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.

Punicalagin protects H9c2 cardiomyocytes from doxorubicin-induced toxicity through activation of Nrf2/HO-1 signaling.

Doxorubicin (DOX) is a wide-spectrum antitumor agent, but its clinical application is largely limited by its cardiotoxicity. Therefore, identification of effective agents against DOX-induced cardiotoxicity is of critical importance. The present study aimed to determine the beneficial role of punicalagin (PUN), a polyphenol isolated from pomegranate, in DOX-induced cardiotoxicity in vitro and explored the underlying mechanisms. H9c2 cardiomyocytes were pretreated with different concentrations (50, 100 and 200 µM) of PUN prior to DOX exposure. The results showed that PUN pretreatment significantly increased cell viability, inhibited lactate dehydrogenase (LDH) release and suppressed cell apoptosis induced by DOX. Additionally, PUN pretreatment attenuated the loss of mitochondrial membrane potential and cytochrome c release. Besides, PUN further enhanced the expression of nuclear Nrf2 and HO-1 in DOX-treated H9c2 cells, and the aforementioned beneficial effects of PUN were partially abolished by small interfering RNA (siRNA)-mediated Nrf2 knockdown. Hence, our findings clearly revealed that PUN might be a promising agent for alleviating the cardiotoxicity of DOX, and Nrf2/HO-1 signaling might serve a critical role during this process.

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.

N,N-dimethylsphingosine attenuates myocardial ischemia-reperfusion injury by recruiting regulatory T cells through PI3K/Akt pathway in mice.

N,N-dimethylsphingosine (DMS) has been documented to be in vitro protective against myocardial ischemia-reperfusion injury (IRI) and can recruit CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs), which may participate in the cardioprotection. We hypothesized that when in vivo applied after a myocardial ischemia, DMS may be cardioprotective by recruiting Tregs. Myocardial IRI was induced in C57BL/6 mice by occluding the left main coronary arteries followed by relaxation, and DMS (0.43 mg/kg) was intravenously injected 5 min after the onset of ischemia. We found that in wild-type (WT) mice, compared with the ischemia-reperfusion group, DMS reduced the infarct size (47.1 ± 8.9 vs. 33.1 ± 3.4 %, p < 0.01), and neutrophil infiltration at 24 h reperfusion (R) evaluated by TTC and immunohistochemical staining, respectively, and increased the aggregation of Tregs [(6 ± 1)/mm(2) vs. (30 ± 4)/mm(2), p < 0.01], peaking at 1 h R by immunofluorescence staining, with reduced gene expression of inflammatory factors at 4 h R in the reperfused myocardium by real-time PCR. This protection was abolished by phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor or Tregs-depleting antibody. Relative to WT mice, the cardioprotection conferred by T cell- and B cell- deficient Rag2 knockout (KO) mice was not strengthened by DMS or by DMS and the adoptive transfer of Tregs from WT mice, but was abolished by DMS and WT non-Tregs and was recaptured by the cotransfer with WT Tregs but not with Akt1(+/-) mice-derived Tregs. In conclusion, applied at an early stage of ischemia, DMS may be in vivo protective against myocardial IRI by recruiting Tregs via PI3K/Akt pathway.