Dipeptidyl peptidase-4 (DPP4) is one of the most potent mammalian serine proteases participated in the pathogenesis of subclinical atherosclerosis. Here we investigated whether the plasma soluble form of DPP4 is associated with the prevalence of coronary artery disease (CAD) with and without diabetes mellitus (DM). A cross-sectional study was conducted of 496 aged 26–81 years with (n = 362) and without (n = 134) CAD. Plasma DPP4 activity, high sensitive C-reactive protein (hs-CRP), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein levels were measured. The coronary atherosclerotic plaques were evaluated by coronary angiography. The CAD patients with (n = 84) and without (n = 278) DM had significantly higher DPP4 levels (11.8 ± 3.1 vs. 6.9 ± 3.5 ng/mL, P<0.01) than the nonCAD subjects. The acute coronary syndrome patients (n = 299) had elevated DPP4 levels than those with stable angina patients (n = 83). CAD patients even without DM had increased plasma DPP4 activities as compared with nonCAD subjects (10.9 ± 4.9 vs. 6.4 ± 3.1, ng/L, P< 0.01). A linear regression analysis revealed that overall, the DPP4 levels were positively associated with LCL-C and hs-CRP levels as well as syntax scores. A multiple logistic regression analysis demonstrated that plasma DPP4 activity was independent predictor of CAD (odds ratio, 1.56; 95% CI, 1.19–1.73; P<0.01). Our study shows that increased DPP4 activity levels are associated with the presence of CAD and that the plasma DPP4 level serves as a novel biomarker for CAD even without DM.

Background:Atrial fibrillation (AF) is the most common type of heart arrhythmia, but the impact of long-term, high-intensity endurance exercise on the risk of AF remains uncertain.Methods:PubMed, EMBASE, and Cochrane library databases were searched till Nov 2017 to retrieve the articles. The included studies were summarized, pooled odds ratio (OR) and its 95% confidence interval (CI) were calculated. Both fixed and random effects models were used to combine the data. Stratified and logistic meta-regression analyses were performed to explore the sources of heterogeneity across studies.Results:Nine studies including 2308 athletes and 6593 controls were eligible. Our results showed that the risk of AF was significantly higher in athletes than in general population (OR = 2.34, 95% CI = 1.04–5.28, Pheterogeneity<.001, I2 = 92.3%). Subgroup analysis based on gender and mean age demonstrated a significantly increased risk in men (OR = 4.03, 95% CI = 1.73–9.42, Pheterogeneity<.001, I2 = 82.7%) and participants with mean age <60 (OR = 3.24, 95% CI = 1.23–8.55, Pheterogeneity<.001, I2 = 84.3%). Furthermore, subgroup analysis based on type of athletes demonstrated a significantly increased risk of AF in participants with single type of sport (OR = 3.97, 95% CI = 1.16–13.62, Pheterogeneity = .018, I2 = 70.4%). Results remained unchanged after performing sensitivity analysis. Meta-regression showed that gender, age, type of study, sample size, and sports mode were unrelated to heterogeneity.Conclusion:Our study confirmed that the risk of AF was significantly higher in athletes than in general population, especially among men and participants aged <60.

Atrial natriuretic peptide (ANP) plays a pivotal role in the regulation of the cardiovascular system. The ANP level increases during atrial fibrillation (AF), suggesting that AF may provoke ANP secretion, but its potential mechanism is still unclear. In the present study, the potential mechanisms of rapid atrial pacing (RAP) regulating ANP secretion was explored. Rabbits were subjected to burst RAP, ANP secretion increased whereas cyclic guanosine monophosphate (cGMP) concentrations decreased during RAP. The p-Akt and p-GSK-3β levels decreased in atrial tissues. Natriuretic peptide receptor A (NPR-A) protein and particulate guanylate cyclase (PGC) activity were detected. The sensitivity of NPR-A to ANP decreased, leading to the decrease of PGC activity. Also, the isolated atrial perfusion system were made in the rabbit model, cGMP was shown to inhibit ANP secretion, and the Akt inhibitor LY294002 (LY) and GSK-3β inhibitor SB216763 (SB) attenuated the inhibitory effects of cGMP on ANP secretion and enhanced the inhibitory effects of cGMP on atrial dynamics. In conclusion, NPR-A interacts with ANP to regulate PGC expression, and influence the expression of cGMP during RAP, which involves in the Akt/GSK-3β signaling pathway. From the aforementioned points we conclude that cGMP regulates ANP secretion by the Akt/GSK-3β signaling pathway during atrial pacing.