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SummaryThe aim of the present study was to evaluate the effects of hypertonic saline solution (C-HSS) with high dose furosemide on hospitalization time, readmission, and mortality in patients with New York Heart Association (NYHA) class III heart failure.Decompensated heart failure patients (NYHA III) with chronic ischemic or nonischemic cardiomyopathy and ejection fraction < 40% were divided into 2 groups in an open-label random manner: the first group received a 1-hour intravenous infusion of furosemide (100 mg) plus compound C-HSS (100 mL) twice daily and underwent serious water restriction (500 mL/day); the second group received furosemide intravenous bolus (100 mg) twice a day and water restriction (500 mL/day), without C-HSS. Both groups had normal sodium (120 mmol sodium) intake. After discharge, the two groups continued to receive 120 mmol Na/day and 500-1000 mL water/day.The first group (132 C-HSS patients) had an increase in urination, a reduction in hospitalization time (4 ± 2 versus 7 ± 2 days, P < 0.01), and a reduction in hospitalization costs (2210 RMB versus 3506 RMB, P < 0.01) compared with the second group (132 without C-HSS patients). During the follow-up period (36 ± 12 months), the first group had a significantly higher average readmission time (31.84 ± 7.58 months versus 15.60 ± 6.25 months, P < 0.01) and lower mortality rate (16.5% versus 31.9%, P < 0.01).The results suggest that periodical C-HSS administration, combined with serious water restriction and a normal sodium diet, significantly reduces the hospitalization time, readmission rate, and mortality in patients with NYHA class III HF. (Int Heart J 2017; 58: 601-607)

Acute oxidative stress and mitochondrial dysfunction are crucial for acute myocardial ischemia-reperfusion (AMI/R) injury, which may induce cell or mitochondrial membrane rupture and myocardial infarction. Plasma homocysteine (Hcy) expression levels are positively associated with risk of cardiovascular disease, and ERK1/2 exert anti-apoptotic and cardioprotective effects on AMI/R injury. However, the precise molecular mechanism of action underlying the effects of Hcy and the ERK1/2 signaling pathway on mitochondrial dysfunction and oxidative stress in AMI/R injury remains unclear. In the present study, AMI/R injury models were established in an animal model treated with Hcy and in H9C2 cells that were treated with hypoxia-reoxygenation. Mitochondrial function and oxidative stress were evaluated. The results demonstrated that Hcy enhanced ERK1/2 protein expression levels and oxidative stress, induced cytochrome c translocation and mitochondria dysfunction, and caused cardiac dysfunction in rats with AMI/R injury. However, an ERK1/2 inhibitor effectively protected AMI/R injury rats from Hcy-induced cardiac dysfunction and oxidative stress. In conclusion, Hcy induced mitochondrial dysfunction and oxidative stress in AMI/R injury through stimulating ROS production and the ERK1/2 signaling pathway. An ERK1/2 inhibitor may be an effective new therapeutic method for treating Hcy-induced cardiac dysfunction in patients with AMI/R injury.

BackgroundThe present study investigated the effects of VEGF-A targeted by miR-126 on myocardial injury after acute myocardial infarction (AMI) in rats, along with the contributions of rosuvastatin to the synergic effect.Material/MethodsSD rats were obtained to construct AMI models by ligating their left anterior descending coronary arteries (LAD). We conducted echocardiography to check the 6 involved indexes: left ventricular ejection fractions (LVEF), fractional shortening (FS), left ventricular end-systolic volume (LVV), left ventricular end-diastolic volume (LVVd), cardiac output (CO), and heart rate (HR). Moreover, antibody sandwich enzyme-linked immunosorbent assay was carried out to determine MI markers: creatine kinase (CK), CK Isoenzyme (CK-MB), and Troponin I (cTn I). Dual-Luciferase Reporter Assay was performed to confirm the targeting of miR-126 and VEGF-A. MTT assay provided insight into the proliferation of myocardial fibroblasts. Finally, RT-RCR and Western blot were used for the detection of miR-126 and VEGF-A expressions in vivo and in vitro.ResultsLuciferase activity assay showed that miR-126 transfection significantly decreased the relative luciferase activity in HEK293T cells when it was bound to normal 3′ UTR of VEGF-A (P<0.05). In comparison to the control group, rats in the AMI model group had significantly lower LVEF, FS, and CO, and substantially higher LVVs, LVVd, HR, CK/U, CK-MB/U, and cTn-1/U (all P<0.05). Down-regulated miR-126 and up-regulated VEGF-A were also observed in MI models (P<0.05).ConclusionsmiR-126 and rosuvastatin have protective effects on AMI risk, and VEGF-A antagonizes effects on AMI is imposed by.