A high‐fat diet (HFD) has been associated with heart failure and arrhythmias; however, the molecular mechanisms underlying these associations are poorly understood. The mitochondria play an essential role in optimal heart performance, most of the energy for which is obtained from the oxidation of fatty acids. As such, chronic exposure to excess fatty acids may cause mitochondrial dysfunction and heart failure. To investigate the effects of a HFD on the mitochondrial function in the myocardium, 40 male rats were randomly divided into two groups and fed with either a normal diet or a HFD for 28 weeks. The myocardial lipid content, cardiac parameters and function, and mitochondrial morphology and function were evaluated. The expression of a number of genes involved in mitochondrial dynamics was measured using quantitative polymerase chain reaction and Western blot analyses. Proteomic analysis was also performed to identify the proteins affected by HFD treatment. Significant fat deposition in the myocardia, cardiac hypertrophy, and cardiac dysfunction were all observed in HFD‐treated rats. Electron microscopy showed abnormal mitochondrial density and morphology. In addition, abnormal expression of genes involved in mitochondrial dynamics, decreased mitochondrial DNA copy numbers, reduced complex I‐III and citrate synthase activities, and decreased mitochondrial respiration were observed in HFD‐treated rats. High performance liquid chromatography showed downregulated adenosine triphosphate (ATP) and adenosine diphosphate levels and an increased adenosine monophosphate (AMP)/ATP ratio. Proteomic analysis confirmed the alteration of mitochondrial function and impaired expression of proteins involved in mitochondrial dynamics in HFD‐treated rats. Mitochondrial dysfunction and impaired mitochondrial dynamics play an important role in heart dysfunction induced by a HFD, thus presenting a potential therapeutic target for the treatment of heart disease.

BackgroundRisk factors for embolism and recurrence of primary cardiac myxoma are not well established. This study aimed to assess the risk factors for embolism and recurrence of cardiac myxoma, as well as the survival of the patients.MethodsThe medical records of 207 consecutive patients treated for primary cardiac myxoma between September 1988 and October 2014 were retrospectively analyzed. All diagnoses were pathologically confirmed. Data were collected to identify the risk factors influencing the prognosis.ResultsMean age at surgery was 44.2 ± 15.8 years. Operative mortality (within 30 days of the surgery) occurred in seven patients. Mean follow-up was 9.35 ± 6.55 years. Embolism occurred in 32 (15.5 %) patients before surgery. Multivariate analysis indicated that small (≤4.5 cm) myxoma (OR = 5.14; 95 % CI, 2.30–11.94; P < 0.0001) and soft, gelatinous myxoma (OR = 5.84; 95 % CI, 1.91–25.61; P = 0.001) were independently associated with the occurrence of embolism. Ten patients experienced recurrences. After excluding the patients who died within 30 days of surgery, survival was 92.7 % at 10 years. Age, sex, tumor size, cardiopulmonary bypass duration, aortic cross clamp duration, tumor appearance, and pre-operative embolism were not associated with early mortality. Multivariate analysis showed that multicentric myxomas were independently associated with recurrence (OR = 9.45, 95 % CI, 2.15–41.3, P = 0.004).ConclusionsThe surgical resection of primary cardiac myxoma is associated with excellent long-term survival. Tumors ≤4.5 cm and soft tumors were independent risk factors for embolism. Multicentric cardiac myxoma was an independent risk factors for recurrence of myxoma.

Sleep deprivation has been shown to be an activator of seizures in clinical and animal studies. Orexin-A was speculated to be involved in the aggravation of seizures by sleep deprivation through the activation of its receptors: orexin-1 and orexin-2 receptor (OX1R and OX2R, respectively). Therefore, we aimed to investigate the effects of pre-treating sleep-deprived Wistar rats with the OX1R or OX2R antagonists, SB334867 (30 nM/kg) or TCS OX2 29 (30 nM/kg), respectively, followed by a convulsive dose of 50 mg/kg pentylenetetrazol administration (seizure induction), on seizure behavior, and hippocampal neurodegeneration and cellular proliferation. Our results revealed that treatment with SB334867 or TCS OX2 29 significantly prolonged the latency and reduced the duration of seizures, while also lowering the mortality rate in sleep-deprived rats exposed to pentylenetetrazol. In addition, SB334867 or TCS OX2 29 reduced the damage to hippocampal CA3 neurons and the number of bromodeoxyuridine-positive cells in the dentate gyrus (particularly in the hilus). Overall, the effect of TCS OX2 29 was greater than that of SB334867. Taken together, these data suggest that OX1R and OX2R antagonists may alleviate the damage of pentylenetetrazol-induced seizures that are exacerbated by sleep deprivation, and furthermore could be associated with a reduction of neuronal damage in the hippocampus and the inhibition of cellular proliferation in the dentate gyrus.

Diabetes mellitus (DM) has been regarded as an important risk factor for Alzheimer's disease (AD), and diabetic patients and animals have shown cognitive dysfunction. More research has shown that the amyloid-β (Aβ), which is a hallmark of AD, was found deposited in the hippocampus of diabetic rats. This Aβ accumulation is regulated by the receptor for advanced glycation end products (RAGE) and low-density lipoprotein receptor-related protein (LRP-1). However, the expression of RAGE and LRP-1 in diabetic rats is not very clear. In the present study, we used streptozotocin (STZ)-induced diabetic rats to investigate whether the expression of RAGE and LRP-1 is related to Aβ deposition at the hippocampus, prefrontal lobe, and amygdala in DM. We found that diabetic rats had longer escape latency and less frequency of entrance into the target zone than that of the control group (P < 0.05) in the Morris water maze (MWM) test. The Aβ expression in the hippocampus and prefrontal lobe significantly increased in the DM group compared to the control group (P < 0.05). RAGE increased (P < 0.05), while LRP-1 decreased (P < 0.05) in the hippocampus tissue and prefrontal lobe tissue of DM rats. The Aβ deposition was correlated with RAGE positively (P < 0.05), but with LRP-1 negatively (P < 0.05). Further, the expression levels of Aβ, RAGE, and LRP-1 were not changed in the amygdala between the diabetic rats and the control group. These findings indicated that upregulating RAGE and/or downregulating LRP-1 at the hippocampus and the prefrontal lobe contributed to the Aβ accumulation and then further promoted the cognitive impairment of diabetic rats.

BackgroundIt is infeasible to occlude a doubly committed juxtaarterial ventricular septal defect (DCVSD) percutaneously. The previous perventricular device closure technique was performed through an inferior median sternotomy approach. The purpose of this study is to evaluate the feasibility, safety and efficacy of perventricular device closure of DCVSDs through a left parasternal approach.MethodsSixty-two patients, with the DCVSD of less than 6 mm in diameter, were enrolled in this study. The pericardial space was approached through a left parasternal mini-incision without entering into the pleural space. Two parallel pursestring sutures were placed on the right ventricular outflow tract for puncture. Under transesophageal echocardiographic guidance, a new delivery sheath loaded with the device was inserted into the right ventricle and advanced through the defect into the left ventricle. The device, connected with a device stay suture, was deployed subsequently.ResultsSuccessful device closure of the defects was achieved in 58/62 patients (94 %). The DCVSD failed to close in 4 (6 %) patients due to device-related aortic regurgitation and device migration. The mean DCVSD diameter was 3.4 ± 1.0 mm (range, 2.0 to 6.0 mm). The implanted device size was 5.2 ± 1.3 mm (range, 4 to 8 mm). Forty-four out of 58 patients (76 %) was implanted with an eccentric occluder. The mean intracardiac manipulation time was 14 ± 13 min (range, 2 to 60 min). The procedure time was 66 ± 15 min (range, 42 to 98 min). During the follow-up period of 180 to 1860 (median 880) days, new mild pulmonary regurgitation occurred in 2 patients. No other device-related complications were found. The complete closure rate was 95 % at discharge, 98 % at 1-, 6- and 12-month, 96 % at 2-year, and 100 % at 3-year follow-up.ConclusionsPerventricular device closure of a DCVSD through a left parasternal approach is feasible, safe, and efficacious in selected patients. This minimally invasive technique permits easy defect crossing and accurate device positioning.

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The purpose of this study was to assess the value of echocardiography for intraoperative guidance during closure of perimembranous ventricular septal defects (pmVSD) and to assess outcomes of these patients. We identified and assessed 78 patients who underwent 2-and 3-dimensional echocardiography-guided mini-invasive per-atrial closure of pmVSD in the cardiac surgery department of our institution, from February 2016 to August 2018, and 76 patients who underwent transcatheter closure of VSD guided by fluoroscopy at the pediatric department (percutaneous control group). All the patients underwent echocardiography. Their clinical data were retrospectively reviewed and analyzed. All patients were followed up using transthoracic echocardiography (TTE) for a maximum of 24 months after the closure. All patients underwent successful device implantation. Echocardiography showed that the major immediate complications included residual shunt, pericardial effusion, and tricuspid regurgitation in the per-atrial group. During the mid-term follow-up period, TTE revealed that the most common complication was tricuspid regurgitation (non-preexisting). There were no cases of VSD recurrence, device displacement, valvular injury, malignant arrhythmias, hemolysis, or death. Moreover, according to the TTE data, the intracardiac structure of the patients were improved. Compared to the control group, the intracardiac manipulation time was shorter and the number of patients with residual shunts, redeployment of devices, or immediate new tricuspid regurgitations was fewer when using 2-and 3-dimensional echocardiography. However, the procedure time in the per-atrial group was slightly longer than that in the control group. Two-and 3-dimensional echocardiography are feasible monitoring tools during mini-invasive per-atrial VSD closure. The short-and mid-term follow-up showed satisfactory results compared to fluoroscopy.