BackgroundTo investigate single and joint associations of body mass index (BMI) and serum high-sensitivity C-reactive protein (hsCRP) with death.MethodsThe study included 1871 coronary artery disease (CAD) patients aged 40–85 year-old recruited from 2008 to 2011. Cox regression models were used to estimate the association of BMI and hsCRP with mortality. The data was analyzed in 2014.ResultsDuring 3.1 years follow-up, 141 deaths were recorded, 110 died of cardiovascular disease (CVD). After adjustment of major CVD risk factors, there was a J-shaped association between BMI and all-cause and CVD mortality, and a positive association between hsCRP and mortality. The J-shaped association of BMI with mortality was present among patients who never smoked or with elevated hsCRP (≥3.0 mg/L). Compared with overweight (BMI 24–27.9 kg/m2) patients with normal hsCRP (<3.0 mg/L), obese patients (BMI≥28 kg/m2) with elevated hsCRP had a 3.41-fold risk of all-cause mortality (95% CI 1.49–7.80) and a 3.50-fold risk of CVD mortality (1.40–8.75), lean patients (BMI<24 kg/m2) with elevated hsCRP concentration had a 2.54-fold risk of all-cause mortality (1.36–4.74) and a 2.36-fold risk of CVD mortality (1.19–4.70).ConclusionsThe association pattern between baseline BMI and mortality changed among different baseline hsCRP concentrations, indicating that low-grade inflammation may be related to BMI and secondary prognosis of CAD.

Objectives: Several studies have investigated the association between serum uric acid (SUA) and the risks of coronary artery disease (CAD) but have yielded inconsistent results. The aim of this study was to assess whether there is an independent association of SUA with all-cause and cardiovascular disease (CVD) mortality in Chinese patients with CAD. Methods: A prospective cohort study of 1,799 patients was conducted. Cox regression models were used to estimate the association of SUA with the risk of death. Results: During a median follow-up of 3.9 years, 177 deaths were recorded and 126 of these were due to CVD. Patients in the highest SUA quartile had a 2.43-fold risk of all-cause mortality and a 2.44-fold risk of CVD mortality compared with those in the lowest quartile. In the subpopulation analysis, the association between SUA and mortality remained similar when participants were stratified by age, gender, body mass index and type of CAD. In contrast, we found a significant interaction with estimated glomerular filtration rate (eGFR). There was a stronger association between SUA and the risk of all-cause and CVD mortality among patients with an eGFR ≥60 ml/min/1.73 m², but no significant association was found in the population with an eGFR <60 ml/min/1.73 m². Conclusions: Elevated SUA levels were positively associated with an increased risk of all-cause and CVD mortality among CAD patients.

BackgroundLipoprotein (a) (Lp [a]) is known being correlated with coronary artery disease (CAD). The SLC22A3-LPAL2-LPA gene cluster, relating with modulating the level of plasma Lp (a), has recently been reported to be associated with CAD in Caucasians. The purpose of this study was to verify whether this finding can be expanded to the Chinese Han population.Methods and ResultsUsing a Chinese Han sample, which consisted of 1012 well-characterized CAD patients and 889 healthy controls, we tested the associations of four SNPs (rs2048327, rs3127599, rs7767084 and rs10755578) in the SLC22A3-LPAL2-LPA gene cluster, and their inferred haplotypes with the risk of CAD. Allelic, genotypic and haplotype association analyses all showed that the gene cluster was not associated with CAD in this Chinese Han sample.ConclusionsWe for the first time explored the association of the four SNPs in the SLC22A3-LPAL2-LPA gene cluster with CAD in a large Chinese Han sample. Nevertheless, this study did not reveal any significant evidence of this gene cluster to increase the risk of CAD in this population.

BackgroundIncreased blood hepcidin may be associated with the presence and promotion of atherosclerosis, the association of hepcidin with mortality among coronary artery disease (CAD) patients remains unknown. We sought to assess the relationship of hepcidin and all-cause and cardiovascular disease (CVD) mortality among CAD patients with and without acute coronary syndrome (ACS).Methods and ResultsThis study included 759 patients with ACS and 526 patients with stable CAD. After an average follow-up of 4.1 years, 154 deaths were recorded, 114 were due to CVD. After adjusting for CVD risk factors and inflammatory markers, the plasma hepcidin was positively associated with all-cause and CVD mortality in the ACS patients, the multivariable-adjusted hazard ratios (HRs) across tertiles of hepcidin were 1.00, 2.18 (95% CI 1.23-3.94), and 2.82 (95% CI 1.59-5.12) for all-cause mortality (Ptrend=0.006), and 1.00, 2.20 (95% CI 1.12-4.05), and 2.64 (95% CI 1.41-5.65) for CVD mortality (Ptrend=0.01). The C-index and net reclassification improvement when including hepcidin in traditional CVD models were 1.6% and 21.5% for all-cause mortality, 1.4% and 23.5% for CVD mortality, respectively, (P<0.001).ConclusionsPlasma hepcidin was positively associated with mortality in ACS patients. Hepcidin may be a potential biomarker for risk prediction in ACS patients.

Proper administration of antithrombotic and antiplatelet drugs after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) and renal insufficiency is a challenging task. In this study, we utilized Fondaparinux and Tirofiban (either separately or combined) to treat post-PCI patients with ACS and concurrent renal insufficiency. The patients were followed-up for 1 year. We observed that combined treatment led to a higher number of significant therapeutic effects and better reduced the frequency of bleeding events. Our findings indicate that combined antithrombotic and antiplatelet treatment improves the prognosis in patients with ACS and renal insufficiency who received PCI treatment.