Radial artery thrombosis is a frequent complication after transradial coronary angiography. Incidence of RA occlusion is underestimated due to the often asymptomatic clinical course. Treatment of symptomatic RA occlusion with low-molecular-weight heparins significantly increases patency rates after 4 weeks.

Enzymes involved in the metabolism nitric oxide (NO) and reactive oxygen species (ROS) may play a role for the decreased availability of NO in atherosclerosis. We, therefore, hypothesized that the pattern of gene expression of these enzymes is altered in atherosclerosis. Myocardial tissue from patients with coronary heart disease (CHD) or without CHD (control group) was investigated. The level of enzymes related to NO/ROS metabolism was determined both at mRNA level and protein level by rt-PCR, real-time PCR, and western blot. The expression of NOS1-3 (synthesis of NO), arginase1 (reduction of L-arginine), p22phox (active subunit of NADPH oxidase), GTPCH (rate limiting enzyme for tetrahydrobiopterin), SOD1-3 (scavengers of superoxide anions), PRTMT1-3, and DDAH2 (involved in the metabolism of ADMA) was determined. All enzymes were found to be expressed in human myocardium. NOS isoforms were decreased in CHD in protein level, but only the downregulation of NOS3 expression reached statistical significance. The expression of PRMT1 and PRMT3 was increased. In addition, the expression of DDAH2 was reduced, both theoretically leading to an increase of ADMA concentration. SOD3 was downregulated in tissue from patients with CHD. Taken together, in myocardial tissue from patients with atherosclerosis, the expression of genes increasing ADMA levels is enhanced in contrast to a reduced expression of genes promoting NO synthesis. These results may contribute to the explanation of increased oxidative stress in atherosclerosis on the level of gene expression.

Abstract. Andrassy M, Volz HC, Riedle N, Gitsioudis G, Seidel C, Laohachewin D, Zankl AR, Kaya Z, Bierhaus A, Giannitsis E, Katus HA, Korosoglou G (University of Heidelberg, Heidelberg, Germany). HMGB1 as a predictor of infarct transmurality and functional recovery in patients with myocardial infarction. J Intern Med 2011; 270: 245-253.Objectives. High-mobility group box 1 (HMGB1) protein is an innate danger signal for the initiation of host defence and tissue repair. The aim of this study was to analyse serum HMGB1 concentration and its correlation with infarct transmurality and functional recovery in patients with ST-elevation (STEMI) and non-ST-elevation myocardial infarction (NSTEMI).Design. We prospectively examined patients with firsttime STEMI (n = 46) or NSTEMI (n = 49), treated according to current guidelines. Contrast-enhanced cardiac magnetic resonance imaging was performed 2-4 days after infarction for the estimation of infarct transmurality and was repeated after 6 months for the estimation of residual left ventricular function. HMGB1 was measured 2-4 days after infarction.Results. High-mobility group box 1 concentration was related to infarct size and to residual ejection fraction in patients with STEMI (r 2 = 0.81 and r 2 = 0.40, respectively, P < 0.001 for both) and NSTEMI (r 2 = 0.74 and r 2 = 0.25, respectively, P < 0.001 for both). Receiver operating characteristic (ROC) curvederived cut-off values of 6.2 and 5.9 ng mL )1 for patients with STEMI and NSTEMI, respectively, were predictive of infarct transmurality greater than 75% (STEMI: area under the curve (AUC) = 0. Conclusion. High-mobility group box 1 serum levels represent a highly valuable surrogate marker for infarct transmurality and for the prediction of residual left ventricular function after MI.

With increasing age of the population and improvement of diagnostic tools, the incidence of abdominal aortic aneurysms (AAA) has been rising steadily. Despite an improvement in operative and interventional treatment options, AAA is the cause of death in 1-3% of men over 65 years of age in industrial countries, mostly due to rupture [1]. Therefore, routine screening for AAA by ultrasonography has been postulated in the past: a 60 year old man with an abdominal aortic diameter of less than 3 cm has a life-time risk of developing AAA close to zero. However, routine screening has not been found to be cost effective. Despite of the results of two well-designed studies, the limits of AAA qualifying the patient for surgery or intervention in contrast to conservative treatment is still a matter of debate. The present review article summarizes the current knowledge of the pathology, incidence, risks, natural course as well as symptoms and current treatment strategies of AAA on the basis of the recent literature.

SummaryIn muscle cells, a complex network of Z-disc proteins allows proper reception, transduction and transmission of mechanical and biochemical signals. Mutations in genes encoding different Z-disc proteins such as integrin-linked kinase (ILK) and nexilin have recently been shown to cause heart failure by distinct mechanisms such as disturbed mechanosensing, altered mechanotransduction or mechanical Z-disc destabilization. We identified core-binding factor  (CBF) as an essential component for maintaining sarcomeric Z-disc and myofilament organization in heart and skeletal muscle. In CBF-deficient cardiomyocytes and skeletal-muscle cells, myofilaments are thinned and Z-discs are misaligned, leading to progressive impairment of heart and skeletal-muscle function. Transcription of the gene encoding CBF mainly depends on JunB activity. In JunB-morphant zebrafish, which show a heart-failure phenotype similar to that of CBF-deficient zebrafish, transcript and protein levels of CBF are severely reduced. Accordingly, ectopic expression of CBF can reconstitute cardiomyocyte function and rescue heart failure in JunB morphants, demonstrating for the first time an essential role of JunB-CBF signaling for maintaining sarcomere architecture and function.