目的:探讨在他汀类药物应用基础上短期内使用依洛尤单抗能否降低急性冠状动脉综合征(ACS)患者经皮冠状动脉介入术(PCI)术后主不良心血管事件(MACEs)的发生风险.方法:回顾性分析2019年1月—2019年10月于同济大学附属第十人民医院CCU收治的128例ACS患者为研究对象,根据是否使用依洛尤单抗分为试验组(41例)和对照组(87例),收集并比较两组患者人口统计学信息、实验室检查、基本临床信息、超声心动图结果、冠状动脉造影结果、基线血脂水平和PCI术后1个月血脂水平.对所有患者进行6个月随访,比较两组患者6个月MACEs发生情况,采用Kaplan-Meier生存分析法比较两组患者6个月随访期间MACEs和再发心肌梗死累积发生率.结果:试验组患者PCI术后1个月低密度脂蛋白胆固醇(LDL-C)水平显著低于对照组0.83(0.54,1.54)mmol/L∶ 1.71(0.98,2.30)mmol/L,P=0.004].经过6个月随访,试验组5例(12.2％)发生MACEs,对照组13例(14.9％)发生MACEs.两组患者在MACEs、死亡、卒中、靶血管再灌注等方面差异无统计学意义(P＞0.05);其中试验组再发心肌梗死0例.对照组再发心肌梗死9例(10.3％),差异有统计学意义(P = 0.027).Kaplan-Meier生存分析显示两组患者累积再发心肌梗死发生率差异有统计学意义(Log-Rank检验P = 0.039).结论:ACS患者在他汀类药物应用基础上短期内使用依洛尤单抗能有效地降低LDL-C水平,同时能降低ACS患者PCI术后6个月再发心肌梗死风险.

Background: Serine proteinase inhibitor A3 (SERPINA3) has been discovered in the pathogenesis of many human diseases, but little is known about the role of SERPINA3 in coronary artery disease (CAD). Therefore, we aim to determine its relationship with CAD and its function in the pathogenesis of atherosclerosis. Methods: In total 86 patients with CAD and 64 patients with non-CAD were compared. The plasma SERPINA3 levels were measured using ELISA. Logistic regression analysis and receiver-operating characteristic (ROC) analysis were performed to illustrate the association between plasma SERPINA3 levels and CAD. In vitro, real-time PCR (RT-PCR) and immunofluorescence staining were used to determine the expression of SERPINA3 in atherosclerotic plaques and their component cells. Then rat aortic smooth muscle cells (RASMCs) were transfected with siRNA to knock down the expression of SERPINA3 and human umbilical vein endothelial cells (HUVECs) were stimulated by SERPINA3 protein. EdU assay and scratch assay were used for assessing the capability of proliferation and migration. The cell signaling pathway was evaluated by western blot and RT-PCR. Results: Patients with CAD [104.4(54.5–259.2) μg/mL] had higher levels of plasma SERPINA3 than non-CAD [65.3(47.5–137.3) μg/mL] (P = 0.004). After being fully adjusted, both log-transformed and tertiles of plasma SERPINA3 levels were significantly associated with CAD. While its diagnostic value was relatively low since the area under the ROC curve was 0.64 (95% CI: 0.55–0.73). Secreted SERPINA3 might increase the expression of inflammatory factors in HUVECs. Vascular smooth muscle cells had the highest SERPINA3 expression among the aorta compared to endothelial cells and inflammatory cells. The knockdown of SERPINA3 in RASMCs attenuated its proliferation and migration. The phosphorylated IκBα and its downstream pathway were inhibited when SERPINA3 was knocked down. Conclusions: Elevated plasma SERPINA3 levels were associated with CAD. SERPINA3 can increase inflammatory factors expression in HUVECs. It can regulate VSMCs proliferation, migration, and releasing of inflammatory factors through the NF-κB signaling pathway. Thus, SERPINA3 played a significant role in the pathogenesis of atherosclerosis.

目的 通过心力衰竭(heart failure,HF)队列研究分析血清白蛋白与射血分数保留的心力衰竭(heartfailure with preserved ejection fraction,HFpEF)患者的预后关系.方法 连续收集2017年7月-2018年12月在同济大学附属第十人民医院住院的HF患者的一般人口学特征、伴随疾病、实验室检查、心脏彩超检查、药物治疗情况等资料(源于GREATWAL研究,编号:NCT04062500).排除其他类型HF等情况后,最终纳入317例HFpEF患者.根据血清白蛋白的中位数把HFpEF患者分为低白蛋白组(＜40 g/L)和正常白蛋白组(≥40 g/L),并比较了两组之间的临床特征差异.此外通过K-M生存曲线和Cox回归模型评估血清白蛋白对HFpEF患者全因死亡率的影响.结果 Spearman相关分析显示,血清白蛋白和C-反应蛋白负相关(rs=-0.242,P＜0.001),与丙氨酸转氨酶、天冬氨酸转氨酶、血尿素氮、血肌酐无关(P＞0.05).在K-M生存曲线分析中,两组间差异有统计学意义(log-rank检验,P=0.011).在单因素Cox回归分析中,低白蛋白分组的HFpEF患者的全因死亡风险比为2.255(95％ CI:1.183～4.301,P=0.014).在多因素Cox回归分析中,低白蛋白分组的HFpEF患者全因死亡风险比为2.095(95％CI:1.098～ 3.998,P=0.025).结论 血清白蛋白可能是HFpEF患者全因死亡的独立预测因素.

Improved non-invasive localization of the epileptogenic foci prior to epilepsy surgery would improve surgical outcome in patients with partial seizure disorders. A critical component for the identification of the epileptogenic brain is the analysis of electrophysiological data obtained during ictal activity from prolonged intracranial recordings. The development of a noninvasive means to identify the seizure onset zone (SOZ) would thus play an important role in treating patients with intractable epilepsy. In the present study, we have investigated non-invasive imaging of epileptiform activity in patients with medically intractable epilepsy by means of a cortical potential imaging (CPI) technique. Eight pediatric patients (1M/7F, ages 4-14 years) with intractable partial epilepsy were studied. Each patient had multiple (6 to 14) interictal spikes (IIS) subjected to the CPI analysis. Realistic geometry boundary element head models were built using each individual's MRI in order to maximize the imaging precision. CPI analysis was performed on the IISs, and extrema in the estimated CPI images were compared with SOZs as determined from the ictal electrocorticogram (ECoG) recordings, as well as the resected areas in the patients and surgical outcomes. The distances between the maximum cortical activities of the IISs reflected by the estimated cortical potential distributions and the SOZs were determined to quantitatively evaluate the performance of the CPI in localizing the epileptogenic zone. Ictal ECoG recordings revealed that six patients exhibited a single epileptogenic focus while two patients had multiple foci. In each patient, the CPI results revealed an area of activity overlapping with the SOZs as identified by ictal ECoG. The distance from the extreme of the CPI images at the peak of IIS to the nearest intracranial electrode associated with the onset of the ictal activity was evaluated for each patient and the averaged distance was 4.6mm. In the group of patients studied, the CPI imaged epileptogenic foci were within the resected areas. According to the follow-up of the eight patients included, two were seizure free and six had substantial reduction in seizure frequency. These promising results demonstrate the potential for noninvasive localization of the epileptogenic focus from interictal scalp EEG recordings. Confirmation of our results may have a significant impact on the process of presurgical planning in pediatric patients with intractable epilepsy by dramatically reducing or potentially eliminating the use of intracranial recording.

Objective To explore the distribution of atrial premature beats( APC)foci following pulmonary vein isolation for atrial fibrillation(AF) and to evaluate the effectiveness of reablation. Methods Twentyone patients( 13 males,mean age of 51.2 ±8. 7 years)were enrolled after a mean of (2. 3 ± 1.1 )months following AF ablation. By 24 h Holter monitoring the mean amount of APC was 12110 ± 375. Pulmonary vein(PV) reisolation was applied if APC were from PV,and 3D mapping and ablation was performed if the origin APC foci were unknown. ECG and Holter were used to evaluate the effectiveness of APC ablation. Results PV re-connection as the APC origin was found in 2 cases and was re-isolated by gaps ablation in initial lesion lines. No PV potentials detected in other 19 cases. APC originated from left atrium(LA) in 14 cases,including from upper postero-superior wall in 2 cases, postero-inferior wall in 4 cases, roof area in 4 cases, and left antero-superior wall in 2 cases. APC originated from right atrium ( RA ) in 7 cases, including from coronary sinus ostium in 1 case ,middle crista terminalis in 2 cases, high RA septum in 2 cases, RA posteo-superior wall in 1 case ,and six o'clock site of tricuspid annulus in 1 case. Catheter ablation eliminated APC in 18 (85.7 % )cases. At the end of( 11.7 ± 4. 2 ) months of follow-up, 17 ( 81% ) cases were free of APC recurrence. Conclusion The distribution of APC foci following paroxysmal AF ablation was discrete. APC originated from LA in two thirds of patients, but usually was uncorrelated with PV conduction recovery. Less commonly APC originated from RA. APC following AF ablation could be treated effectively by 3-D mapping and ablation.

当前肥胖的迅速流行已成为全球的首要健康问题，特别是腹型肥胖发生心血管疾病的危险性明显增加。大量研究表明，脂肪组织不仅是能量储存器官，还是一个能分泌多种生物活性因子如瘦素、脂联素(adiponectin)、抵抗素、IL-6、TNF-α等的内分泌和代谢器官，其中，脂联素是与代谢综合征、心血管疾病惟一呈负相关的一种脂肪因子，自1995年被发现，因其在一、二级预防中的预测价值和血管保护作用而受到日益广泛关注。血清脂联素在肥胖、2型糖尿病（DM）、高血压和冠心病患者中明显降低，具有广泛的生物学活性，如抗炎，改善胰岛素敏感性、调节糖脂代谢和抗动脉粥样硬化作用。分子流行病学研究表明脂联素的表达受基因的调节并共同影响冠心病的发生和发展。现就脂联素及其基因多态性与冠心病的研究进展作一综述。