OBJECTIVE:This Mendelian randomization (MR) study aimed to investigate the relationships between type 1 diabetes (T1D), type 2 diabetes (T2D), and glycemic traits, including fasting insulin, fasting glucose, and HbA1c, with cardiovascular diseases (CVDs).METHODS:We selected genetic instruments for predisposition to T1D, T2D, fasting insulin, fasting glucose, and HbA1c based on published genome-wide association studies. Using a 2-Sample MR approach, we assessed associations with 12 common CVDs sourced from the FinnGen and UK Biobank studies, along with stroke subtypes obtained from the GIGASTROKE and MEGASTROKE Consortium.RESULTS:T1D was associated with SVS. T2D showed associations with AIS, LAA, CES, SVS, coronary heart disease, myocardial infarction, pulmonary embolism, DVT of lower extremities, peripheral vascular diseases. Genetically predicted higher HbA1c levels were associated with eight CVDs. The results of MVMR aligned with the primary findings for T1D and T2D.CONCLUSIONS:T1D and T2D exhibit different genetic predisposition to CVDs. BMI, LDL, and HDL play intermediary roles in connecting TID and T2D to specific types of CVDs, providing insights into the potential underlying pathways and mechanisms involved in these relationships. Strategies aimed at achieving sustained reductions in HbA1c levels may offer potential for reducing the risk of various CVDs.

Background: No evidence exists on the impact of bivalirudin in patients with the acute coronary syndrome undergoing rotational atherectomy. This study aimed to evaluate the impact of bivalirudin on patients with acute coronary syndrome undergoing rotational atherectomy. Methods: This was a retrospective cohort study conducted in our hospital between January 2017 and December 2019. The study included patients with acute coronary syndrome undergoing rotational atherectomy. Furthermore, 2 cohorts were included in this study (bivalirudin cohort and control cohort unfractionated heparin). The primary end-point was in-hospital net adverse clinical events. The secondary endpoint was all-cause mortality at 23 months. Results: The study included 157 patients with 33 (21.0%) in the bivalirudin cohort and 124 (79.0%) in the control cohort. Net adverse clinical events during hospitalization in the bivalirudin cohort were higher than that in the control cohort [9 (27.3%) vs. 14 (11.3%), P = .021]. However, there was no significant difference in all-cause mortality at 23 months between the 2 cohorts [25 (20.2%) vs. 10 (30.3%), P =.214]. After adjusting for potential confounders, the usage of bivalirudin was not associated with net adverse clinical event (odds ratio = 0.90; 95% CI: 0.18-4.45; P =.890), and the hazard ratio for all-cause mortality at 23 months was 1.01 (95% CI: 0.33-3.15; P =.983). Conclusion: Bivalirudin appears to exhibit a similar impact as unfractionated heparin on patients with acute coronary syndrome undergoing rotational atherectomy in real-life setting.

目的 探讨冠状动脉旋磨术中发生旋磨头嵌顿的处理方法.方法 回顾分析2018年1月至2020年12月中国科学技术大学附属第一医院行冠状动脉旋磨术患者362例,其中发生旋磨头嵌顿14例.分析及归纳旋磨头嵌顿的不同处理方法.结果 分析14例发生旋磨头嵌顿患者的原因和处理方法,总结取出嵌顿旋磨头的几种方法:(1)旋磨头低速或高速交替旋转并同时前送及后退取出旋磨头;(2)通过另一根导丝送入球囊至旋磨头嵌顿位置反复扩张松解局部组织,取出旋磨头;(3)采用Guidezilla延长导管套在旋磨导管上取出旋磨头.结论 旋磨头嵌顿是一种少见但非常严重的旋磨并发症.根据本中心的经验,采取规范的处理流程和操作方法可以成功取出嵌顿的旋磨头.

目的 探讨合并心原性休克(CS)的急性心肌梗死(AMI)患者行急诊经皮冠状动脉介入治疗(PCI)后1年内死亡的预测因素.方法 连续纳入中国科学技术大学附属第一医院2014年1月至2018年1月符合入选条件的所有患者298例.根据1年随访时患者生存情况分为死亡组111例(37.2％)和存活组187例(62.8％).分析两组患者临床资料,绘制随访1年生存曲线.采用多因素Cox回归分析PCI术后影响远期预后的危险因素.结果 通过多因素Cox回归分析发现有意义的死亡预测因素有4个,分别是年龄≥75岁(HR 1.68,95％CI 1.31～2.16,P<0.001),PCI术后靶血管心肌梗死溶栓治疗试验(TIMI)血流分级≤Ⅱ级(HR 3.57,95％CI 2.06～6.18,P<0.001)、左心室射血分数<40％(HR 0.45,95％CI 0.26～0.78,P=0.004)以及首次医疗接触至球囊扩张(FMC-to-B)时间>12 h(HR 7.52,95％CI 3.28～17.24,P<0.001).1年随访Kaplan-Meier生存曲线显示AMI合并CS患者行急诊PCI术后3个月内死亡率高.结论 主动脉内球囊反搏是AMI合并CS最常用的机械循环辅助救治手段.在众多危险因素中FMC-to-B时间延迟、PCI术后靶血管TIMI血流分级≤Ⅱ级、高龄、左心室射血分数低是AMI合并CS患者PCI术后1年内死亡的预测因素.

目的:基于非标记蛋白组学方法筛选冠状动脉(冠脉)严重钙化病变患者外周血浆中的特异性蛋白质标志物.方法:采用数据非依赖采集质谱技术检测30例冠脉严重钙化病变患者与30例非钙化对照人群血浆,生物信息学软件进一步分析差异表达蛋白质数据.结果:冠脉严重钙化病变患者与非钙化人群血浆相比较,共筛选出表达量差异2倍以上的差异蛋白共28种(其中表达上调的蛋白20种,表达下调的蛋白8种),基因本体论(GO)分析差异表达蛋白主要分布于细胞外区域、细胞外泌体和胞外细胞器部分;生物学过程主要涉及细胞过程、肌动蛋白细胞骨架和应激反应、白细胞介导的免疫和细胞活化;而其分子功能与蛋白质结合、信号受体结合和肌动蛋白结合相关.京都基因与基因组百科全书(KEGG)分析显示差异表达蛋白与补体和凝血级联、糖酵解/糖异生作用、细胞凋亡、HIF-1和Rap1信号通路相关.结论:冠脉严重钙化病变患者和非钙化人群的血浆蛋白质组学存在显著差异,这些差异表达蛋白质有望成为冠脉严重钙化病变鉴别诊断的新型生物标志物.

目的:探讨经皮冠状动脉腔内旋磨术(RA)在冠状动脉严重钙化的非ST段抬高型急性冠脉综合征(NSTE-ACS)患者中的安全性.方法:纳入2017年1月至2019年12月在安徽省立医院接受RA联合经皮冠状动脉介入术(PCI)的冠状动脉粥样硬化性心脏病(冠心病)患者共248例.排除近3个月内发生过急性ST段抬高型心肌梗死(STEMI)并行溶栓或急诊介入手术10例,最终纳入238例,分为NSTE-ACS组120例和稳定型冠心病(SCAD)组118例,比较两组的基线特征、即刻手术成功率、围术期并发症、院内以及1年和3年的主要不良心血管事件(MACEs).结果:在基线资料中,NSTE-ACS组的心率、N末端脑钠肽前体(NT-proBNP)水平以及替罗非班使用明显高于SCAD组,而左室射血分数(LVEF)明显低于SCAD组(P均＜0.05).冠状动脉造影显示NSTE-ACS组单支血管病变比例更高,而SCAD组多支病变的比例更高(P＜0.05),其余介入术中相关资料比较均未见统计学差异.2组患者RA术中冠状动脉慢血流/无复流、夹层、穿孔等并发症的发生率相当,且住院期间以及1年、3年内的MACEs发生率均无统计学差异.结论:对于冠状动脉严重钙化的NSTE-ACS患者,由于斑块不稳定,RA造成冠状动脉慢血流或无复流、冠状动脉夹层的风险可能高于SCAD,但其即刻手术成功率、院内及远期预后无显著差异.对于严重钙化的NSTE-ACS患者,RA是一种安全可行的方法.

心脏骤停是一种对人体危害非常大的疾病,在很短时间内就会危及患者的生命.虽经心肺复苏但自主循环恢复伴有良好的神经功能状态的患者极少,长期生存率极低,是世界所有国家面临的难题.各个国家对长期生存率研究数据不同且也较少,影响脑复苏的因素较多,就本例老年患者在家中突发心脏骤停进行心肺脑复苏成功全程报告,并进行探讨,以提高脑复苏的成功率.

目的 评价冠状动脉旋磨术(RA)治疗冠状动脉弥漫性钙化病变(长度≥25 mm)的有效性及安全性.方法 将158例严重冠状动脉钙化患者按照冠脉造影显示病变长度分为研究组(长度≥25 mm)和对照组(长度<25 mm),比较两组患者的主要心血管不良事件(MACE)发生率、即刻成功率、临床终点的差异.结果 所有患者手术成功率96.2％;两组患者术中冠状动脉穿孔、慢血流或无复流、B型以上冠状动脉夹层发生率差异无统计学意义(P>0.05);两组患者术后随访主要MACE发生率差异无统计学意义(P>0.05).结论 冠状动脉旋磨术在冠状动脉弥漫性钙化病变的应用中是有效且安全的.

目的 探讨泛素羧基末端水解酶L1在小鼠心肌纤维化发生发展中可能的分子机制.方法 雄性小鼠(每组6只)皮下植入缓释泵持续灌注血管紧张素Ⅱ(Ang Ⅱ),并给小鼠腹腔注射UCHL1特异性抑制剂LDN57444.14 d后检测小鼠心脏功能变化,天狼猩红染色方法检测小鼠心肌纤维化程度.分离纯化小鼠心肌成纤维细胞,随机分为3组:对照组(细胞+培养基)、P组(细胞+培养基+PDGF-DD)、PL组(细胞+培养基+PDGF-DD+LDN57444),荧光定量PCR检测mRNA表达水平,蛋白印迹法检测蛋白表达水平.结果 动物实验中与对照组比较,Ang Ⅱ灌注2周后小鼠收缩压升高,心脏机构功能发生改变,应用UCHL1特异抑制剂LDN57444处理后可抑制Ang Ⅱ诱导的这些作用,天狼猩红染色心肌纤维化程度降低.qRT-PCR法显示PL组中Ⅰ型胶原蛋白的mRNA表达水平低于P组,P、PL组中UCH-L1的mRNA表达水平高于对照组.Western blot法显示P组中PDGFRβ/p-PDGFRβ、UCH-L1、pRb/Rb、Col Ⅰ 的蛋白表达水平均高于对照组,PL组中PDGFRβ/p-PDGFRβ、Col Ⅰ、pRB/RB的蛋白表达量低于P组.染色质免疫共沉淀检测显示NF-κB蛋白调控下游UCH-L1基因转录.结论 UCH-L1参与调控小鼠的心脏成纤维细胞增殖,机制可能是通过PI3K、AKT和NF-κB信号轴通路调节UCH-L1表达,UCH-L1调控下游Rb蛋白的表达,通过调控细胞周期,抑制UCH-L1可减轻小鼠心肌纤维化.

背景 既往研究认为冠状动脉慢性完全闭塞性病变(CTO)患者行经皮冠状动脉介入治疗(PCI)后可以改善临床症状,而临床症状的改善与哪种心电复极指标改变相关,目前研究较少,且对其的认识处于初级阶段.目的 本研究旨在了解单支及多支血管CTO患者CTO-PCI后心电复极指标变化情况,从而为不同类型CTO患者进行CTO-PCI提供更多电生理方面的客观证据.方法 选取2017年5月—2019年5月于中国科学技术大学附属第一医院心内科住院并成功行PCI(PCI成功的标准:CTO-PCI后血管残余狭窄<30％,前向血流TIMI>3级)的CTO患者249例.按照主要冠状动脉(前降支、回旋支、右冠状动脉)CTO的血管支数分为单支CTO组(n=192例);多支(两支或三支)CTO组(n=57例).比较两组患者心率、侧支循环Rentrop分级、校正QT间期(QTc)、QT离散度(QTd)、T波尖峰-T波末尾时限(Tp-Te)、T波改善比例以及所有患者随访6个月,比较纽约心功能分级及主要心血管不良事件(MACE)发生率.结果 单支CTO组和多支CTO组的侧支循环Rentrop分级比较,差异无统计学意义(P>0.05).术后多支CTO组QTc小于单支CTO组,T波改善比例高于单支CTO组(P<0.05).术后随访6个月,单支CTO组MACE发生率高于多支CTO组(P<0.05).结论 CTO患者血运重建后,复极指标均有改善,多支CTO患者复极指标改善更为明显,临床受益可能来自于细胞活力增强和复极离散指标的双重改善.

The ubiquitin-proteasome system (UPS) plays an essential role in cellular homeostasis and myocardial function. Ubiquitin carboxy-terminal hydrolase 1 (UCHL1) is involved in cardiac remodeling, but its underlying mechanisms are largely unknown. Here, we observed that the UCHL1 was significantly up-regulated in angiotensin II-infused heart and primary cardiac fibroblast (CF). Systemic administration of the UCHL1 inhibitor LDN57444 significantly ameliorated cardiac fibrosis and improved cardiac function induced by angiotensin II. Also, LDN57444 inhibited CF cell proliferation as well as attenuated collagen I, and CTGF gene expression in the presence of Ang II. Mechanistically, UCHL1 promotes angiotensin II-induced fibrotic responses by way of activating nuclear factor kappa B (NF-κB) signaling. Moreover, suppression of the NF-κB pathway interfered with UCHL1 overexpression-mediated fibrotic responses. Besides, the chromatin immunoprecipitation assay demonstrated that NF-κB can bind to the UCHL1 promoter and trigger its transcription in cardiac fibroblasts. These findings suggest that UCHL1 positively regulates cardiac fibrosis by modulating NF-κB signaling pathway and identify UCHL1 could be a new treatment strategy for cardiac fibrosis.

目的 探讨血清胱抑素C及左心室射血分数(LVEF)对经皮冠状动脉介入治疗(PCI)的急性心肌梗死(AMI)患者1年全因死亡的预测价值.?方法 选取2017年1月至2018年12月中国科学技术大学附属第一医院住院且行急诊PCI的AMI患者306例,对患者进行为期12个月的随访,随访结束后根据患者是否死亡分为存活组280例和死亡组26例.收集患者住院期间的相关临床资料、实验室检查及超声心动图检查指标,采用多因素Logistic回归分析AMI患者术后1年全因死亡的风险因素,采用ROC曲线分析血清胱抑素C及LVEF对AMI患者术后1年全因死亡率的预测价值.?结果 两组患者Gensini评分、年龄、肌酐、尿素氮、胱抑素C、N端B型脑钠肽前体(NT-proBNP)、LVEF、红细胞计数、吸烟及合并糖尿病情况比较差异均有统计学意义(t/χ2=-2.498、-3.610、-4.661、-3.812、-5.356、-4.812、6.843、-2.564、8.052、5.326,P<0.05).多因素Logistic回归分析显示,胱抑素C是AMI患者术后1年死亡的危险因素[OR(95％CI)=4.382(1.331～14.428),P<0.05],LVEF是AMI患者术后1年死亡的保护因素[OR(95％CI)=0.894(0.853～0.936),P<0.05].血清胱抑素C及LVEF对AMI术后患者1年全因死亡的预测界值分别为1.205 mg/L、54.5％,敏感度分别为0.69,0.88,特异度分别为0.81,0.63.?结论 胱抑素C和LVEF是AMI患者PCI术后1年全因死亡的重要影响因素,能够有效预测AMI患者术后1年死亡的发生.

目的探讨个性化护理在冠状动脉钙化病变病人冠脉旋磨术围手术期中的应用效果。方法选取2016年3月至2018年3月我院收治的冠脉钙化病变并行冠脉旋磨术治疗的110例病人作为研究对象,将其随机分为对照组（55例）和观察组（55例）。对照组病人采用冠状动脉旋磨术围手术期常规护理,观察组病人在此基础上进行个性化的护理干预,评估并比较2组病人术后的并发症发生率、护理水平及护理满意度。结果观察组慢血流发生率明显低于对照组,护理水平评分及病人对护理工作的满意度明显高于对照组,且差异均有统计学意义（P＜0. 05）。结论冠状动脉旋磨术围手术期采用个性化的护理方式较围手术期常规护理可以提高临床护理的护理质量水平和病人对护理工作的满意程度,减少病人并发症的发生率,值得临床上相关科室进一步推广和应用。

目的 探讨单支冠状动脉慢性完全闭塞病变患者(CTO),经皮冠状动脉介入术(PCI)前后T波振幅、Tpeak-Tend (Tp-Te)等十二导联心电指标以及随访6个月比较纽约心功能(NYHA)分级的改善情况.方法 纳入成功行CTO-PCI的单支血管CTO患者192例,按有无合并陈旧性心肌梗死分为合并陈旧性心肌梗死的CTO组(MICTO组,106例)、不合并陈旧性心肌梗死的CTO组(non-MI CTO组,86例),比较两组心电指标术前术后变化情况以及6个月后NYHA分级.结果 两组患者心电指标中,术前下壁导联的T波振幅,下壁、前壁导联Tp-T指标差异有统计学意义(P＜0.05);术后仅有Ⅰ、Ⅲ导联的Tp-Te差异有统计学意义(P＜0.05).MI CTO组术后心电复极指标T波振幅、Tp-Te均有导联,较术前差异有统计学意义(P＜0.05).non-MI CTO组血运重建后,7个导联(Ⅰ导联、Ⅲ导联、AVR导联、AVF导联、V4导联、V5导联、V6导联)的Tp-Te差异有统计学意义(P＜0.05),随访6个月,组间比较NYHA分级差异无统计学意义,而组内比较NYHA分级差异有统计学意义(P＜0.05).结论 CTO患者血运重建后心电复极指标和心功能分级均会改善,non-MI CTO患者,由Tp-Te改善引起,而MICTO患者是因为T波振幅和Tp-Te的双重改善引起.

目的 研究Culotte techniques(DK-Mini-Culotte)双支架术及Crush techniques(DK-Mini-Crush)双支架术式治疗冠状动脉分叉病变主要不良心脏事件发生情况.方法 纳入2015年7月至2019年1月中国科学技术大学附属第一医院收治的221例冠状动脉分叉病变患者,按照手术方式分两组,其中观察组行DK-Mini-Crush术(154例),对照组接受DK-Mini-Culottc术(67例).比较两组造影特征及经皮冠状动脉介入治疗(PCI)情况(包括主支病变长度、分支病变长度、主支支架长度、分支支架长度、平均支架植入数、手术时间、造影剂总量、住院天数及病变分布特点、手术成功率、最终对吻球囊扩张成功率、主支即刻造影成功率、分支即刻造影成功率),分析两组术后主要不良临床事件发生情况.结果 两组主支病变长度、分支病变长度、主支支架长度、分支支架长度、平均支架植入数、手术时间、造影剂总量、住院天数及病变分布情况、手术成功率、最终对吻球囊扩张成功率、主支即刻造影成功率、分支即刻造影成功率比较差异均无统计学意义(JP＞0.05).观察组术后支架内再狭窄率为1.30％,显著低于对照组的7.46％(x2=3.948,P＜ 0.05),出血、再发心绞痛、心源性死亡、病变血运重建所占比例较对照组比较差异均无统计学意义(P＞0.05). 结论 DK-Mini-Crush术与DK-Mini-Culotte术治疗冠状动脉分叉病变最终对吻球囊扩张成功率均较高,均具有良好的临床及造影结果,但后者支架内再狭窄率相对较高,临床应引起足够重视.

Induction of autophagy promotes cardiomyocyte survival and confers a cardioprotective effect on acute myocardial infarction (AMI). Our previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse AMI. Herein, this study further investigated whether the mechanisms by which MALAT1 enhanced cardiomyocyte apoptosis involved the autophagy regulation. To address this, cardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The cell apoptosis was evaluated using TUNEL staining and Western blot analysis of apoptosis-related proteins. The autophagy level was assessed using GFP-LC3 immunofluorescence and Western blot analysis of autophagy-related proteins. The results showed that H/R injury increased MALAT1 expression. Furthermore, MALAT1 overexpression significantly enhanced apoptosis and regulated autophagy of cardiomyocytes, whereas MALAT1 knockdown exerted the opposite effect. Moreover, rapamycin (an autophagy activator) effectively attenuated the MALAT1-mediated enhancement of cardiomyocyte apoptosis. Overall, our findings demonstrated that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis, at least in part, through autophagy modulation.

目的:探讨急性心肌梗死(AMI)患者院内死亡的影响因素,构建预测AMI患者院内死亡的列线图模型.方法:收集中国科学技术大学附属第一医院心内科2017-01--2018-12收治的331例行急诊冠脉介入治疗的AMI患者,按住院期间是否发生院内死亡分为院内死亡组(25例)和非院内死亡组(306例),利用最小绝对收缩选择算子(least absolute shrinkage and selection operator,LASSO)回归法和多因素Logistic回归分析AMI患者院内死亡的影响因素,并建立预测AMI患者院内死亡的列线图模型.结果:LASSO回归及Logistic回归分析结果均提示,NT-proBNP、心率、随机血糖、血肌酐、中性粒细胞绝对值为AMI患者发生院内死亡的独立影响因素(P＜0.05).利用上述指标构建列线图模型,经内部验证(Bootstrap重抽样1 000次)后可知,该模型预测AMI患者院内死亡发生的曲线下面积(AUCROC)为0.927(95％CI:0.855～0.998),灵敏度为88.00％,特异度为94.10％.结论:本研究结果显示NT-proBNP、心率、随机血糖、血肌酐、中性粒细胞绝对值为AMI患者发生院内死亡的独立危险因素,依此绘制的列线图模型能直观、简洁地为AMI患者提供个体化的院内死亡风险预测.

背景 单核细胞与高密度脂蛋白胆固醇比值(MHR)是近年发现的一种新型炎性标志物,与人体内氧化应激和炎性反应密切相关.目前已证实,MHR升高与冠心病的病理过程及不良预后有关,且与冠心病患者的心血管事件发生相关.高尿酸血症参与了炎性反应,在理论上会提高MHR,从而加速冠状动脉粥样硬化病变进展,但相关研究较少.目的 分析MHR在冠心病合并高尿酸血症患者中的变化,并探讨其与冠心病患者冠状动脉狭窄程度的关系.方法 选取2017年6月—2018年6月于中国科学技术大学附属第一医院经冠状动脉造影确诊的冠心病患者1337例,根据尿酸水平分为高尿酸血症组(n=318)和尿酸正常组(n=1019);根据冠状动脉造影结果分为轻度狭窄组(n=507)、中度狭窄组(n=482)和重度狭窄组(n=348);选取同期于本院体检健康者204例为对照组.比较对照组、尿酸正常组和高尿酸血症组与对照组、轻度狭窄组、中度狭窄组和重度狭窄组受试者一般资料和实验室检查指标,MHR与冠心病患者冠状动脉狭窄程度的相关性分析采用Pearson相关分析;冠心病患者冠状动脉狭窄程度的影响因素分析采用多因素Logistic回归分析.结果 对照组受试者低密度脂蛋白胆固醇(LDL-C)、MHR低于高尿酸血症和尿酸正常组(P<0.05),尿酸正常组患者MHR低于高尿酸血症组(P<0.05).对照组受试者LDL-C、尿酸及MHR低于轻度狭窄组、中度狭窄组和重度狭窄组(P<0.05),轻度狭窄组患者糖尿病病史率、吸烟史率、LDL-C、MHR低于中度狭窄组和重度狭窄组(P<0.05),中度狭窄组患者糖尿病病史率、吸烟史率、LDL-C、MHR低于重度狭窄组(P<0.05);Pearson相关分析结果显示,MHR与冠心病患者冠状动脉狭窄程度呈正相关(r=0.826,P<0.001).多因素Logistic回归分析结果显示,LDL-C〔OR=3.228,95％CI(1.374,7.588)〕、MHR〔OR=3.597,95％CI(1.024,12.634)〕是冠心病患者冠状动脉狭窄程度的影响因素(P<0.05).结论 MHR在冠心病合并高尿酸血症患者中较高,与冠心病患者冠状动脉狭窄程度呈正相关,且是冠心病患者冠状动脉狭窄程度的影响因素.

Myocardial injury has been deemed as a major cause of heart diseases including myocarditis and coronary heart disease, which have brought multiple mortalities globally. Long non-coding RNAs (lncRNAs) are widely recognized in diverse diseases. However, the role of circular RNA HIPK2 (circ-HIPK2) remains unclear in myocardial injury induced by H2O2. We attempted to investigate the probable role of circ-HIPK2 in myocardial injury induced by H2O2. This study discovered that the treatment of H2O2 inhibited cell proliferation but boosted cell apoptosis and autophagy. ATG101 was upregulated in primary mouse neonatal cardiomyocytes under H2O2 treatment. ATG101 knockdown promoted proliferation and limited apoptosis by attenuating autophagy in H2O2-injured mouse neonatal cardiomyocytes. Furthermore, miR-485-5p was validated to combine with ATG101 and circ-HIPK2, and circ-HIPK2 positively regulated ATG101 expression by sponging miR-485-5p. At last, silenced circ-HIPK2 mediated the promotion of cell proliferation, and repression of cell apoptosis was restored by ATG101 amplification. In a word, circ-HIPK2 facilitates autophagy to accelerate cell apoptosis and cell death in H2O2-caused myocardial oxidative injury through the miR-485-5p/ATG101 pathway, indicating a novel therapeutic target point for patients with myocardial injury.

The aim of the study was to compare the clinical efficacy and safety of ticagrelor and clopidogrel in patients with coronary heart disease one year after percutaneous coronary intervention (PCI), and to explore their association with the CYP2C19 gene polymorphism. A total of 971 patients with coronary heart disease who were hospitalized and underwent PCI from April 2016 to May 2017 were studied. All 971 patients were divided into three subgroups according to CYP2C19 gene types as fast metabolizing, slow metabolizing and very slow metabolizing type. Patients were also classified according to the oral antiplatelet aggregation drugs they received: clopidogrel group and ticagrelor group. The incidence of major adverse cardiac events (MACE) and bleeding events in the clopidogrel-treated and ticagrelor-treated groups and in patients with fast, slow, and very slow CYP2C19 metabolisms were compared. Binary logistic regression analysis was carried out to analyze the risk factors associated with MACEs and hemorrhagic events. Patients on ticagrelor had a greater number of bleeding complications compared to those on clopidogrel (P<0.001), with no difference in MACE between the two groups (P=0.399). The incidence of MACE was significantly higher in very slow metabolizing patients receiving clopidogrel (P<0.001) while the incidence of bleeding complications was significantly higher in fast metabolizing patients receiving ticagrelor (P<0.001). The regression analysis revealed that the CYP2C19 gene mutation, a dual-antiplatelet therapy, and a stroke history were all significantly associated with MACE. By contrast, a dual-antiplatelet therapy and a stroke history were significantly associated with bleeding events. Findings of the present study indicated that clopidogrel and ticagrelor were equally efficacious post-PCI. Efficacy of clopidogrel was reduced in patients with very slow CYP2C19 genotype while bleeding complications were higher in patients with fast CYP2C19 genotype receiving ticagrelor. CYP2C19 genotyping may be used to provide guidance to optimize individual antiplatelet treatment.