Previous studies of implantable cardiac resynchronization therapy plus defibrillator (CRT-D) therapy used for primary prevention of sudden cardiac death have suggested that CRT-D therapy is less effective in patients with mild heart failure and a wide QRS complex. However, the long-term benefits are variable. We performed a meta-analysis of randomized trials identified in systematic searches of MEDLINE, EMBASE, and the Cochrane Database. Three studies (3858 patients) with a mean follow-up of 66 months were included. Overall, CRT-D therapy was associated with significantly lower all-cause mortality than was implantable cardioverter defibrillator (ICD) therapy (OR, 0.78; 95 % CI, 0.63–0.96; P = 0.02; I2 = 19 %). However, the risk of cardiac mortality was comparable between two groups (OR, 0.74; 95 % CI, 0.53–1.01; P = 0.06). CRT-D treatment was associated with a significantly lower risk of hospitalization for heart failure (OR, 0.67; 95 % CI, 0.50–0.89; P = 0.005; I2 = 55 %). The composite outcome of all-cause mortality and hospitalization for heart failure was also markedly lower with CRT-D therapy than with ICD treatment alone (OR, 0.67; 95 % CI, 0.57–0.77; P < 0.0001; I2 = 0 %). CRT-D therapy decreased the long-term risk of mortality and heart failure events in patients with mild heart failure with a wide QRS complex. However, long-term risk of cardiac mortality was similar between two groups. More randomized studies are needed to confirm these findings, especially in patients with NYHA class I heart failure or patients without LBBB.

Polymorphisms of the NR3C1 (glucocorticoid receptor) gene have been reported to be associated with altered glucocorticoids sensitivity and changes in body composition and metabolic parameters. This study explored the relationship between single nucleotide polymorphisms (SNPs) of the NR3C1 gene and metabolic syndrome (MetS) in a Chinese population. Fourteen tag-SNPs and five functionally important SNPs in the NR3C1 gene were genotyped in MetS patients (n = 431) and normal controls (n = 461) using the high-throughput Sequenom genotyping platform. Genotype, allelic and haplotype associations were examined using logistic regression and Haploview. There are four SNPs significantly associated with MetS. The T allele of rs2963156 was associated with an increased risk effect for MetS (adjusted OR = 1.66, 95 % CI 1.25–2.22, P = 0.001). By contrast, rs10052957 A allele carriers were significantly associated with a decreased risk of MetS (adjusted OR = 0.58, 95 % CI 0.42–0.80, P = 0.001). Rs41423247 GG genotype (adjusted OR = 2.01, 95 % CI 1.25–3.22, P = 0.004), and rs7701443 AA genotype (adjusted OR = 1.88, 95 % CI 1.24–2.83, P = 0.003) were significantly associated with an increased risk of MetS. Haplotype CGGA is risk conferring (adjusted OR = 1.53, 95 % CI 1.06–2.20, P = 0.023), whereas haplotype CCAG was protective (adjusted OR = 0.30, 95 % CI 0.20–0.47, P < 0.001). Polymorphism of NR3C1 gene is associated with MetS and may contribute to the susceptibility of MetS.

To investigate the association of tag-SNPs and haplotype structures of the CIDEA gene with obesity in a Han Chinese population. Five single nucleotide polymorphisms (SNPs) (rs1154588/V115F, rs4796955/SNP1, rs8092502/SNP2, rs12962340/SNP3 and rs7230480/SNP4) in the CIDEA gene were genotyped in a case–control study. Genotyping was performed using the sequenom matrix-assisted laser desorption/ionization time-of-flight mass spectrometry iPLEX platform. There were significant differences between the obese and control groups in genotype distributions of V115F (P < 0.001), SNP1 (P = 0.006) and SNP2 (P = 0.005). Carriers of V115F-TT, SNP1-GG and SNP2-CC genotypes had a 2.84-fold (95 % CI 1.73–4.66), 2.19-fold (95 % CI 1.09–4.38) and 4.37-fold (95 % CI 1.21–15.08) increased risk for obesity, respectively. Haplotype analysis showed that GTTC (SNP1/SNP2/V115F/SNP4) had 1.41-fold (95 % CI 1.02–1.95) increased risk for obesity; whereas, haplotype TTGC had 0.48-fold (95 % CI 0.24–0.96) decreased risk for obesity. Using the multifactor dimensionality reduction method, the best model including SNP1, SNP2, V115F and SNP4 polymorphisms was identified with a maximum testing accuracy to 59.32 % and a perfect cross-validation consistency of 10/10 (P = 0.011). Logistic analysis indicated that there was a significant interaction between SNP1 and V115F associated with obesity. Subjects having both genotypes of SNP1/GG and V115F/TT were more susceptible to obesity in the Han Chinese population (OR 2.66, 95 %: 1.22–5.80). Genotypes of V115F/TT, SNP1/GG and SNP2/CC and haplotype GTTC of CIDEA gene were identified as risk factors for obesity in the Han Chinese population. The interaction between SNP1 and V115F could play a joint role in the development of obesity.

N-glycans play an essential role in biological process and are associated with age, gender, and body mass parameters in Caucasian populations, whereas no study has been reported in Chinese populations. To investigate the correlation between N-glycan structures and metabolic syndrome (MetS) components, we conducted a population-based study in 212 Chinese Han individuals. The replication study was performed on 520 unrelated individuals from a Croatian island Korčula. The most prominent observation was the consistent positive correlations between different forms of triantennary glycans and negative correlations between glycans containing core-fucose with MetS components including BMI, SBP, DBP, and fasting plasma glucose (FPG) simultaneously. Significant differences in a number of N-glycan traits were also detected between normal and abnormal groups of BMI, BP, and FPG, respectively. In the multivariate analysis, the level of monosialylated glycans (structure loadings = −0.776) was the most correlated with the MetS related risk factors, especially with SBP (structure loadings = 0.907). Results presented here are showing that variations in the composition of the N-glycome in human plasma could represent the alternations of human metabolism and could be potential biomarkers of MetS.