BackgroundNT-proBNP has been widely regarded as a useful tool for diagnosis or exclusion of heart failure (HF) in many settings. However, in patients with acute exacerbation of chronic bronchitis (AECB), its roles have not been well described. The objective of this study was to evaluate the diagnostic performance of NT-proBNP for identifying left ventricular (LV) failure in such patients.Methods and Results311 AECB patients and 102 stable chronic bronchitis patients with no history of HF were enrolled. Plasma NT-proBNP concentrations were measured using Roche Elecsys. The European Society of Cardiology (ESC) diagnostic principles were adopted to identify HF and the diagnostic performance of NT-proBNP was evaluated by ROC. Our results showed, the median NT-proBNP level in patients with LV failure [4828.4 (2044.4–9203.6) ng/L] was significantly higher than that in those without LV failure [519.2 (179.1–1409.8) ng/L, p<0.001] and stable controls [207.5 (186.5–318.2) ng/L, p<0.001]. LV failure, renal function, atrial fibrillation and systolic pulmonary artery pressure were independent predictors of NT-proBNP levels (all p<0.05). The area under ROC curve (AUC) of NT-proBNP for identifying LV failure was 0.884, significantly superior to clinical judgment alone (AUC 0.835, p = 0.0294). At the optimal cutoff value of 935.0 ng/L, NT-proBNP yielded sensitivity 94.4%, specificity 68.2%, accuracy 74.3% and negative predictive value 97.6%. Adding the results of NT-proBNP to those of clinical judgment improved the diagnostic accuracy for LV failure.ConclusionAs a tool for diagnosis or exclusion of HF, NT-proBNP can help physicians identify LV failure in patients with AECB.

KCNN3 rs13376333 polymorphism was associated with lone AF in the Chinese Han population and the T allele carriers may be an independent predictive factor for lone AF.

The aim of this study was to compare renal impairment in patients with propylthiouracil (PTU)-induced small-vessel vasculitis and patients with primary anti-neutrophil cytoplasmic antibody (ANCA)-induced small-vessel vasculitis. The study compared the pathology and clinical conditions of 10 patients with PTU-associated small-vessel vasculitis and 18 patients with primary ANCA-associated small-vessel vasculitis. All patients showed manifestations of renal impairment. Compared with the primary ANCA-induced small-vessel vasculitis, patients with PTU-induced small-vessel vasculitis were mostly female (P<0.05) and deleloped the disease at a younger age (P<0.05). They had a higher positive rate of perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA; P<0.05), lower 24 h proteinuria content, lower serum creatinine (P<0.05) and milder histopathological lesions (P<0.05). A number of them had gross hematuria (P<0.05). They rarely used hormone and cytotoxic drugs (P<0.05) during treatment and had a better prognosis (P<0.05). In conclusion, PTU-induced small-vessel vasculitis has a milder pathology and clinical manifestations with a better prognosis.

ABSTRACT.We investigated the effect of atorvastatin on vascular endothelial function in moderately nicotine-dependent smokers. One hundred and sixty moderately nicotine-dependent smokers were randomly divided into the atorvastatin group (N = 80) and the control group (N = 80). Total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose levels, aspartate aminotransferase, total bilirubin, creatine phosphokinase, and brachial artery flow-mediated vasodilation function (FMD) were measured before and 12 months after atorvastatin treatment. After a 12-month atorvastatin therapy, the TC and LDL-C levels of patients were decreased significantly (P < 0.05) and the FMD of patients were improved significantly (P < 0.05). Compared with the control group, TC and LDL-C of the patients were significantly decreased (P < 0.05) and the FMD of the patients were significantly improved (P < 0.05). Atorvastatin may significantly improve endothelial function in moderately nicotinedependent smokers.

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The aim of this study was to determine the defibrillation threshold (DFT) of implantable cardioverter-defibrillators (ICDs) and outcomes of treatment. Sixty-four patients received cardioverter-defibrillator implantation. During implantation, the DFT was determined by the defibrillation safety margin (DSM). All patients were followed up for 12–48 months after the implantation. The overall DFT was 14.27±2.56 J and the DSM was 18.40±1.89 J. Malignant ventricular arrhythmias occurred in 42 patients following cardioverter-defibrillator implantation including 500 episodes of non-sustained ventricular tachycardia (VT) and 289 episodes of persistent VT. VT was treated using antitachycardia pacing (ATP); 265 episodes were treated successfully by a single ATP treatment (91.69%) and 12 episodes were treated successfully by two ATP treatments (4.15%). Twelve episodes were converted by low-energy electrical cardioversion (4.15%). A total of 175 ventricular fibrillation (VF) episodes were identified, of which 18 episodes automatically terminated prior to treatment. In total, 146 episodes were converted by a single cardioversion with a defibrillation energy of 13.21±2.58 J and 11 episodes were converted by two cardioversions with a defibrillation energy of 16.19±2.48 J. It is safe and feasible to determine the DFT by DSM measurement during cardioverterdefibrillator implantation.