Randomized comparison of Glidesheath Slender with conventional 5Fr arterial sheaths for coronary angiography through the distal radial artery.

BACKGROUND: The potential benefits of the thin-walled 5F Glidesheath Slender sheath in the distal transradial access (dTRA) have not been investigated. This study aimed to compare the Glidesheath Slender versus conventional 5Fr arterial sheaths in patients undergoing diagnostic coronary angiography (CAG) through the dTRA. METHODS: A total of 352 consecutive patients with an indication for CAG were randomized (1:1) to Glidesheath Slender 5Fr versus a conventional 5Fr arterial sheath for dTRA. The primary endpoint was the rate of successful hemostasis at 30 minutes after sheath removal. Follow-up ultrasound of the right radial and distal radial artery was performed 7-10 days after the procedure. RESULTS: After exclusion of patients where a 6Fr sheath or crossover of access site was required, 108 patients in the Glidesheath Slender and 105 patients in the conventional 5Fr arterial sheath group were included in the analysis. The crossover rate to conventional radial access and the rate of successful hemostasis at 30 minutes after sheath removal were similar between the two groups (18.9% in the Glidesheath slender vs. 22% in the control group; P=0.460, and 62% vs. 51.4%; P=0.118, respectively). The level of pain associated with the procedure was significantly lower in the Glidesheath Slender group (2.69 vs. 3.29 in the control group; P=0.02). No significant difference was recorded between the two groups in the rate of access-related complications. CONCLUSIONS: Use of Glidesheath Slender for dTRA did not increase the rate of early hemostasis compared with conventional arterial sheath.

The role of noncoding genetic variants in cardiomyopathy.

Cardiomyopathies remain one of the leading causes of morbidity and mortality worldwide. Environmental risk factors and genetic predisposition account for most cardiomyopathy cases. As with all complex diseases, there are significant challenges in the interpretation of the molecular mechanisms underlying cardiomyopathy-associated genetic variants. Given the technical improvements and reduced costs of DNA sequence technologies, an increasing number of patients are now undergoing genetic testing, resulting in a continuously expanding list of novel mutations. However, many patients carry noncoding genetic variants, and although emerging evidence supports their contribution to cardiac disease, their role in cardiomyopathies remains largely understudied. In this review, we summarize published studies reporting on the association of different types of noncoding variants with various types of cardiomyopathies. We focus on variants within transcriptional enhancers, promoters, intronic sites, and untranslated regions that are likely associated with cardiac disease. Given the broad nature of this topic, we provide an overview of studies that are relatively recent and have sufficient evidence to support a significant degree of causality. We believe that more research with additional validation of noncoding genetic variants will provide further mechanistic insights on the development of cardiac disease, and noncoding variants will be increasingly incorporated in future genetic screening tests.

Advanced Gene-Targeting Therapies for Motor Neuron Diseases and Muscular Dystrophies.

Gene therapy is a revolutionary, cutting-edge approach to permanently ameliorate or amend many neuromuscular diseases by targeting their genetic origins. Motor neuron diseases and muscular dystrophies, whose genetic causes are well known, are the frontiers of this research revolution. Several genetic treatments, with diverse mechanisms of action and delivery methods, have been approved during the past decade and have demonstrated remarkable results. However, despite the high number of genetic treatments studied preclinically, those that have been advanced to clinical trials are significantly fewer. The most clinically advanced treatments include adeno-associated virus gene replacement therapy, antisense oligonucleotides, and RNA interference. This review provides a comprehensive overview of the advanced gene therapies for motor neuron diseases (i.e., amyotrophic lateral sclerosis and spinal muscular atrophy) and muscular dystrophies (i.e., Duchenne muscular dystrophy, limb-girdle muscular dystrophy, and myotonic dystrophy) tested in clinical trials. Emphasis has been placed on those methods that are a few steps away from their authoritative approval.