Objective This study examined the separate and joint associations between modifiable behavioral risk factors (daily sitting time (DST), physical activity (PA) levels) and all-cause and premature mortality among individuals diagnosed with Cardiovascular Disease (CVD). Methods This retrospective cohort study analyzed data from 2,530 adult CVD patients in the National Health and Nutrition Examination Survey (2007–2018), and linked records to the National Death Index through December 31, 2019. Physical activity was categorized as high (≥500 MET-min/week) or low (<500 MET-min/week), while daily sitting time was classified as low (<7 hours/day) or high (≥7 hours/day). We used survey-weighted Cox regression, restricted cubic splines (RCS), and Kaplan-Meier survival analysis to evaluate relationships and conducted subgroup analyses to verify consistency. Results The cohort had a weighted mean age of 59.12±0.27 years (56.61% men, 68.01% non-Hispanic White), with 531 all-cause mortality (374 premature deaths). PA≥500 MET-min/week was associated with lower all-cause (HR = 0.49, 95% CI:0.37–0.64) and premature mortality (HR=0.44, 95% CI:0.32–0.61); Each 1-SD increase in PA was linked to 52% and 51% lower risks of all-cause and premature mortality. DST≥7 hours/day increased all-cause (HR=1.67, 95% CI:1.32–2.11) and premature mortality (HR=1.74, 95% CI:1.30–2.32); Each 1-SD increase in DST was linked to 31% and 33% higher risks of all-cause and premature mortality. The lowest mortality risk was among those with DST <7 hours/day and PA ≥500 MET-min/week (all-cause: HR = 0.37; premature: HR = 0.31). RCS showed linear positive associations for DST ( P for nonlinearity >0.05) and nonlinear negative associations for PA ( P for nonlinearity < 0.05) with mortality; subgroup analyses confirmed stable associations. Conclusions This study suggests that increasing physical activity and reducing daily sitting time may be associated with lower risks of all-cause mortality and premature death in patients with CVD, with more favorable effects observed when the two behaviors are combined. Promoting a combination of higher PA and lower DST may be a useful reference of routine CVD risk management.

Intense or exhaustive exercise is known to increase the risk of ventricular arrhythmias. One important mechanism is the disruption of intracellular calcium homeostasis. Exercise preconditioning (EP) has been reported to exert cardioprotective effects. However, under exercise-induced stress, how EP reduces arrhythmia susceptibility through regulation of calcium-handling signaling pathways remains unclear. This study aimed to investigate whether EP reduces exercise-induced arrhythmias by modulating the CaMKII–RyR2–PLN signaling pathway. In this study, a rat model of repeated exhaustive exercise (EE) was established. The effects of EE and EP on myocardial electrophysiological properties were compared. The results showed that EE significantly shortened exhaustion time. EE also increased the incidence of electrically induced ventricular arrhythmias. In addition, EE markedly altered the expression of proteins related to calcium homeostasis. Specifically, EE significantly increased CaMKII activation and enhanced RyR2 phosphorylation at the Ser2814 site. These changes were accompanied by reduced SERCA2a expression and elevated PP1 levels. These findings indicated impaired sarcoplasmic reticulum calcium reuptake and increased calcium leakage. EP significantly prolonged exhaustion time and preserved myocardial structural integrity. EP reduced the occurrence of ventricular arrhythmias. Moreover, EP suppressed CaMKII activity and prevented excessive RyR2 phosphorylation. SERCA2a expression was restored, and PP1 levels were partially normalized. The CaMKII inhibitor KN-93 acted synergistically with EP. This result further confirmed the central role of CaMKII overactivation in exercise-induced ventricular arrhythmias. EP effectively reduced susceptibility to exercise-induced ventricular arrhythmias by regulating the CaMKII–RyR2–PLN signaling pathway and maintaining calcium homeostasis. These findings highlight CaMKII as a potential therapeutic target. In addition, they provide mechanistic evidence for the cardioprotective effects of exercise preconditioning under extreme exercise stress.

BACKGROUND:Hypoxia has a major regulatory impact on the electrical activity transmission in the myocardium, and it is involved in the development of tachyarrhythmia disease. Anchor protein G (ankyrin-G, ANK-G) is associated with voltage-gated Na+ channels (Nav1.5), but its specific role and mechanism have not been fully defined. In this experiment, we investigated the role and mechanism of hypoxia on cardiomyocyte electrophysiology of voltage-gated Na+ channel, as well as the intervention effect of ankyrin-G by simulating the environment of cardiomyocytes during hypoxia through hypoxia-treated murine atrial myocytes (HL-1). METHODS:The HL-1 cells were divided into 6 groups: normoxia group (NO), hypoxia group (HO), ANK-G-overexpressing hypoxia-negative group (ANK-G NC), ANK-G-overexpressing hypoxia group (ANK-G), ANK-G-silenced hypoxia-negative group (shANK-G NC), and ANK-G-silenced hypoxia group (shANK-G). ANK-G overexpression was induced using lentiviral vectors through the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 system. The characteristics of sodium ion channel current (INa) were observed through the whole-cell patch clamp technique. Western blotting was used to detect the expression of ANK-G and Nav1.5 channel proteins, and the distribution of Nav1.5 channel on HL-1 cells was observed by confocal microscope. RESULTS:Under hypoxic conditions, the INa peak current amplitude (p < 0.01) and density (p < 0.01) of HL-1 cells increased. Compared with the normoxia group, the steady-state inactivation curve of the hypoxia group shifted to the right. The protein levels of ANK-G and Nav1.5 channels were increased under hypoxia (p < 0.001). In the ANK-G group, the upregulation of ANK-G protein increased the distribution of Nav1.5 channel in the cell membrane under the hypoxic condition (p < 0.01). CONCLUSIONS:Hypoxia increases the INa amplitude and density of HL-1 cells, and the gating mechanism of INa is related to steady-state inactivation. Hypoxic condition triggers the upregulation of the ANK-G protein expression, which promotes the redistribution of Nav1.5 channel proteins in the cell membrane, thereby augmenting INa peak current amplitude and density.

Robotic-assisted percutaneous coronary intervention (R-PCI) is an innovative way of performing percutaneous coronary intervention (PCI) whereby the operator can manipulate coronary intraluminal guidewires and catheter devices by using remotely controlled technology. Performing tele-R-PCI from a remote location via fifth generation network communication technology has never been reported in China; however, if this were possible, the technique could be used to treat many patients with coronary artery disease who would otherwise not have the opportunity of treatment. The case of a 73-year-old male patient with coronary artery disease who underwent successful tele-R-PCI at 800 km from the operators is presented. Performing long-distance tele-R-PCI in patients with coronary artery disease is feasible with predictably successful outcomes when reliable network connectivity and local cardiac catheterization facilities are present.

2008年《The New England Journal of Medicine》刊登了de Winter教授发表的文章,该文首次描述了冠状动脉(冠脉)前降支(LAD)完全闭塞时心电图改变不表现为显著的ST段抬高,而表现为一种特殊类型即ST段上斜型压低伴T波高尖,即de Winter ST-T改变[1,2],这是LAD近段闭塞的一种特殊的心电图表现(LAD近段急性闭塞).

Age-related cardiac fibrosis is a risk factor for heart failure and a marker for heart aging. However, the mechanisms underlying age-related cardiac fibrosis remain unclear. Ischemia and hypoxia are inevitable events in the aging process, which are direct causes of mitochondrial dysfunction and metabolic alterations. In this study, we identified metabolic changes and determined the mechanisms by which succinate (a tricarboxylic acid cycle intermediate) accumulation promotes fibroblast activation and apoptosis resistance in the aging heart. We also assessed its significance in relation to cardiac fibrosis and diastolic dysfunction.We first investigated how aging promotes persistent cardiac fibrosis. Following this, the metabolic alterations of the aging heart were identified by untargeted metabolomics, and the succinate level was verified via quantitative analysis. Furthermore, the correlations between succinate and fibrosis or diastolic dysfunction in older mice/people were assessed. We also described the role of succinate and its receptor SUCNR1/GPR91 in establishing a fibrosis network during diastolic dysfunction with age using SUCNR1-/- mouse model and an AAV9-based approach. We further identified the specific mechanisms involved in PKM2 dimerization, which regulate fibroblast activation and apoptosis resistance.We demonstrated that aging promotes fibrogenesis and diastolic dysfunction, which are linked to fibroblast activation and apoptosis resistance in the heart. Succinate levels were correlated with diastolic dysfunction and cardiac fibrosis in older mice and people. Functionally, succinate promoted fibroblast activation and apoptosis resistance, which aggravate cardiac fibrosis formation in both young and old mice. This was attributed to the ability of succinate to stimulate PKM2 dimerization via succinate receptor SUCNR1. Furthermore, dimeric PKM2 translocated to the nucleus and mitochondria, where it promoted fibroblast activation and apoptosis resistance, respectively. Accumulated PKM2 in the nucleus interacted with HIF-1α, increasing the DNA binding of HIF-1α and the expression of fibrogenic genes, resulting in fibroblast activation. In the mitochondria, accumulated PKM2 phosphorylated VDAC1 at T93 and increased VDAC1 degradation by promoting SYVN1-based E3 ligase binding to VDAC1, which is associated with increased apoptosis resistance and fibrosis persistence. We found that targeting succinate accumulation by metformin can inhibit fibroblast activation and apoptosis resistance in mice, which is a potential strategy to control age-related cardiac fibrosis and diastolic dysfunction.Our findings indicate that targeting metabolic dysregulation has significant implications for the treatment of age-related cardiac fibrosis and diastolic dysfunction. We further demonstrate a novel mechanism by which succinate induces fibroblast activation and apoptosis resistance by promoting PKM2 dimerization. Hence, inhibiting succinate generation or blocking its downstream effects is potentially a promising new strategy for slowing the heart aging.

Regular moderate physical exercise is beneficial for the cardiovascular system. Our prior study has demonstrated a long-term moderate exercise (4-week of 60-min 74.0% V̇O2max treadmill running) is optimal in protecting from exhaustive exercise-induced cardiac ischemic injury. This study is aimed to investigate the effect of long-term moderate exercise on myocardial metabolome in rats. Thirteen male Sprague-Dawley rats were randomly assigned into the control group (C) and the long-term moderate exercise group (E). The targeted metabolomics of the myocardium was analyzed by ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS) system. Results showed that the metabolites categories of bile acids (BAs), fatty acids (FAs), and phenylpropanoic acids were significantly decreased. The biosynthesis of unsaturated FAs pathway was significantly downregulated. The altered metabolites in the E Group included decreased FAs (pentadecanoic acid, 10Z-heptadecenoic acid, dihomo-gamma-linolenic acid, docosahexaenoic acid, docosapentaenoic acid, and 10Z-nonadecenoic acid), decreased BAs (chenodeoxycholic acid and beta-muricholic acid), decreased organic acids (glycolic acid and 2-hydroxyglutaric acid), decreased carbohydrate (N-acetylneuraminic acid, Neu5Ac), decreased amino acids (α-aminobutyric acid and norvaline), decreased phenylpropanoic acids (hydroxyphenyllactic acid), and benzoic acids (4-hydroxybenzoic acid and phthalic acid). The results indicated that long-term moderate exercise has promoted lipids utilization in myocardium while exerted little influence on carbohydrate metabolism and diminished many detrimental metabolites. Notably, decrease of myocardial carbohydrate Neu5Ac after long-term moderate exercise might predict a prospective metabolomics biomarker for cardioprotection. This research has displayed the effect of long-term moderate exercise on myocardial metabolomic profiling in rats and indicated some promising metabolites which can be applied for exercise benefits in future.

Objective::This study aimed to evaluate the major adverse cardiovascular and cerebrovascular events (MACCEs) and overall safety profile associated with iodixanol in Chinese patients undergoing percutaneous coronary intervention (PCI).Methods::Patients at 30 centers in China registered in the OpenClinic v3.6 database from October 30, 2013, to October 7, 2015, were included in the study. The primary endpoint was in-hospital MACCEs including target lesion revascularization (TLR), stroke, stent thrombosis, cardiac death, and PCI-related myocardial infarction (MI) within 72 h post-PCI. Secondary endpoints were MACCEs from 72 h to 30 d post-PCI and other safety events within 30 d post-PCI.Results::A total of 3,042 patients were enrolled. The incidence of MACCEs within 72 h post-PCI was 2.33% ( n = 71), including cardiac death (0.03%, n = 1) and PCI-related MI (2.30%, n = 70). The incidence of MACCEs from 72 h to 30 d post-PCI was 0.16% ( n = 5), including cardiac death (0.10%, n = 3), PCI-related MI (0.03%, n = 1), and TLR for stent thrombosis (0.03%, n = 1). The incidence of composite angiographic or procedural complications was 2.86% ( n = 87); 233 (7.86%) patients had results suggesting contrast-induced acute kidney injury. Conclusions::These findings indicate that the use of iodixanol in Chinese patients undergoing PCI is associated with a low incidence of MACCEs, confirming its safety in this population.

目的 探讨替罗非班在急性前壁心肌梗死合并糖尿病患者介入治疗中不同用药途径的疗效差异.方法 选择急性前壁心肌梗死伴糖尿病并行急诊介入治疗患者200例,随机分为冠脉内推注替罗非班组(研究组)及静脉推注替罗非班组(对照组),各100例.比较2组TIMI血流分级、心电图回落程度、心绞痛发作次数、心功能指标、NT-ProBNP、ESR、CRP、CK-MB、TNI、Cre、Ure水平以及住院期间不良事件发生情况、安全性指标.结果 术后研究组TIMI血流3级人数高于对照组.研究组心电图回落程度高于对照组(P＜0.05).治疗后,2组心绞痛发作持续时间均明显缩短,研究组治疗后3d、7 d心绞痛发作持续时间低于对照组(P＜0.05);2组LVEF增加,LVEDD降低(P＜0.05),且研究组LVEF水平高于对照组,LVEDD低于对照组(P＜0.05);2组BNP、ESR、CRP水平显著下降(P＜0.05),且研究组NT-ProBNP、ESR、CRP的水平低于对照组(P＜0.05);2组血清CK-MB及TNI水平均显著下降(P＜0.05),且研究组血清CK-MB及TNI 水平显著低于对照组(P＜0.05).2组住院期间不良事件发生率比较,研究组无病死病例,对照组出现2例病死,2组无再次血运重建、新发心肌梗死出现.2组安全性指标比较,研究组出现2例出血,对照组出现1例心绞痛、8例出血.2组组间比较差异无统计学意义(P＞0.05).结论 替罗非班在急性前壁心肌梗死伴糖尿病行急诊介入治疗中,疗效较好,与静脉推注替罗非班相比,冠脉内推注替罗非班疗效更佳,且安全性较好,对肾功能指标改善效果较好.

The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.

目的 探究碎裂QRS波在新战士复检中的发生率、 分布特点及在训练中的预警意义.方法 回顾性分析某部3954例(男性3631例,女性323例)入伍新战士复检心电图,收集静息状态下的常规12导联心电图,筛选出fQRS波,统计fQRS波的发生率及发生部位.依据年龄18～25岁划分为八个组,男兵按兵种分为六组:空军1部、陆军1部、武警、通讯、空军2部、陆军2部,再按fQRS波出现导联分为肢导组、胸导组、胸导+肢导组.结果 fQRS波的整体发生率在性别和年龄上无统计学差异(P>0.05).fQRS发生率在入伍战士各年龄段无统计学差异(P>0.05).六个兵种男兵fQRS波发生率之间存在统计学差异(P<0.05).fQRS波同时发生于胸导和肢导的比例明显大于单纯发生于胸导/肢导的比例,具有显著差异(P<0.05).结论 fQRS波的发生率与运动强度之间具有一定联系,这种不同运动强度造成的fQRS波发生率之间差异可能与心肌损伤有一定关系.

OBJECTIVE:To investigate the effects of mitochondrion-targeted cyanine fluorescent small molecule IR-61 on cardiac injury induced by exhaustive exercise in rats.METHODS:Thirty-six adult male SD rats were randomly divided into 3 groups(n=12),control group (Ctrl), exhaustive exercise group (EE) and IR-61+ exhaustive exercise group (IR-61+EE). IR-61+EE group were intraperitoneally injected with 2 mg/kg IR-61 at the same time on day 1, 4 and 7. One hour after the end of the last drug administration, the two exhaustive exercise groups were subjected to exhaustive exercise modeling. The rats were placed on an animal treadmill with a slope of 0° at a speed of 10~15 m/min to coordinate their limbs running posture, and then ran at a speed of 25~30 m/min until exhaustion about 15 minutes later. After the animal models established, ECG was recorded by physiological recorder, myocardial injury was observed by light microscope, mitochondrial injury was observed by transmission electron microscope, myocardial cell apoptosis was detected by TUNEL method, markers of myocardial injury were detected by ELISA, and myocardial mitochondrial respiration rate was measured by high-resolution Oxygraph-2K mitochondrial instrument.RESULTS:① Compared with Ctrl group, heart rate was increased, PR interval was shortened, QRS interval was prolonged, QTc was prolonged and ST segment was depressed significantly in EE group (P＜0.05). In EE group, myocardial fiber fracture and mitochondrial inner chamber swelling were obvious, mitochondrial crest was fuzzy, mitochondrial outer membrane was incomplete, and a large number of mitochondrial rupture and fusion were visible. In EE group, TUNEL staining cells were abundant, chromatin concentration and marginalization, nuclear membrane lysis, chromatin fragmentation into massive apoptotic bodies, apoptosis score increased (P＜0.05). The levels of creatine kinase isoenzyme-MB (CK-MB), cardiac troponin I(cTn-I) and N-terminal B-type natriuretic peptide (NT-proBNP) were increased in EE group (P＜0.05). Basal respiration rate, oxidative respiration rate of fatty acids and respiration rate of complex Ⅰ, Ⅱ and Ⅳ were all decreased (P＜ 0.05). ② Compared with EE group, the heart rate in IR-61+EE group was increased, PR interval was prolonged, QRS interval was shortened, QTc was shortened, ST segment was not significantly depressed (P＜0.05). In IR-61+EE group, myocardial fiber arrangement was loose, no obvious fracture was observed, mitochondrial inner ventricle was swelling, mitochondrial outer membrane was intact, TUNEL stained cells and unstained cells were observed, the overall morphology was more similar to Ctrl group. Apoptosis index was decreased (P＜0.05), the levels of CK-MB and cTn-I were decreased in IR-61+EE group (P＜0.05). The oxidative respiration rate of fatty acids and the respiration rate of complex Ⅱ and Ⅳ were increased (P＜0.05).CONCLUSION:Mitochondrion-targeted cyanine fluorescent small molecule IR-61 can improve cardiac electrical activity, reduce myocardial cell injury and mitochondrial injury, reduce myocardial cell apoptosis, and improve the myocardial mitochondrial energy metabolism condition in exhausted rats.

妊娠期高血压(HDCP)是妊娠期的特发疾病,以妊娠20周后出现高血压、水肿、蛋白尿为主要表现的全身各器官和系统损害的一种妊娠期并发症,严重影响母婴健康,是孕产妇和围生儿患病及死亡的主要原因之一[1,2].降压治疗是HDCP的重要治疗手段,目的是预防子痫、心脑血管意外和胎盘早剥等严重母胎并发症,保证母儿安全,有效改善妊娠结局.我国2015年HDP诊治指南[3]参考了国际指南并结合我国国情建议:收缩压≥160 mmHg和(或)舒张压≥110 mmHg(1 mmHg=0.133 kPa)给予降压药物治疗,目标血压控制在130～155/80～105 mmHg,合并器官功能损伤,应控制130～139/80～89 mmHg,降压过程应平稳,避免过度波动,且血压不应低于130/80 mmHg,以保证子宫-胎盘的血流灌注[4].

To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague–Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.

运动导致的心源性猝死一直是运动医学领域重要问题.近年来,研究人员通过对运动员、部队作训人员等参与高强度运动训练者发生猝死的类型、频率及发病机理进行研究,在实验室从细胞及分子水平研究和探讨运动致心脏损伤的病理基础与发生机制,深入研究心脏损伤与运动性猝死的关系,从而制订出更加科学、合理的运动训练方案,科学指导各类作训人员进行运动训练,进而预防和减少心源性猝死事件的发生.

Stimulation with a low frequency electromagnetic field (LF-EMF) has proven to represent a powerful method for the suppression of seizures, as demonstrated in select clinical and laboratory studies. However, the mechanism by which LF-EMF suppresses seizures remains unclear. The purpose of the present study was to explore the modulatory effect of LF-EMF on epileptiform discharges (EDs) using rat hippocampal slices and investigate the underlying mechanisms that mediate these effects. EDs in hippocampal slices was induced by magnesium-free (zero-Mg2+) artificial cerebrospinal fluid (ACSF) and recorded using an in vitro micro-electrode array (MEA). A small sub-decimeter coil was designed and incorporated in a flexible magnetic stimulation device that allowed electromagnetic fields with different parameters to be delivered to slices. After a stable ED event was recorded, magnetic fields of 0.5 Hz (30 min) with a magnetic intensity of 0.13 mT (5 Vpp voltage input) and 0.25 mT (20 Vpp voltage input) were applied. The results indicated that a high-amplitude 0.5 Hz magnetic field could lead to persistent suppression of ictal discharges (IDs), while low-amplitude magnetic fields did not influence IDs. The persistent suppression of complex ED was prevented if the magnetic fields were applied in the presence of 10 μmol/L bicuculline (BIC), a γ-aminobutyric acid type A (GABAA) receptor antagonist, while the application of BIC subsequent to a magnetic field application led to the reappearance of ID. The addition of BIC resulted in EDs that had previously been inhibited by magnetic fields, reappearing. Low-frequency magnetic stimulation was able to inhibit the conversion from interictal discharges (IIDs) or preictal discharges (PIDs) to IDs. This suppression was attributed to the modulation of GABAA receptor activity.

目的 探讨心电图T波峰末间期(Tp-Te)、Tp-Te/QT比值对恶性室性心律失常(MVA)的诊断价值.方法 连续入选2017年1月1日至2018年1月1日于保定市第一中心医院西院心电图、脑电图二室行24 h 12导联动态心电图检查的患者412例为研究对象.根据是否发生恶性室性心律失常分为两组:恶性室性心律失常组72例;无恶性室性心律失常组340例.分别测定两组患者Tp-Te间期、QT间期,计算出Tp-Te间期、QTc间期及Tp-Te/QT比值,并对两组患者Tp-Te间期、QTc间期及Tp-Te/QT比值进行统计学分析.结果 恶性室性心律失常组的Tp-Te间期、Tp-Te/QT比值均较非恶性室性心律失常组明显增加(P<0.001).结论 Tp-Te间期、Tp-Te/QT比值增加对于恶性室性心律失常的发生均有预测价值.

目的 通过建立大鼠急性低氧运动模型,观察大鼠单个心室肌细胞瞬时外向钾电流(Ito)的改变,在细胞水平探究模拟高原低氧条件下力竭运动对心脏电生理的影响.方法 将40只健康雄性清洁级SD大鼠随机分为低氧运动组、低氧安静组、常氧运动组和常氧安静组,每组10只.利用小动物低压氧舱和常氧状态下进行力竭运动试验.取出各组大鼠心脏,利用灌流酶解法分离大鼠单个心室肌细胞,采用全细胞膜片钳技术记录大鼠单个心室肌细胞的瞬时外向钾电流.采用SPSS 20.0统计软件进行数据处理,多组间比较采用ANOVA方差分析,组间两两比较采用SNK-q检验.结果 与常氧安静组比较,+40 mV时,低氧运动组的Ito电流密度显著降低,且低于低氧安静组及常氧运动组,此效应呈现电压依赖性.门控机制研究显示,低氧运动时大鼠心肌细胞Ito稳态激活曲线失活向超极化方向移动,而稳态失活曲线则向去极化方向移动,二者综合效应使Ito电流显著降低.结论 急性低氧运动可通过改变钾通道稳态激活与稳态失活过程,降低大鼠心室肌细胞Ito,这可能是急性低氧运动导致心律失常的主要原因之一.

This study was to optimize the exercise preconditioning (EP) intensity in protecting from exhaustive exercise-induced cardiac injury (EECI). A total of 98 male Sprague-Dawley rats were divided into 7 groups (n ​= ​14): the control group (C), the exhaustive exercise group (EE) and the EP ​+ ​EE groups, which include the V10 (53.0%̇O2max), V15 (58.4%̇O2max), V20 (67.0%̇O2max), V26 (74.0%̇O2max) and V30 (80.0%̇O2max) groups. Except the C group, the other groups were subjected to treadmill running. The serum contents of N terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTn-I) were detected by the enzyme-linked immunosorbent assay method, ECG was recorded, heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway (ET pathway) complexes I, Ⅱ and IV were measured by high-resolution respiration instrument. Compared to the EE group, the EP groups have shown decrease of NT-proBNP and cTn-I, improvement of mitochondrial respiratory function and cardiac function. Compared to other EP groups, the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function. The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%̇O2max-74.0%̇O2max. High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I, improve electrical derangement and the left ventricular function, and raise the activities of ET pathway complexes I, Ⅱ and IV. The protection of EP on EECI was improved as the EP intensity was increased from 53.0%̇O2max to 74.0%̇O2max and when EP intensity was 74.0%̇O2max, the effect was the most obvious among all the setting EP groups.