Influence of Body Mass Index on the Prognostic Value of N-Terminal Pro-B-Type Natriuretic Peptide Level in Chinese Patients with Heart Failure.

N-terminal pro-B-type natriuretic peptide (NT-proBNP) is an essential biomarker for the prediction of heart failure (HF), but its prognostic ability across body mass index (BMI) categories needs to be clarified. Our study aimed to explore the association between BMI and NT-proBNP and assess the effect of BMI on the prognostic ability of NT-proBNP in Chinese patients with HF. We retrospectively analyzed clinical data from the FuWai Hospital HF Center in Beijing, China. According to the Chinese adult BMI standard, 1,508 patients with HF were classified into four groups: underweight (BMI < 18.5 kg/m2), normal weight (BMI 18.5-23.9 kg/m2, as a reference category), overweight (BMI 24-27.9 kg/m2), and obesity (BMI ≥ 28 kg/m2). NT-proBNP was examined for its prognostic role in adverse events as an endpoint. BMI was independently and negatively associated with NT-proBNP (ß = -0.074; P < 0.001), and NT-proBNP levels tended to decrease as BMI increased across the different BMI categories. The results of our study differ from those of other studies of European-American populations. In this study, NT-proBNP was a weak predictor of a 4-year adverse prognosis in underweight patients (BMI < 18.5 kg/m2). In other BMI categories, NT-proBNP was an independent predictor of adverse events in HF. BMI and sex significantly affected the optimal threshold for NT-proBNP to predict the risk of adverse events. There is a negative correlation between BMI and NT-proBNP, and NT-proBNP independently predicts adverse HF events in patients with a BMI of ≥ 18.5 kg/m2. The optimal risk prediction cutoffs are lower in patients who are overweight and obese.

Comparison of platelet reactivity between prasugrel and ticagrelor in patients with acute coronary syndrome: a meta-analysis.

BACKGROUND: This meta-analysis aimed to compare the effects of prasugrel and ticagrelor on high (HTPR) and low on-treatment platelet reactivity (LTPR) in patients with acute coronary syndrome (ACS). METHODS: Eligible studies were retrieved from PubMed, Embase, and the Cochrane Library. HTPR and LTPR were evaluated on the basis of the vasodilator-stimulated phosphoprotein platelet reactivity index (VASP-PRI) and P2Y12 reaction units (PRUs). HTPR and LTPR were analyzed using risk ratios (RRs) and their 95% confidence intervals (CIs). Weighted mean difference (WMD) and 95% CI were used to calculate the pooled effect size of platelet reactivity (PR). RESULTS: Fourteen eligible studies were obtained, which included 2629 patients treated with ticagrelor (n = 1340) and prasugrel (n = 1289). The pooled results showed that the prasugrel-treated patients had higher platelet reactivity than the ticagrelor-treated patients (PRU: WMD = - 32.26; 95% CI: - 56.48 to - 8.76; P < 0.01; VASP-PRI: WMD = - 9.61; 95% CI: - 14.63 to - 4.60; P = 0.002). No significant difference in HTPR based on PRU was identified between the ticagrelor and prasugrel groups (P = 0.71), whereas a lower HTPR based on VASP-PRI was found in the ticagrelor-treated patients than in the prasugrel-treated patients (RR = 0.30; 95% CI: 0.12-0.75; P = 0.010). In addition, the results showed a lower LTPR was observed in the prasugrel group than in the ticagrelor group (RR = 1.40; 95% CI: 1.08-1.81; P = 0.01). CONCLUSIONS: Prasugrel might enable higher platelet reactivity than ticagrelor. Ticagrelor could lead to a decrease in HTPR and increase in LTPR. However, this result was only obtained in pooled observational studies. Several uncertainties such as the nondeterminancy of the effectiveness of ticagrelor estimated using VASP-PRI or the definition of HTPR (a high or modifiable risk factor) might have affected our results.

Exploration of Novel Biomarkers in Vasculitis by Integrated Bioinfomatic Approaches.

Angiitis, also known as vasculitis, is a chronic inflammatory disease characterized by the infiltration of inflammatory cells in surroundings of blood vessels, accompanied by vascular damage including fibrin deposition, collagen fiber degeneration, myocyte, and endotheliocyte necrosis. This work aimed to perform an integrated bioinformatic analysis of three data sets concerning vasculitis to explore and examine the potential diagnostic and therapeutic makers contributing to illuminating the pathomechanisms of vasculitis. We collected three sets of gene expression data designed by dual-channel method from Gene Expression Omnibus, which were based on the same platform (Agilent-014850 Whole Human Genome Microarray 4x44K G4112F). The meta-analysis was used to analyze the gene expression profiles and screen the differentially expressed genes followed by functional features identification. Subsequently, a protein-protein interaction and transcriptional regulation network were conducted for further investigation of expression mechanisms of vasculitis. Totally, 73 consistently upregulated genes, 49 consistently downregulated genes, and 26 genes with different expression directions were identified. Functional enrichment and transcription regulation analysis suggested upregulated genes (PPBP, PLAU, and HIST1H2BH) and downregulated genes such as IL23A gene were predominately associated with immune responses and cytokine receptors function. In addition, specific cancer-related genes such as MRVI1 was also extracted and considered as promising biomarkers of the development and progression of vasculitis. This study established an integrated meta-analysis approach and identified novel biomarkers involved in vasculitis, which further facilitate to explore and unravel the etiopathogenesis of vasculitis.