Sarcoidosis And Atrial Fibrillation: A Rare Association And Interlink With Inflammation

We report a case of sarcoidosis presenting initially as atrial fibrillation(AF). His response to anti-arrhythmic treatment strategy was suboptimal. On initiation of immunosuppressive therapy, AF was better controlled. This interesting case highlights a likely link between inflammation and pathogenesis of atrial fibrillation.     

急性下壁心肌梗死急诊PCI术中应用临时起搏器与阿托品的对比研究

目的：探讨临时起搏器与阿托品在急性下壁心肌梗死急诊经皮冠状动脉介入治疗（PCI）中应用的疗效。方法：入选2012 年2 月至2013 年8 月我院收治的发病12 小时内,诊断为急性下壁心肌梗死并接受急诊PCI治疗的患者92 例,依据治疗方法的不同 将病例分为临时起搏组和阿托品组,并对病例进行为期一年的追踪随访,收集患者平均住院天数、平均住院费用、再灌注心律失 常、心肌梗死后心绞痛、心肌梗死后心衰发生率资料。结果：临时起搏组的平均住院天数、平均住院费用、心肌梗死后心绞痛、心肌 梗死后心衰发生率均显著低于阿托品治疗组（P 均<0.05）,阿托品治疗组的再灌注心律失常发生率则明显低于临时起搏组（P<0. 05）。结论：急性下壁心肌梗死急诊PCI中应用临时起搏器,具有治疗成本低,降低心血管事件发生率的优点,而阿托品治疗在改 善再灌注心律失常的疗效上则显著优于临时起搏治疗。     

The effects of intraoperative dexamethasone on left atrial function and postoperative atrial fibrillation in cardiac surgical patients

Postoperative new-onset atrial fibrillation (PNAF) is very common after cardiac surgery and postoperative inflammation may contribute to PNAF by inducing atrial dysfunction. Corticosteroids reduce inflammation and may thus reduce atrial dysfunction and PNAF development. This study aimed to determine whether dexamethasone protects against left atrial dysfunction and PNAF in cardiac surgical patients. Cardiac surgical patients were randomised to a single dose of dexamethasone (1 mg.kg⁻¹) or placebo after inducing anaesthesia. Transoesophageal echocardiography was performed in patients before and after surgery. Primary outcome was left atrial total ejection fraction (LA-TEF) after sternal closure; secondary outcomes included left atrial diameter and PNAF. 62 patients were included. Baseline characteristics were well balanced. Postoperative LA-TEF was 36.4 % in the dexamethasone group and 40.2 % in the placebo group (difference −3.8 %; 95 % confidence interval (CI) -9.0 to 1.4 %; P = 0.15). Postoperative left atrial diameter was 4.6 and 4.3 cm, respectively (difference 0.3; 95 % CI −0.2 to 0.7; P = 0.19). The incidence of PNAF was 30 % in the dexamethasone group and 39 % in the placebo group (P = 0.47). Intraoperative high-dose dexamethasone did not protect against postoperative left atrial dysfunction and did not reduce the risk of PNAF in cardiac surgical patients.     

Isolation and sequence determination of peptide components of atrial natriuretic factor

The independent isolation and sequence determination in our laboratories of three closely related Atrial Natriuretic Factor peptides from rat atria confirm the sequences of ANF peptides reported by Seidah et al and synthesized by Nutt et al [Proc. Natl. Acad. Sci., (1984) in press] and contain the sequences reported by Flynn et al [Biochem. Biophys. Res. Commun. (1983) 117: 859-865] and by Currie et al [Science (1984) 223: 67-69]. In addition, we provide proof for a C-terminal tyrosine rather than tyrosine amide in our isolated peptides.     

Trafficking of astrocytic vesicles in hippocampal slices

The increasingly appreciated role of astrocytes in neurophysiology dictates a thorough understanding of the mechanisms underlying the communication between astrocytes and neurons. In particular, the uptake and release of signaling substances into/from astrocytes is considered as crucial. The release of different gliotransmitters involves regulated exocytosis, consisting of the fusion between the vesicle and the plasma membranes. After fusion with the plasma membrane vesicles may be retrieved into the cytoplasm and may continue to recycle. To study the mobility implicated in the retrieval of secretory vesicles, these structures have been previously efficiently and specifically labeled in cultured astrocytes, by exposing live cells to primary and secondary antibodies. Since the vesicle labeling and the vesicle mobility properties may be an artifact of cell culture conditions, we here asked whether the retrieving exocytotic vesicles can be labeled in brain tissue slices and whether their mobility differs to that observed in cell cultures. We labeled astrocytic vesicles and recorded their mobility with two-photon microscopy in hippocampal slices from transgenic mice with fluorescently tagged astrocytes (GFP mice) and in wild-type mice with astrocytes labeled by Fluo4 fluorescence indicator. Glutamatergic vesicles and peptidergic granules were labeled by the anti-vesicular glutamate transporter 1 (vGlut1) and anti-atrial natriuretic peptide (ANP) antibodies, respectively. We report that the vesicle mobility parameters (velocity, maximal displacement and track length) recorded in astrocytes from tissue slices are similar to those reported previously in cultured astrocytes.     

Gastric Pacing for Morbid Obesity: Plasma Levels of Gastrointestinal Peptides and Leptin

Objective: A gastric pacemaker has been developed to treat morbid obesity. Patients experience increased satiety, the ability to reduce food intake, and a resultant weight loss. However, the mechanism behind the changed eating behavior in paced patients is still under investigation. Research Methods and Procedures: This study was performed on 11 morbidly obese patients (mean BMI, 46.0 kg/m²) treated with gastric pacing. The peripheral blood levels of satiety signals of cholecystokinin (CCK), somatostatin, glucagon‐like peptide‐1 (GLP‐1), and leptin were studied 1 month before gastric pacer implantation, 1 month after implantation, and 6 months after activation of electrical stimulation. Blood samples were drawn 12 hours after fasting and in response to a hypocaloric meal (270 kcal). Patients were followed monthly for vital signs and weight level. Results: Gastric pacing resulted in a significant weight loss of a mean of 10.4 kg (4.4 BMI units). No negative side effects or complications were observed during the treatment. After activation of the pacemaker, meal‐related response of CCK and somatostatin and basal levels of GLP‐1 and leptin were significantly reduced (p < 0.05) compared with the tests before gastric pacing. The weight loss correlated significantly with a decrease of leptin levels (R = 0.79, p < 0.01). Discussion: Gastric pacing is a novel and promising therapy for morbid obesity. Activation of the gastric pacer was associated with a decrease in plasma levels of CCK, somatostatin, GLP‐1, and leptin. More studies are necessary to elucidate the correlations between satiety, weight loss, and digestive neuro‐hormone changes.     

经食道心房调搏术及食道心电图在心律失常中的应用

目的:分析经食道心房调搏术(TEAP)及食道内心电图(EECG)在心律失常中的应用价值。方法:选取2018年6月至2019年12月于我院行食道心电图及经食道调搏的患者189例,其中男80例,女109例,年龄11~83岁。结果:54例为房室结折返性心动过速(AVNRT),34例为房室折返性心动过速(AVRT),8例为房性心动过速(AT),4例为心房扑动(AF),6例为心房颤动(Af),5例为室性心过速,78例为室早或其他。共105例心律失常患者拟行食道心房调搏终止心动过速,所有AVNRT和AVRT患者及17例AT患者经食道心房调搏S1S1成功转为窦律,50例AVNRT、32例AVRT、6例AT、3例AF及2例VT患者通过射频消融术成功根治。其中1例11岁AT患者因无法耐受食道调搏,未能转为窦律,患者经静推普罗帕酮后次日转为窦律。共97例患者拟行食道心房调搏诱发,共49例诱发出心动过速,1例左后分支型室速经静滴异丙肾上腺素后诱发心动过速,且仍需静滴异丙肾上腺素后经心房食道调博终止心动过速,后经射频消融术成功根治。结论:TEAP及EECG可用于复杂心律失常的诊断及治疗,是一种相对安全、临床容易掌握的技术,值得推广。     

CYP2J2/EET reduces vulnerability to atrial fibrillation in chronic pressure overload mice

Growing evidence has well established the protective effects of CYP2J2/EET on the cardiovascular system. The aim of the present study was to determine whether CYP2J2/EET has a preventive effect on atrial fibrillation (AF) and to investigate the underlying mechanisms. Wild‐type mice were injected with or without AAV9‐CYP2J2 before abdominal aortic constriction (AAC) operation. After 8 weeks, compared with wild‐type mice, AAC mice display higher AF inducibility and longer AF durations, which were remarkably attenuated with AAV9‐CYP2J2. Also, AAV9‐CYP2J2 reduced atrial fibrosis area and the deposit of collagen‐I/III in AAC mice, accompanied by the blockade of TGF‐β/Smad‐2/3 signalling pathways, as well as the recovery in Smad‐7 expression. In vitro, isolated atrial fibroblasts were administrated with TGF‐β1, EET, EEZE, GW9662, SiRNA Smad‐7 and pre‐MiR‐21, and EET was demonstrated to restrain the differentiation of atrial fibroblasts largely dependent on Smad‐7, due to the inhibition of EET on MiR‐21. In addition, increased inflammatory cytokines, as well as activated NF‐κB pathways induced by AAC surgery, were also significantly blunted by AAV9‐CYP2J2 treatment. These effects of CYP2J2/EET were partially blocked by GW9662, the antagonist of PPAR‐γ. In conclusion, this study revealed that CYP2J2/EET ameliorates atrial fibrosis through modulating atrial fibroblasts activation by disinhibition of MiR‐21 on Smad‐7, and attenuates atrial inflammatory response by repressing NF‐κB pathways, reducing the vulnerability to AF, and CYP2J2/EET exerts its role at least partially through PPAR‐γ activation. Our findings might provide a novel upstream therapeutic strategy for AF.     

Protective mechanism of SIRT1 on Hcy‐induced atrial fibrosis mediated by TRPC3

High plasma levels of homocysteine (Hcy) are regarded as a risk factor for atrial fibrillation (AF), which is closely associated with the pathological consequence of atrial fibrosis and can lead to heart failure with a high mortality rate; here, we show that atrial fibrosis is mediated by the relationship between canonical transient receptor potential 3 (TRPC3) channels and sirtuin type 1 (SIRT1) under the stimulation of Hcy. The left atrial appendage was obtained from patients with either sinus rhythm (SR) or AF and used to evaluate the relationship between the concentration of Hcy and a potential mechanism of cardiac fibrosis mediated by TRPC3 and SIRT1. We next performed transverse aortic constriction (TAC) in mouse to investigate the relationship. The mechanisms underlying atrial fibrosis involving TRPC3 and SIRT1 proteins were explored by co‐IP, BLI and lentivirus transfection experiments. qPCR and WB were performed to analyse gene and protein expression, respectively. The higher level of atrial fibrosis was observed in the HH mouse group with a high Hcy diet. Such results suggest that AF patients may be more susceptible to atrial fibrosis and possess a high probability of progressing to hyperhomocysteinemia. Moreover, our findings are consistent with the hypothesis that TRPC3 channel up‐regulation leads to abnormal accumulation of collagen, with the down‐regulation of SIRT1 as an aetiological factor of high Hcy, which in turn predisposes to atrial fibrosis and strongly enhances the possibility of AF.