Background. Obstruction of the access vein following cardiac pacemaker and defibrillator implantation is a common complication. However, the exact incidence and contributing risk factors are unknown. The aim of this study is to determine the incidence and analyze the contribution of each risk factor.Methods. 57 consecutive patients candidate for their first transvenous pacemaker, implantable cardioverter-defibrillator (ICD), or cardiac resynchronization therapy device implantation were enrolled. After implantation, venography of the ipsilateral peripheral arm was performed. Patients underwent their second venography after the follow-up period of 3 to 6 months.Results. 42 patients (13 females, mean age 59.71 ± 12.33) completed the study. The followup venography showed significant venous obstruction (more than 50%) in 9 (21%) patients, but in none of the individuals, venography revealed total occlusion of the veins. Patients with obstruction had more leads in their veins (2.56 ± 0.53 vs 1.58 ± 0.71, P = 0.001). Venous obstruction was significantly more prevalent in patients with implanted cardiac resynchronization therapy device compared with an ICD or pacemaker (p = 0. 01). Age, gender, diabetes mellitus, hypertension, ischemic heart disease and antiplatelet consumption did not reveal any other contribution to the risk of thrombosis. In multivariate analysis, total lead number was a positive predictor for venous occlusion (P = 0.015, OR:19.2, and CI: 1.7-207.1).Conclusion. Venous obstruction is relatively frequent after pacemaker or ICD implantation. This study also shows that pacemaker and ICD leads have a similar risk for lead-related venous obstruction. However, patients with multiple leads are associated with an increased risk.

PLR and NLR are two easily calculated and efficient indexes for predicting the no-reflow phenomenon in patients with STEMI undergoing PPCI. Therefore, they might be employed in accurate risk stratification when a patient is a candidate for PPCI and in accurately referring patients who would benefit greatly from PPCI.

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Coronary artery disease (CAD) is a multicellular disease characterized by chronic inflammation. Peripheral blood-mononuclear cells (PBMCs), as a critical component of immune system, actively cross-talk with pathophysiological conditions induced by endothelial cell injury, reflecting in perturbed PBMC expression. STAT1 is believed to be relevant to CAD pathogenesis through regulating key inflammatory processes and modulating STAT1 expression play key roles in fine-tuning CAD-related inflammatory processes. This study evaluated PBMC expressions of STAT1, and its regulators (miR-150 and miR-223) in a cohort including 72 patients with CAD with significant ( ≥ 50%) stenosis, 30 patients with insignificant ( < 50%) coronary stenosis (ICAD), and 74 healthy controls, and assessed potential of PBMC expressions to discriminate between patients and controls. We designed quantitative real-time polymerase chain reaction (RT-qPCR) assays and identified stable reference genes for normalizing PBMC quantities of miR-150, miR-223, and STAT1 applying geNorm algorithm to six small RNAs and five mRNAs. There was no significant difference between CAD and ICAD patients regarding STAT1 expression. However, both groups of patients had higher levels of STAT1 than healthy controls. miR-150 and miR-223 were differently expressed across three groups of subjects and were downregulated in patients compared with healthy controls, with the lowest expression levels being observed in patients with ICAD. ROC curves suggested that PBMC expressions may separate between different groups of study subjects. PBMC expressions also discriminated different clinical manifestations of CAD from ICADs or healthy controls. In conclusion, the present study reported PBMC dysregulations of STAT1, miR-150, and miR-223, in patients with significant or insignificant coronary stenosis and suggested that these changes may have diagnostic implications. K E Y W O R D Scoronary artery disease, microRNA, miR-150, miR-223, PBMC, peripheral blood mononuclear cell, STAT1

Background Cardiac involvement by sarcoidosis may affect any part of the heart such as the pericardium, atriums, ventricles, and papillary muscles. In this regard, the use of two‐dimensional speckle‐tracking strain has been reported to be valuable in detecting heart sarcoidosis and its distinction from cardiomyopathy. The aim of this study was to investigate subclinical cardiac involvement using 2D speckle tracking and its associated factors in patients with normal systolic function by 2D transthoracic echocardiography (TTE). Methods In this study, 55 patients with extra‐cardiac sarcoidosis and 21 normal people were evaluated by 2D speckle tracking. The mean longitudinal global strain for the left ventricle was calculated as an average of 16 segments per patient. Results The comparison of the mean 2D speckle‐tracking indices including GCS (global circumferential strain) SAXA, GCSSAXM, Average GCS, AP2LS, AP3LS, AP4LS, and also Average GLS (global longitudinal strain) showed a significant difference between the two groups. Also, the evaluation of each of the above indices with a specific cutoff point as well as a high sensitivity and acceptable specificity predicted the presence of sarcoidosis. The occurrence of changes in the above indices was independent of ventricular function by 2D echocardiography in these patients. Conclusions The marked changes in the 2D speckle‐tracking parameters in patients with extra‐cardiac sarcoidosis can be of great value in the prediction of cardiac involvement. The occurrence of the abovementioned cardiac changes can be completely independent of the involvement of left ventricular function and is therefore predictable in patients with normal ventricular function.

BackgroundSulfur mustard (SM) is a blister-forming agent that has been used as a chemical weapon. Sulfur mustard can cause damage in various organs, especially the skin, respiratory system, and eyes. Generally, the multiple complications of mustard gas result from its alkalizing potency; it reacts with cellular components like DNA, RNA, proteins, and lipid membranes.TGF-β is a multi-functional cytokine with multiple biological effects ranging from cell differentiation and growth inhibition to extracellular matrix stimulation, immunosuppression, and immunomodulation. TGF-β has 3 isoforms (TGF-β 1, 2, 3) and its signaling is mediated by its receptors: R1, R2 and intracellular Smads molecules.TGF-β has been shown to have anti-inflammatory effects. TGF-βs and their receptors also have an important role in modulation of skin inflammation, proliferation of epidermal cells, and wound healing, and they have been implicated in different types of skin inflammatory disorders.MethodsSeventeen exposed SM individuals (48.47 ± 9.3 years), 17 chronic dermatitis patients (46.52 ± 14.6 years), and 5 normal controls (44.00 ± 14.6 years) were enrolled in this study.Evaluation of TGF-βs and their receptors expressions was performed by semiquantitative RT-PCR. Only TGF1was analyzed immunohistochemically.ResultsOur results showed significant decreases in the expression percentages of TGF-β 1, 2 and R1, R2 in chemical victims in comparison with chronic dermatitis and normal subjects and significant decreases in the intensity of R1 and R2 expressions in chemical victims in comparison with chronic dermatitis and normal controls. (P value < 0.05)ConclusionsTGF-βs and their receptors appear to have a noticeable role in chronic inflammatory skin lesions caused by sulfur mustard.