BackgroundIt is demonstrated that elevated serum levels of alkaline phosphatase (ALP) and phosphate indicate a higher risks of cardiovascular disease (CVD) and total mortality in population with chronic kidney disease (CKD), but it remains unclear whether this association exists in people with normal or preserved renal function.MethodClinical trials were searched from Embase and PubMed from inception to 2013 December using the keywords “ALP”, “phosphate”, “CVD”, “mortality” and so on, and finally 24 trials with a total of 147634 patients were included in this study. Dose-response and semi-parametric meta-analyses were performed.ResultsA linear association of serum levels of ALP and phosphate with risks of coronary heart disease (CHD) events, CVD events and deaths was identified. The relative risk(RR)of ALP for CVD deaths was 1.02 (95% confidence interval [CI], 1.01–1.04). The RR of phosphate for CVD deaths and events was 1.05 (95% CI, 1.02–1.09) and 1.04 (95% CI: 1.03–1.06), respectively. A non-linear association of ALP and phosphate with total mortality was identified. Compared with the reference category of ALP and phosphate, the pooled RR of ALP for total mortality was 1.57 (95% CI, 1.27–1.95) for the high ALP group, while the RR of phosphate for total mortality was 1.33 (95% CI, 1.21–1.46) for the high phosphate group. It was observed in subgroup analysis that higher levels of serum ALP and phosphate seemed to indicate a higher mortality rate in diabetic patients and those having previous CVD. The higher total mortality rate was more obvious in the men and Asians with high ALP.ConclusionA non-linear relationship exists between serum levels of ALP and phosphate and risk of total mortality. There appears to be a positive association of serum levels of ALP/phosphate with total mortality in people with normal or preserved renal function, while the relationship between ALP and CVD is still ambiguous.

Plasma dipeptidyl-peptidase-4 activity (DPP4a) is inversely associated with left ventricular function in patients with heart failure (HF) or diabetes. However, the association between DPP4a and left ventricular function in ST-segment elevation myocardial infarction (STEMI) patients has not been reported. We studied this association in 584 consecutive STEMI patients at a tertiary referral center from July 2014 to October 2015. DPP4a and plasma N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) levels were quantified by enzymatic assays. The median serum NT-proBNP levels were highest in patients of the lowest tertile (T1) of DPP4a compared with that of the highest tertile (T3) (p = 0.028). The STEMI patients in T1 exhibited lower left ventricular systolic function (T1 vs. T3: left ventricular ejection fraction (LVEF): 50.13 ± 9.12 vs. 52.85 ± 6.82%, p = 0.001). Multivariate logisticregression analyses (adjusted for confounding variables) showed that a 1 U/L increase in DPP4a was associated with a decreased incidence of left ventricular systolic dysfunction (LVSD) (adjusted odds ratio: 0.90; 95% CI: 0.87-0.94; p < 0.01). In conclusion, low DPP4a is independently associated with LVSD in STEMI patients, which suggests that DPP4 may be involved in the mechanisms of LVSD in STEMI patients.Left ventricular systolic dysfunction (LVSD), whose representative indicator is left ventricular ejection fraction (LVEF), is an important marker of poorer prognosis in patients after an acute myocardial infarction (AMI), for both in-hospital and long-term follow-up 1, 2 . Plasma biomarkers may provide insight into the pathogenesis of LVSD while also providing prognostic information in MI patients.Dipeptidyl-peptidase-4 (DPP4) is a widely expressed enzyme, cleaving off proteins containing a position 2 alanine or proline, and thus inactivating peptides 3 . DPP4 plays an important role in glucose metabolism and is responsible for the degradation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide. DPP4 regulates immune responses via cleavage of many cytokines and chemokines, such as stromal-cell-derived factor-1 (SDF-1) 4 . Inhibition of DPP4 enhances endothelial regeneration and reduces atherosclerotic progression via the SDF1/chemokine receptor (CXCR)-4 axis 5 . Soluble DPP4 circulating in the plasma exerts catalytic activity cleaving oxyntomodulin 6 and SDF-1 7 , as does membrane-type DPP4. Soluble DPP4 plays a role in the development of insulin resistance, smooth muscle cell (SMC) proliferation, inflammation, and vasorelaxation 8 . Increased soluble DPP4 levels are associated with coronary artery disease 9 and heart failure (HF) 10 . We found that plasma DPP4 activity (DPP4a) is decreased in patients with MI compared with those with only chest pain or unstable angina pectoris. Also, we found that elevated DPP4a is associated with no-reflow phenomenon and a decreased rate of major bleeding events in ST-segment elevation myocardial infarction (STEMI) patients treated with percutaneous coronary ...