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The circulating concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) has been shown to be a diagnostic tool for the detection of heart failure. Several factors influence NT-proBNP levels including age, sex, and body mass index (BMI). Therefore, the diagnostic sensitivity of NT-proBNP level for heart failure is relatively higher, but its specificity is low. This study aims to improve the diagnostic accuracy rate of this test by including multiple variables in the diagnostic test.The suspected chronic heart failure outpatients were divided into heart failure with reduced ejection fraction, heart failure with mid-range ejection fraction, heart failure with preserved ejection fraction, and normal heart function groups. Area under the receiver-operating characteristic (ROC) curve, cut-off value, and logistic regression analysis were used to select the model variables, sensitivity and specificity.In all, 436 subjects enrolled into this study were divided in 2 groups: model establishment (n = 300) and model validation (n = 136). In the model establishment group, the area under the curve (AUC) and cut-off value of NT-proBNP was 0.926 and 257.4 pg/mL, respectively. When age, glomerular filtration rate, BMI, atrial fibrillation, and sex were entered into the diagnosis model, AUC, sensitivity, and specificity further increased to 0.955 (95% confidence interval [CI] 0.934, 0.976), 94.2% (from 93.0%), and 86.7% (from 74.2%). The ROC curve of corrected NT-proBNP diagnostic formula for heart failure was also significantly higher (P = .037).The corrected NT-proBNP diagnostic formula was found to improve the diagnostic accuracy of chronic heart failure.

Introduction The mortality due to cardiogenic shock complicating acute myocardial infarction (AMI) is high even in patients with early revascularization. Infusion of low dose recombinant human brain natriuretic peptide (rhBNP) at the time of AMI is well tolerated and could improve cardiac function.Objective The objective of this study was to evaluate the hemodynamic effects of rhBNP in AMI patients revascularized by emergency percutaneous coronary intervention (PCI) who developed cardiogenic shock.Methods A total of 48 patients with acute ST segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock and whose hemodynamic status was improved following emergency PCI were enrolled. Patients were randomly assigned to rhBNP (n=25) and control (n=23) groups. In addition to standard therapy, study group individuals received rhBNP by continuous infusion at 0.005 µg kg−1 min−1 for 72 hours.Results Baseline characteristics, medications, and peak of cardiac troponin I (cTnI) were similar between both groups. rhBNP treatment resulted in consistently improved pulmonary capillary wedge pressure (PCWP) compared to the control group. Respectively, 7 and 9 patients died in experimental and control groups. No drug-related serious adverse events occurred in either group.Conclusion When added to standard care in stable patients with cardiogenic shock complicating anterior STEMI, low dose rhBNP improves PCWP and is well tolerated.

Background/Aims: Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction. Methods: Wild type mice (n=37), mice with cardiac-specific SIRT1 knockout (n=29), or overexpression (n=29), and corresponding controls, were randomized into four groups: sham MI (myocardial infarction) +sham STNx (subtotal nephrectomy); MI+sham STNx; sham MI+STNx; and MI+STNx. To establish the CRS model, subtotal nephrectomy (5/6 nephrectomy, SNTx) and myocardial infarction (MI) (induced by ligation of the left anterior descending (LAD) coronary artery) were performed successively to establish CRS model. At week 8, the mice were sacrificed after sequential echocardiographic and hemodynamic studies, and then pathology and Western-blot analysis were performed. Results: Neither MI nor STNx alone significantly influenced the other healthy organ. However, in MI groups, STNx led to more severe cardiac structural and functional deterioration, with increased remodeling, increased BNP levels, and decreased EF, Max +dp/dt, and Max -dp/dt values than in sham MI +STNx groups. Conversely, in STNx groups, MI led to renal structural and functional deterioration, with more severe morphologic changes, augmented desmin and decreased nephrin expression, and increased BUN, SCr and UCAR levels. In MI+STNx groups, SIRT1 knockout led to more severe cardiac structural and functional deterioration, with higher Masson-staining score and BNP levels, and lower EF, FS, Max +dp/dt, and Max -dp/dt values; while SIRT1 overexpression had the opposite attenuating effects. In kidney, SIRT1 knockout resulted in greater structural and functional deterioration, as evidenced by more severe morphologic changes, higher levels of UACR, BUN and SCr, and increased desmin and TGF-β expression, while SIRT1 overexpression resulted in less severe morphologic changes and increased nephrin expression without significant influence on BUN or SCr levels. The SIRT1 knockout but not overexpression resulted in increased myocardial expression of CHOP and GRP78. Cardiac-specific SIRT1 knockout or overexpression resulted in increased or decreased renal expression of CHOP, Bax, and p53 respectively. Conclusions: Myocardial SIRT1 activation appears protective to both heart and kidney in CRS models, probably through modulation of ER stress.

Permanent left bundle branch area pacing (LBBP) is a promising physiological pacing technique that has emerged in recent years. However, LBBP is almost exclusively clinically applied in adult patients. The feasibility and safety of the use of LBBP in children have not been well-assessed. Here, we report the case of a 6-year-old child with a third-degree atrioventricular block after surgical aortic valve replacement who successfully received a permanent LBBP.congenital heart disease, left bundle branch area pacing, third-degree atrioventricular block

Chronic BNP infusion can provide beneficial effects against adverse post-MI remodelling.

Background: Syncope is a perplexing challenge that often receives thorough evaluation, yet the diagnosis remains unclear. Usually, the emergency department is the first point at which patients present with syncope. However, diverse medical factors, including low diagnostic rates and inconsistent management by doctors, add to healthcare costs and delay diagnosis for syncope patients. Methods:Patients who had been to the emergency department at least once but were not given a clear diagnosis of syncope were recruited into our study at the time they visited syncope clinic staffed by a multidisciplinary team. Complete medical histories and clinical examinations were conducted by both experienced cardiologists and neurologists. If patients were not given a conclusive diagnosis at the syncope clinic on the basis of outpatient examinations, they were admitted for further evaluation.Results: A total of 209 consecutive patients claiming "syncope" visited the syncope clinic, yet only 167 patients were formally diagnosed with syncope. For these 167 patients, the mean age was 55.93 ± 17.40 years old, and 41.3% were male. The proportions of cardiac syncope, reflex syncope, orthostatic hypotension (OH), and syncope of uncertain etiology were 19.8%, 64.1%, 7.8%, and 8.4%, respectively. The diagnostic rate was 91.6%, and the hospitalization rate was 23.4%. Patients with reflex syncope and OH were younger than patients with cardiac syncope. Cardiac syncope tends to occur more frequently in males, while reflex syncope is more likely in females. Conclusions:The cooperation of professional cardiologists and neurologists will play an important role in improving diagnostic rates, lowering admission rates, and reducing medical costs. K E Y W O R D S diagnosis, multidisciplinary team, syncope, syncope clinicThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Background: Myocardial ischemia/reperfusion (I/R) injury is common during the treatment of cardiovascular diseases. Neuronal PAS Domain Protein 2 (NPAS2) is one of the core genes that control the rhythm of the biological clock. NPAS2 also regulates the biological rhythm. Results: The rat I/R model showed that the expression of NPAS2 decreased with the increase of reperfusion time. Overexpressing NPAS2 adenovirus (ad-NPAS2) was injected into IR rat which demonstrated that ad-NPAS2 ameliorated rats I/R injury. A hypoxia/reoxygenation (H/R) model in rat cardiomyocytes showed that ad-NPAS2 inhibited cardiomyocyte apoptosis. Co-Immunoprecipitation results showed that there is an interaction between NPAS2 and Cry2. Knockdown of Cry2 aggravated the cardiomyocyte apoptosis induced by H/R. Additionally, NPAS2 directly act on the promoter region of CX3CL1. Knockdown of CX3CL1 reverse the protective effect of ad-NPAS2 on rat myocardial ischemia-reperfusion injury and H/R-induced cardiomyocyte apoptosis. CX3CL1 also regulates autophagy through the downstream AKT/mTOR pathway. Conclusions: research demonstrated that overexpression of NPAS2 interacts with Cry2 and promotes the transcriptional activity of CX3CL1. Moreover, overexpression of NPAS2 regulates the downstream AKT/mTOR pathway to inhibit autophagy in order to improve rat cardiac I/R injury.