A Case of Using the Distal Radial Artery to Open an Occluded Radial Artery.

We describe a case of radial artery occlusion caused by previous percutaneous coronary intervention. The occluded radial artery was opened through the distal radial artery, and left main coronary artery intervention was subsequently performed. Follow-up vascular ultrasound showed that the radial artery had smooth blood flow and no stenosis. (Level of Difficulty: Intermediate.).

Atrial overexpression of microRNA-27b attenuates angiotensin II-induced atrial fibrosis and fibrillation by targeting ALK5.

Atrial fibrosis influences atrial fibrillation (AF) development by transforming growth factor beta 1 (TGF-ß1)/Smad pathway. Although microRNAs are implicated in the pathogenesis of various diseases, information regarding the functional role of microRNAs in atrial dysfunction is limited. In the present study, we found that microRNA-27b (miR-27b) was the dominant member of miR-27 family expressed in left atrium. Moreover, the expression of miR-27b was significantly reduced after angiotensin II (AngII) infusion. Masson's trichrome staining revealed that delivery of miR-27b adeno-associated virus to left atrium led to a decrease in atrial fibrosis induced by AngII. The increased expression of collagen I, collagen III, plasminogen activator inhibitor type 1 and alpha smooth muscle actin was also inhibited after miR-27b upregulation. In isolated perfused hearts, miR-27b restoration markedly attenuated AngII-induced increase in interatrial conduction time, AF incidence and AF duration. Furthermore, our data evidence that miR-27b is a novel miRNA that targets ALK5, a receptor of TGF-ß1, through binding to the 3' untranslated region of ALK5 mRNA. Ectopic miR-27b suppressed luciferase activity and expression of ALK5, whereas inhibition of miR-27b increased ALK5 luciferase activity and expression. Additionally, miR-27b inhibited AngII-induced Smad-2/3 phosphorylation without altering Smad-1 activity. Taken together, our study demonstrates that miR-27b ameliorates atrial fibrosis and AF through inactivation of Smad-2/3 pathway by targeting ALK5, suggesting miR-27b may play an anti-fibrotic role in left atrium and function as a novel therapeutic target for the treatment of cardiac dysfunction.

Effects of dabigatran regulates no­reflow phenomenon in acute myocardial infarction mice through anti­inflammatory and anti­oxidative activities and connective tissue growth factor expression.

Pradaxa is a novel oral anticoagulant, which was originally used to prevent thrombosis following joint replacement surgery. The aim of the current study was to investigate the effect dabigatran on acute myocardial infarction through regulating no­reflow phenomenon and oxidative stress, neutrophil intraplaque infiltration and apoptosis. In the present study, dabigatran significantly inhibited the infarct size, increased arterial pressure and reduced no­reflow phenomenon in acute myocardial infarction (AMI) vehicle rabbits. Treatment with dabigatran significantly inhibited the P65 of nuclear factor κB, tumor necrosis factor α, interleukin (IL)­1ß and IL­6 activities and significantly enhanced the catalase and superoxide dismutase activities in the AMI rabbits. In addition, dabigatran significantly suppressed inducible nitric oxide synthase (iNOS), collagen I, transforming growth factor ß1 (TGF­ß1), α­smooth muscle actin (α­SMA) and connective tissue growth factor (CTGF) protein expression in AMI rabbits. Taken together, these results suggest that the effects of dabigatran inhibit no­reflow phenomenon, infarct size and enhance arterial pressure in AMI through anti­inflammatory and anti­oxidative activity, and regulating iNOS, collagen I, TGF­ß1, α­SMA and CTGF protein expression in AMI rabbits.