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Background Glycated albumin (GA) has been shown to be a better indicator than glycosylated hemoglobin A1c (HbA1c) in terms of severity of renal impairment in patients with type 2 diabetes mellitus (T2DM). This study aimed to determine whether elevated serum GA levels are associated with an increased risk for contrast-induced acute kidney injury (CI-AKI) and worse clinical outcome in patients with T2DM and at least moderate renal insufficiency (RI) undergoing coronary angiography. Methods Serum levels of fasting blood glucose (FBG), HbA1c and GA were measured in 1030 patients with T2DM and moderate to severe RI (eGFR 15–59mL/min/1.73m 2 ). CI-AKI was defined as ≥25% increase in serum creatinine within 72h after the procedure. Receiver-operating characteristic curve was constructed to assess the predictive value of GA, HbA1c and FBG for CI-AKI. Multivariable logistic regression model was developed to identify risk factors for CI-AKI, and Kaplan–Meier curve analysis was used to compare the rates of dialysis and major adverse cardiac events (MACE) during one-year follow-up. Results The overall rate of CI-AKI was 11.1%. GA was significantly higher in patients with CI-AKI than in those without, and correlated positively with changes of renal function after the procedure. After adjusting for age, sex, left ventricular ejection fraction, multi-vessel disease, type and volume of contrast media, FBG, and HbA1c, GA remained an independent risk factor for CI-AKI. GA≥21% was associated with increased rates of dialysis and MACE during one-year follow-up in patients with or without CI-AKI. Conclusions Increased GA level serves as a valuable risk factor for CI-AKI and indicates poor one-year clinical outcome in patients with T2DM and moderate to severe RI.

Background We investigated whether an additional intracoronary tirofiban bolus administration following upstream intravenous treatment could further improve myocardial reperfusion and clinical outcome in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Methods A total of 453 eligible STEMI patients were randomly allocated to intracoronary bolus administration of tirofiban (10μg/kg; n=229) or saline (10mL; n=224) during primary PCI, followed by intravenous tirofiban infusion (0.15μg/kg/min) for 24–36h. Serum levels of P-selectin, vWF, CD40L and serum amyloid A (SAA) in the coronary sinus were measured before and after intracoronary bolus administration. The primary endpoint was ST-segment resolution (STR) at 90min after the procedure. Second endpoints included corrected TIMI frame count (cTFC), left ventricular volumes and ejection fraction (EF), and major adverse cardiac events (MACE) at 30-day and 6-month follow-up. Results Intracoronary tirofiban administration resulted in a higher rate of completed STR (59.0% vs. 44.6%, P=0.002), lower cTFC (21.6±5.4 vs. 23.7±7.8, P=0.048), and significantly reduced coronary sinus levels of P-selectin, vWF, CD40L and SAA. Patients treated with intracoronary tirofiban had a trend toward less MACE at 30days (3.1% vs. 6.7%, P=0.072). At 6months, left ventricular end-systolic volume was smaller, EF was higher and MACE-free survival was improved (96.1% vs. 90.6%, P=0.020) in the intracoronary tirofiban group. Conclusions An additional intracoronary tirofiban bolus administration following upstream intravenous treatment reduces coronary circulatory platelet activation and inflammatory process, and significantly improves myocardial reperfusion and left ventricular function as well as 6-month MACE-free survival for STEMI patients undergoing primary PCI.

Background Atrial fibrillation (Af) is frequently observed in patients with rheumatic heart disease (RHD). The hyperactivity of autonomic nervous system is known to contribute to the occurrence of Af in RHD patients. This study investigated the association between the autonomic density and the risk of Af in RHD patients. Methods Seventy-five patients were enrolled: (1) RHD patients with Af (N=25, Group 1); (2) RHD patients without Af (N=25, Group 2); (3) congenital heart disease patients without Af (N=25, Group 3). The baseline characteristics and the blood concentrations of renin, C-reaction protein and angiotensin II were collected from all patients. The tissues were obtained from the right atrial appendage during the open-heart surgery and then stained using immunohistochemical methods with autonomic antibodies. Results The sympathetic nerve density was significantly higher in RHD patients with Af than RHD patients without Af and congenital heart disease patients, both endocardially and epicardially. The parasympathetic nerve density did not show significant difference among the three groups. The left atrial diameter was larger in RHD patients with Af than the other two groups. The blood concentrations of renin and angiotensin II were higher in RHD patients with Af than the other two groups. The erythrocyte sedimentation rate and blood concentrations of C-reaction protein did not show significant change among the three groups. Conclusion This study provided direct evidence of the increase in sympathetic nerve density in atrium in patients with RHD. This phenomenon may be associated with the development of Af in RHD patients.

Objective To study the potential mechanisms of hepatocyte growth factor (HGF) mediating improvement of the cardiac function of dilated cardiomyopathy mice (DCM). Methods and results We established experimental model of dilated cardiomyopathy by repetitive coxsickievirus B3 (CVB3) infection in Balb/c mice and half of the experimental group mice were injected 0.2 µg recombinated human HGF through tail vein every 2 days starting from the 5th month. At the 5th month, dilated cardiomyopathy occurred in experimental group mice. The HGF level and N-cadherin expression in myocardium of experimental group was downregulated. At the 7th month, after HGF supplement, the HGF level and N-cadherin expression in the myocardium of the mice were increased, the fibrosis of myocardial and cells apoptosis were ameliorated and cardiac function was improved. In vitro experiment, we found that N-cadherin expression was increased in cultured myocardial cells treated with rHGF. Conclusion Increasing in N-cadherin expression may be one of the potential mechanisms of HGF mediating Improvement of cardiac function of dilated cardiomyopathy mice.

a Dept. of Pediatric Cardiology, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China b Dept. of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China c Dept. of Ultrasound Cardiography, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China d Dept. of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China e Key Laboratory of Ob&G and Pediatric Diseases and Birth Defects of Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China f Program for Yangtze River Scholars and Innovative Research Team in University, West China Medical Center, West China Second University Hospital, Sichuan University, Chengdu 610041, PR China