miR­351­5p aggravates lipopolysaccharide­induced acute lung injury via inhibiting AMPK.

Inflammation and oxidative stress have indispensable roles in the development of acute lung injury (ALI). MicroRNA (miRNA/miR)­351­5p was initially identified as a myogenesis­associated miRNA; however, its role in lipopolysaccharide (LPS)­induced ALI remains unclear. The aim of the present study was to investigate the role and potential mechanisms of miR­351­5p in ALI. ALI was induced through a single intratracheal injection of LPS for 12 h, and miR­351­5p agomir, antagomir or their corresponding negative controls were injected into the tail vein before LPS stimulation. Compound C, 2',5'­dideoxyadenosine and H89 were used to inhibit AMP­activated protein kinase (AMPK), adenylate cyclase and protein kinase A (PKA), respectively. miR­351­5p levels in the lungs were significantly increased in response to LPS injection. miR­351­5p antagomir alleviated, while miR­351­5p agomir aggravated LPS­induced oxidative stress and inflammation in the lungs. The present results also demonstrated that miR­351­5p antagomir attenuated LPS­induced ALI via activating AMPK, and that the cAMP/PKA axis was required for the activation of AMPK by the miR­351­5p antagomir. In conclusion, the present study indicated that miR­351­5p aggravated LPS­induced ALI via inhibiting AMPK, suggesting that targeting miR­351­5p may help to develop efficient therapeutic approaches for treating ALI.

Prevention of Contrast-Induced Nephropathy by Inferior Vena Cava Ultrasonography-Guided Hydration in Chronic Heart Failure Patients.

INTRODUCTION: Contrast-induced nephropathy (CIN) is a common complication resulting from the administration of contrast media. This study was designed to determine whether inferior vena cava (IVC) ultrasonography (IVCU)-guided hydration can reduce the risk of CIN in chronic heart failure patients undergoing coronary angiography or coronary angiography with percutaneous coronary intervention compared with standard hydration. METHODS: This prospective clinical trial enrolled 207 chronic heart failure patients from February 2016 to November 2017, who were randomly assigned to either the IVCU-guided hydration group (n = 104) or the routine hydration group (n = 103). In the IVCU-guided group, the hydration infusion rate was set according to the IVC diameter determined by IVCU, while the control group received intravenous infusion of 0.9% saline at 0.5 mL/(kg·h). Serum Cr was measured before and 48-72 h after the procedure. All patients were followed up for 18 months. The incidence of nephropathy and major adverse cardiovascular or cerebrovascular events (MACCEs) was also compared between the 2 groups. RESULTS: Statistically significant difference between the 2 groups regarding the occurrence of CIN was observed (12.5 vs. 29.1%, p = 0.004). The hydration volume of the IVCU-guided group was significantly higher than that of the routine group (p < 0.001). In addition, patients receiving IVCU-guided hydration had significantly lower risk of developing MACCEs than patients in the control group during the 18-month follow-up (14.4 vs. 27.2%, p = 0.027). CONCLUSION: Our findings support that IVCU-guided hydration is superior to standard hydration in prevention of CIN and may substantially reduce longtime composite major adverse events.

A propensity score matched valuation on feasibility of low frame rate fluoroscopy during primary percutaneous coronary intervention for patients with STEMI.

The present study aimed to evaluate the feasibility of low frame rate fluoroscopy during primary percutaneous coronary intervention (PPCI) for patients with acute ST elevation myocardial infarction (STEMI). From January 2016 to December 2017, 165 consecutive patients with STEMI who underwent PPCI were retrospectively divided into two groups: the 7.5-frame group (fluoroscopy at 7.5 frames/s) and the 15-frame group (fluoroscopy at 15 frames/s), according to the frame rate of fluoroscopy used in their treatment. Reduction of radiation and safety of fluoroscopy at 7.5 frames/s were compared by a method of propensity score matching (PSM) with fluoroscopy at 15 frames/s. After PSM, there were 56 patients in each group. There were no differences in patients' baseline characteristics between two groups. The 7.5-frame protocol resulted in 48.9% reduction of DAP (9917 ± 5543 cGycm2 vs. 14766 ± 7272 cGycm2, P < 0.001) and 61.1% reduction of AK (1209 ± 562 mGy vs. 1948 ± 1105 mGy, P < 0.001) with comparable procedural time (38.1 ± 15.3 min vs. 38.8 ± 17.2 min, P = 0.830), fluoroscopy time (13.0 ± 7.2 min vs. 13.5 ± 8.1 min, P = 0.703) and contrast volume (122.3 ± 39.4 ml vs. 119.3 ± 49.4 ml, P = 0.725) to the 15-frame group. Meanwhile, this new protocol didn't increase the incidence of contrast-induced nephropathy (23.2% vs. 25.0%, OR = 0.907, 95% CI 0.381-2.157, P = 0.825) and peri-PPCI cumulative adverse events (30.4% vs. 28.6%, OR = 1.090, 95% CI 0.483-2.456, P = 0.836). In conclusion, low frame rate fluoroscopy at 7.5 frames/s is a safe and feasible strategy for reducing radiation during PPCI.

Elevated endocan concentration is associated with coronary slow flow.

We sought to assess whether serum endocan concentration is correlated with coronary slow flow (CSF). We measured serum endocan concentration in 93 patients with CSF and in 206 controls. Serum endocan concentration was measured by enzyme-linked immunosorbent assay (ELISA). The presence of CSF was assessed by thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. We demonstrated that serum endocan concentration is significantly higher in CSF patients (n = 93) than that in controls (n = 206) (1.03 [range 0.63-1.33] vs. 0.80 [range 0.52-1.09] ng/mL, p = 0.002). Multivariate logistic regression analysis revealed that serum endocan concentration was independently associated with the presence of CSF (odds ratio 1.774, 95% confidence interval 1.064-2.958; p = 0.028). Serum endocan concentration was positively correlated with mean-TFC in CSF patients (r = 0.289, p = 0.005). These results revealed that endocan might be a useful biomarker for predicting the presence and severity of CSF. Therapeutic interventions by down-regulating endocan to delay the progressive process of CSF warrants further investigations.