent implantation when used to treat DES-ISR. On the basis of these, as well as previous randomized trial data, PCB angioplasty offers an effective treatment for DES-ISR without the necessity of implanting additional metal layers for drug release. (A Safety and Efficacy Study of Paclitaxel-Eluting Balloon to Paclitaxel-Eluting Stent [PEPCAD]; NCT01622075).

Results of this large series of consecutive patients who underwent unprotected LM-PCI suggested that the SS-II has better long-term prognostic power in terms of mortality compared with the original purely angiographic SS.

TF-TAVR and MIAVR increased while SAVR and TA-TAVR trended down in the latter periods, which underscore a paradigm shift in the treatment of severe AS and the importance of surgeon adoption of TF-TAVR and MIAVR techniques. As the demand for minimally invasive modalities increases, further studies comparing MIAVR versus TF-TAVR in low and intermediate risk patients are warranted.

Twelve-month TVF was significantly higher in the highest rSS group; rSS with a cut-off of 5 might therefore allow the risk stratification of patients with complex lesions treated with a second-generation drug-eluting stent (Clinical-Trials.gov identifier: NCT 01157455).

The ventricular septal defect (VSD) is the most common congenital heart defect and no candidate susceptibility gene has been identified. Endocardial cushion and outflow septal morphogenesis, malalignment of which induces VSD, have been suggested to be mediated by the vascular endothelial growth factor (VEGF). Three single-nucleotide polymorphism (SNP) variants in promoter and 5 0 -UTR region of the VEGF gene, CÀ2578A (rs699947), GÀ1154A (rs1570360) and GÀ634C (rs2010963), were reported to alter its expression. We assessed the association in a Chinese population between these SNPs and VSD using a double approach: case-control and TDT designs. Among the three SNPs, only À634C allele was less frequently present in 222 patients compared to 352 controls (odds ratio: 0.76, 95% CI: 0.59 -0.97, X 2 ¼ 5.06, P ¼ 0.024, not significant after a Bonferroni correction). This was significantly less transmitted to VSD patients (trios: 142) (odds ratio: 0.39, 95% CI: 0.25-0.62, X 2 ¼ 8.11, df ¼ 1, P ¼ 0.004, corrected P ¼ 0.024). A similar result was observed for haplotype À2578C/À1154G/À634C allele in both studies (in TDT: X 2 ¼ 7.51, df ¼ 1, P ¼ 0.006, corrected P ¼ 0.048). All these associations for the first time demonstrated that -634C allele was in a significant protective association against VSD, suggesting that VEGF dysregulation was involved in the pathological processes of VSD.