Acute coronary syndrome (ACS) is a serious cardiovascular condition and a leading cause of mortality worldwide. Notably, 12/15-lipoxygenase (ALOX15) can be regulated by the long non-coding RNA ENST00000538705.1, thereby facilitating the progression of ACS. However, the downstream regulatory mechanisms involving ALOX15 remain unclear. The viability and migration of human primary coronary artery endothelial cells (HCAECs) were assessed using the Cell Counting Kit-8 and scratch assays, respectively. Reverse transcription-quantitative PCR was performed to assess the mRNA expression levels of ALOX15 and fibroblast growth factor receptor 2 (FGFR2). Protein-protein interactions between ALOX15 and FGFR2 were verified by co-immunoprecipitation (CO-IP). An ACS rat model was established to examine the effects of ALOX15 on blood lipid levels. Hematoxylin and eosin staining was executed to assess the histological changes. The levels of the FGFR2/PI3K/AKT signaling pathway-related proteins were assessed by western blotting. The results revealed elevated expression levels of ALOX15 and FGFR2 in patients with ACS. In HCAECs, transfection of overexpressed ALOX15 markedly enhanced cell viability and migration, while small interfering RNA-ALOX15 transfection produced the opposite effects. CO-IP assays confirmed the interaction between ALOX15 and FGFR2 in HCAECs. Additionally, knockdown of ALOX15 reduced blood lipid levels and alleviated myocardial injury in rats with ACS. ALOX15 silencing inhibited the expression of proteins associated with the FGFR2/PI3K/AKT signaling pathway in both HCAECs and rats with ACS. Both the overexpression of FGFR2 and the supplementation with insulin like growth factor 1 (a specific agonist of the PI3K/AKT pathway) significantly mitigated the inhibitory effects of ALOX15 knockdown on the migratory and proliferative capacities of HCAECs. The findings of the present study indicated that silencing of ALOX15 alleviates ACS progression via inhibiting the FGFR2/PI3K/AKT signaling pathway, providing a theoretical basis for ACS therapy in clinic.

Acute coronary syndrome (ACS), the acute manifestation of ischemic heart disease, remains a major cause of morbidity and mortality worldwide. The present study aimed to elucidate the preliminarily biological role and underlying mechanism of the long non-coding RNA (lncRNA) transcription factor AP-2α (TFAP2A)-AS1 in ACS. The viability, apoptosis, invasion, and migration of human coronary artery endothelial cells (HCAECs) were assessed using Cell Counting Kit-8, flow cytometric, Transwell, and wound healing assays. In addition, reverse transcription-quantitative PCR was performed to examine the expression levels of TFAP2A-AS1 and TFAP2A. Western blotting was performed to determine the protein level of TFAP2A. Furthermore, a mouse model of ACS was established to investigate the effects of TFAP2A-AS1 and TFAP2A on blood lipid levels. Histological changes were evaluated through hematoxylin and eosin staining. The results revealed high levels of TFAP2A-AS1 and TFAP2A expression in patients with ACS and in mouse models. In HCAECs, knockdown of TFAP2A-AS1 resulted in decreased TFAP2A expression, whereas silencing of TFAP2A did not affect the expression of TFAP2A-AS1. Interference with either TFAP2A-AS1 or TFAP2A in HCAECs led to suppressed cell viability, invasion, and migration, as well as an increased apoptosis rate. Furthermore, it was demonstrated that the absence of both TFAP2A-AS1 and TFAP2A reduced blood lipid levels and improved myocardial injury in a mouse model of ACS. In conclusion, groundbreaking findings revealed that the suppression of TFAP2A-AS1 could effectively mitigate the progression of ACS by reducing the expression of TFAP2A. This finding not only offers crucial insight into the pathogenesis of ACS but also provides a solid theoretical foundation for the development of novel therapeutic interventions in clinical settings.

Objective Exploring the Correlation between Mitochondrial Function of T Cells and the Severity of Coronary Artery Disease. Methods A total of 118 patients with coronary heart disease were divided into 32 cases in the ACS group and 25 cases in the stable angina pectoris (SAP) group. Meanwhile, 61 non-coronary heart disease patients who were hospitalized during the same period were selected as the control group. The expression levels of CD3 + T lymphocytes, CD4 + T lymphocytes and CD8 + T cells, CD4-MM, CD8-MM,CD4-MMP,CD8-MMP in the plasma of the three groups were detected by a flow cytometry instrument and the human lymphocyte mitochondrial function. Results In the SAP and ACS groups, CD4MMP and CD8MMP were significantly lower than those in the control group, while CD4MM was significantly higher than that in the control group(P<0.05).However, there were no differences in CD4MMP, CD8MMP, and CD4MM between the SAP group and the ACS group(P > 0.05). CD4MM in the STEMI group was higher than that in the UA/NSTEMI group. Conclusion In the peripheral blood of patients with coronary heart disease, the levels of CD4MMP and CD8MMP are significantly decreased, while CD4MM is significantly increased. These indicators can be used as predictive markers for the occurrence of coronary heart disease.

BACKGROUND AND AIMS:Human vascular smooth muscle cells (HA-VSMCs) are an important cell type involved in atherosclerosis. Low density lipoprotein (LDL) is a lipoprotein particle that carries cholesterol into peripheral tissue cells, and oxidized modified LDL (ox-LDL) is a well-known inducer of the atherosclerosis-related phenotype switch in VSMCs, leading to the occurrence of atherosclerosis. Accumulating studies have revealed that long non-coding RNAs (lncRNAs) mediate the effect of ox-LDL on the atherosclerosis-related biological activities of HA-VSMCs, including proliferation, migration, and apoptosis. However, the mechanism of small nucleolar RNA host gene 12 (SNHG12) in ox-LDL-induced phenotype switch of VSMCs remains unclear. Thus, this research dug in whether SNHG12 mediated the influence of ox-LDL on HA-VSMCs and the potential mechanism.METHODS:Fundamental experiments and functional assays were performed to measure the function of SNHG12 on HA-VSMCs. Then, mechanism assays and rescue assays were performed to study the regulatory mechanism of SNHG12 in HA-VSMCs.RESULTS:SNHG12 reversed the influence of ox-LDL treatment in enhancing cell proliferative and migratory abilities and weakening apoptotic ability in HA-VSMCs. SNHG12 was a competitive endogenous RNA (ceRNA) competing with sprouty RTK signaling antagonist 2 (SPRY2) to bind to miR-1301-3p, thus up-regulating SPRY2 expression in ox-LDL-treated HA-VSMCs. Besides, SNHG12 recruited serine and arginine rich splicing factor 1 (SRSF1) to stabilize negative regulator of ubiquitin like proteins 1 (NUB1) expression.CONCLUSIONS:This study illustrated that SNHG12 inhibited cell proliferation, migration and facilitated cell apoptosis in ox-LDL-induced HA-VSMCs by up-regulating SPRY2 and NUB1.

Abstract Objective to evaluate the clinical efficacy and safety of sacubitril valsartan in the treatment of heart failure (HF) with midrange ejection fraction after acute myocardial infarction (AMI) in diabetic patients. From January 2015 to July 2020, HF patients with diabetes mellitus complicated with AMI were retrospectively analyzed. According to the medication, they were divided into 2 groups, that is, sacubitril valsartan group (84 cases) and valsartan group (86 cases). Valsartan group took valsartan capsule (80 mg/capsule, Beijing Novartis Pharmaceutical Co., Ltd) 80 mg, qd, on the basis of routine treatment. On the basis of routine treatment, the sacubitril valsartan group took sacubitril valsartan sodium tablets (50 mg/tablet, Beijing Novartis Pharmaceutical Co., Ltd), the initial dose was 25 mg, bid, and gradually increased to the target dose according to the patient's blood pressure. After 12 months of treatment, the independent sample t test showed that the left ventricular end diastolic dimension in the sacubitril valsartan group was lower than that in the valsartan group [(47.26 ± 4.71) mm vs (50.05 ± 5.62) mm, P < .001]. The left ventricular ejection fraction in the sacubitril valsartan group was higher than that in the valsartan group [(54.76 ± 4.24)% vs (49.28 ± 3.74)%, P < .001]. χ2 inspection showed that the readmission rate in the sacubitril valsartan group was lower than that in the valsartan group (7.14% vs 18.60%, P < .05). Sacubitril valsartan has good safety and tolerability in patients with diabetes mellitus complicated with AMI who have HF with midrange ejection fraction. Compared with valsartan, sacubitril valsartan can improve the left ventricular function better and reduce the readmission rate due to HF in these patients.

Objective Acute coronary syndrome (ACS) is the most dangerous and deadly form of coronary heart disease. Herein, we aimed to explore ACS-specific circulating lncRNAs and their regulatory mechanisms. Methods This study collected serum samples from ACS patients and healthy controls for microarray analysis. Dysregulated circulating lncRNAs and mRNAs were determined with |log2fold − change| > 1 and p < 0.05. lncRNA-mRNA coexpression analysis was carried out. ENST00000538705.1 and ALOX15 expression was further verified in serum specimens. In human coronary artery endothelial cells (HCAECs), ENST00000538705.1 and ALOX15 were knocked out through transfecting specific siRNAs. Thereafter, proliferation and migration were investigated with CCK-8 and wound-healing assays. Myocardial infarction rat models were established and administrated with siRNAs against ENST00000538705.1 or ALOX15. Myocardial damage was investigated with H&E staining, and serum TC, LDL, and HDL levels were measured. Results Microarray analysis identified 353 dysregulated circulating lncRNAs and 441 dysregulated circulating mRNAs in ACS. Coexpression analysis indicated the interaction between ENST00000538705.1 and ALOX15. RT-qPCR confirmed the remarkable upregulation of circulating ENST00000538705.1 and ALOX15 in ACS patients. In HCAECs, ENST00000538705.1 knockdown lowered the expression of ALOX15 but ALOX15 did not alter the expression of ENST00000538705.1. Silencing ENST00000538705.1 or ALOX15 weakened the proliferation and migration of HCAECs. Additionally, knockdown of ENST00000538705.1 or ALOX15 relieved myocardial damage, decreased serum TC and LDL levels, and elevated HDL levels in myocardial infarction rats. Conclusion Collectively, our findings demonstrate that circulating ENST00000538705.1 facilitates ACS progression through modulating ALOX15, which provide potential targets for ACS treatment.

蛋白激酶C-βⅡ(PKC-βⅡ)是单个多肽链,包含由5个可变区(V1～V5)间隔的4个保守结构域(C1～C4).高糖环境可导致组织中二酰甘油水平普遍升高,进而激活PKC-βⅡ.而PKC-βⅡ能够激活一系列下游信号通路,引发多组织器官发生病变,导致糖尿病并发症发生,如糖尿病肾病等.PKC-βⅡ抑制剂LY333531可以通过抑制PKC-βⅡ的激活来阻断下游信号通路,从而起到治疗糖尿病肾病的作用.近年来关于PKC-βⅡ在糖尿病肾病中的研究越来越多,本文就其相关研究进展作一综述.

Objective. This study is aimed at investigating the therapeutic effects of tetrandrine (Tet) on myocardial ischemia reperfusion (I/R) injury and probe into underlying molecular mechanism. Methods. H9C2 cells were divided into hypoxia/oxygenation (H/R) group, H/R+Tet group, H/R+Tet+negative control (NC) group, and H/R+Tet+miR-202-5p inhibitor group. RT-qPCR was utilized to monitor miR-202-5p and TRPV2 expression, and TRPV2 protein expression was detected via western blot and immunohistochemistry in H9C2 cells. Cardiomyocyte apoptosis was evaluated through detection of apoptosis-related markers and flow cytometry. Furthermore, myocardial enzyme levels were detected by ELISA. Rats were randomly separated into sham operation group, I/R group, I/R+Tet group (50 mg/kg), I/R+Tet+NC group, and I/R+Tet+miR-202-5p inhibitor group. miR202-5p and TRPV2 mRNA expression was assessed by RT-qPCR. TRPV2 protein expression was detected through western blot and immunohistochemistry in myocardial tissues. Apoptotic levels were assessed via apoptosis-related proteins and TUNEL. Pathological changes were observed by H&E staining. Myocardial infarction size was examined by Evans blue-TCC staining. Results. Abnormally expressed miR-202-5p as well as TRPV2 was found in H/R H9C2 cells and myocardial tissues of I/R rats, which was ameliorated following Tet treatment. Tet treatment significantly suppressed H/R- or I/R-induced cardiomyocyte apoptosis. ELISA results showed that CK-MB and LDH levels were lowered by Tet treatment in H/R H9C2 cells and serum of I/R rats. H&E staining indicated that Tet reduced myocardial injury in I/R rats. Also, myocardial infarction size was lowered by Tet treatment. The treatment effects of Tet were altered following cotreatment with miR-202-5p inhibitor. Conclusion. Our findings revealed that Tet may ameliorate myocardial I/R damage via targeting the miR-202-5p/TRPV2 axis.

The present study aimed to determine whether tetrandrine could attenuate left ventricular dysfunction and remodeling in rats with myocardial infarction. Sprague-Dawley rats were randomly divided into six groups (n=5/group) as follows: i) Healthy control group; ii) sham operation group; iii) myocardial infarction model group; iv) myocardial infarction + low-dose tetrandrine group (10 mg/kg); v) myocardial infarction + medium-dose tetrandrine group (50 mg/kg); and vi) myocardial infarction + high-dose tetrandrine group (80 mg/kg). Left ventricular end-diastolic diameter (LVIDd), left ventricular end-systolic diameter (LVIDs), ejection fraction (EF%) and left ventricular fractional shortening rate (FS%) were measured using ultrasonography. The pathological changes were observed by hematoxylin and eosin (H&E) staining. Left ventricular tissue section TUNEL staining was also performed. Furthermore, the triglyceride (TG), total cholesterol (TC), high density lipoprotein (HDL) and low-density lipoprotein (LDL) in the arterial blood were examined by biochemical testing. Expression levels of intracellular Ca2+ homeostasis-related proteins including ryanodine receptor calmodulin, CaM-dependent protein kinase II delta, protein kinase A, FK506 binding protein 12.6 were measured using western blot analysis. Ultrasonography results showed that in the myocardial infarction model rats, the levels of LVIDd and LVIDs were significantly higher; however, the levels of EF% and FS% were lower compared with those in the sham operation group, which was alleviated by tetrandrine. H&E results showed that tetrandrine alleviated the pathological characteristics of myocardial infarction model rats. Furthermore, tetrandrine significantly inhibited myocardial cell apoptosis in rats with myocardial infarction. Tetrandrine significantly inhibited the levels of TG, TC and LDL and increased the levels of HDL in the arterial blood of rats with myocardial infarction. These findings revealed that tetrandrine could attenuate left ventricular dysfunction in rats with myocardial infarction, which might be associated with intracellular Ca2+ homeostasis.

目的 分析起搏器植入术后起搏诱导性心肌病(pacing induced cardiomyopathy,PICM)的临床特征和相关因素.方法 2008年1月至2013年12月温州市人民医院心内科行起搏器植入且术前左心室射血分数(LVEF)>50％的患者204例,根据术后随访心脏超声结果分为PICM组和非PICM组,比较两组起搏器植入前后心脏超声、心电图数据及起搏器程控数据,分析PICM的危险因素及对患者远期预后的影响.结果 204例植入起搏器的患者中,PICM组26例,非PICM组178例,PICM发病率为12.7％.与非PICM组患者比较,PICM组术前左心室舒张末期内径(LVEDd)、左心室收缩末期内径(LVESd)和左心室质量指数(LVMI)较大,LVEF较低,术后心电图起搏QRS时间较长,心室起搏比例较高,差异均有统计学意义(均P<0.05).其中起搏QRS时间(>155.5 ms),心室起搏比例(>28.5％)及术前LVMI(>129.1 g/m2)均为PICM的危险因素(均P<0.05).PICM组术后心力衰竭住院率较高(P<0.05).结论 起搏QRS时间、心室起搏比例及LVMI与PICM的发生有关.

目的 探讨粉防己碱改善心肌梗死大鼠心功能的作用及潜在机制.方法 将48只雄性SD大鼠按随机数字表法分成正常组、假手术组、心肌梗死组、心肌梗死+粉防己碱低剂量(10 mg/kg)组、心肌梗死+粉防己碱中剂量(50 mg/kg)组、心肌梗死+粉防己碱高剂量(80 mg/kg)组,每组8只.采用永久结扎左冠状动脉方法 建立心肌梗死模型.利用超声心动图评估大鼠心脏功能[包括左室舒张末期内径(LVIDd)、收缩末期内径(LVIDs)、射血分数(EF)、左室短轴缩短率(FS)],ELISA法检测大鼠血清乳酸盐脱氢酶(LDH)、磷酸肌酸激酶同工酶(CK-MB)水平,Masson染色法测定心肌组织纤维化面积百分比,Western blot、RT-qPCR法分别检测心肌组织B淋巴细胞瘤-2(Bcl-2)、BCL2-Associated X的蛋白质(Bax)蛋白及mRNA相对表达量.结果 与假手术组相比,心肌梗死组大鼠的LVIDd、LVIDs,血清LDH、CK-MB水平,心肌组织纤维化面积百分比,心肌组织Bax蛋白及mRNA相对表达量均明显升高(均P<0.05);EF、FS,心肌组织Bcl-2蛋白及mRNA相对表达量均明显降低(均P<0.05).与心肌梗死组相比,心肌梗死+粉防己碱高、中剂量组大鼠血清LDH、CK-MB水平明显降低(均P<0.05);心肌梗死+粉防己碱高、中、低剂量组大鼠的LVIDd、LVIDs,心肌组织纤维化面积百分比,心肌组织Bax蛋白及mRNA相对表达量均明显降低(均P<0.05);而EF、FS,Bcl-2蛋白及mRNA相对表达量均明显升高(均P<0.05).结论 粉防己碱能改善心肌梗死大鼠的心室重塑和心肌细胞凋亡,其潜在的机制可能与Bax/Bcl-2有关.

Background: Contrast induced diabetic nephropathy (CIN) is an important cause of hospital-acquired acute renal failure. Our aim was to observe the effect of protein kinase C β2 (PKCβ2) knockdown on human proximal tubular epithelial cells (HK-2 cells) against meglumine diatrizoate and advanced glycation end products (AGEs)-induced apoptosis and autophagy. Methods: Cell viability was detected using cell counting kit-8 (CCK-8) assay in HK-2 cells after disposal with meglumine diatrizoate and AGEs with or without PKCβ2 siRNA/inhibitor LY333531. Flow cytometry and western blot were used to test cell apoptosis and the related protein levels in meglumine diatrizoate and AGEs co-treated HK-2 cells with or without PKCβ2 siRNA/inhibitor LY333531. Autophagy related proteins were detected using western blot. Immunofluorescence staining was used to examine the autophagy-specific protein light chain 3 (LC3), and autophagosome and autolysosome formation was observed under a transmission electron microscopy. Results: CCK-8 assay results showed that meglumine diatrizoate inhibited AGEs-induced HK-2 cell viability. Furthermore, meglumine diatrizoate promoted cell apoptosis and the expression level of caspase3 in AGEs-induced HK-2. Western blot results showed that meglumine diatrizoate elevated the expression levels of PKCβ2 and p-PKCβ2 in AGEs-induced HK-2 cells, and up-regulated the expression level of Beclin-1 and the ratio of LC3 II/LC3 I, and down-regulated the expression level of p62 in AGEs-induced HK-2 cells. We found that PKCβ2 knockdown alleviated meglumine diatrizoate and AGEs-induced HK-2 cell apoptosis and autophagy. Intriguingly, PKCβ2 inhibitor LY333531 reversed 3-methyladenine (3-MA)-induced autophagy inhibition in meglumine diatrizoate and AGEs-induced HK-2 cells. Conclusions: Our findings reveal that inhibiting PKCβ2 protects HK-2 cells against meglumine diatrizoate and AGEs-induced apoptosis and autophagy, which provide a novel therapeutic insight for CIN in diabetic patients.

目的:分析紫檀芪对急性心肌梗死大鼠心肌功能、心肌纤维化和炎症反应的作用及对Notch1/eIF3a信号通路的影响.方法:选取SPF级Wistar雄性大鼠75只,分为5组,紫檀芪低、中、高剂量组在造模前采用紫檀芪溶液预处理,灌胃剂量为10、20及40 mg/kg的紫檀芪溶液;模型组和正常组灌胃等剂量生理盐水.除正常组外,其他大鼠制备急性心肌梗死(AMI)模型.观察大鼠左心室功能、心脏血流动力指标、心肌组织病理形态和纤维化情况、心肌炎症因子含量、eIF3a与Notch1蛋白、mR-NA表达.结果:模型组大鼠左室短轴缩短率(LVFS)、左室射血分数(LVEF)较正常组降低,左心室舒张末期内径(LVEDd)、左心室收缩末期内径(LVESd)、收缩末期左室容积(LVESV)和舒展末期左室容积(LVEDV)较正常组升高;紫檀芪低、中、高剂量组大鼠LVFS、LVEF较模型组升高,LVEDd、LVESd、LVESV、LVEDV较模型组降低,差异有统计学意义(P<0.05);模型组大鼠左室压力最大降低速率(-dp/dtmax)、左室压力最大升高速率(+dp/dtmax)、左心室收缩压(LVSP)较正常组下降,左室舒张末压(LVEDP)较正常组升高;紫檀芪低剂、中、高剂量组大鼠-dp/dtmax、+dp/dtmax、LVSP较模型组升高,LVEDP较模型组降低,差异有统计学意义(P<0.05);模型组大鼠心肌组织白细胞介素(IL)-6、IL-1β及TNF-α含量较正常组升高;紫檀芪低剂、中、高剂量大鼠心肌组织IL-6、IL-1β及TNF-α含量较模型组降低,差异有统计学意义(P<0.05);模型组大鼠心肌组织eIF3a、Notch1蛋白与mRNA表达较正常组升高;紫檀芪低、中、高剂量大鼠心肌组织eIF3a、Notch1蛋白与mRNA表达较模型组降低,差异有统计学意义(P<0.05).结论:AMI大鼠心肌炎症和纤维化发展可能和Notch信号通路下游eIF3a表达增加有联系,紫檀芪预处理可明显改善AMI大鼠心室重构,其作用机制可能和抑制eIF3a、Notch1表达有关.

OBJECTIVE:To examine whether the influence of hypertension (HTN) status on longitudinal changes in brain glucose metabolism was modified by the apolipoprotein 4 (APOE4) status among older people with normal cognition.METHODS:In this study, we included 217 older individuals with normal cognition from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Participants were divided into the HTN and no HTN groups based on self-reported medical history. Brain glucose metabolism was assessed by 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET). Linear mixed model was fitted to examine the association between the HTN × APOE4 interaction and longitudinal changes in brain glucose metabolism after controlling for several covariates.RESULTS:In the present study, we found that the association between HTN status and longitudinal changes in brain glucose metabolism varied as a function of the APOE4 status, such that the HTN/APOE4+ group showed a steeper decline in FDG SUVR than all other groups (No HTN/APOE4-, HTN/APOE4-, and No HTN/APOE4+). Nevertheless, there was no significant difference in the rate of decline in FDG SUVR among other groups (No HTN/APOE4-, HTN/APOE4-, and No HTN/APOE4+).CONCLUSION:The APOE4 genotype interacted with hypertension status to affect longitudinal changes in brain glucose metabolism among older individual with normal cognition, such that the HTN/APOE4+ group showed a steeper decline in FDG SUVR than other groups.

Abstract Rationale: BMPR2 mutation is the most common cause of heritable pulmonary arterial hypertension (HPAH), but rare in hereditary hemorrhagic telangiectasia (HHT). ACVRL1, ENG and SMAD4 are the most common gene mutations reported in HPAH with HHT. Patient concerns: We report a 11-year-old boy with a definite diagnosis of pulmonary hypertension and suspected HHT with recurrent epistaxis. The results of gene detection showed that there was a nosense mutation in BMPR2. The results of gene detection of ACVRL1, ENG and SMAD4 were normal. Diagnoses: Heritable pulmonary arterial hypertension with suspected hereditary hemorrhagic telangiectasia. Interventions: Patient was treated with ambrisentan 2.5 mg qd. About a month later, the patient developed massive gastrointestinal bleeding and sudden convulsions. The patient's vital signs were stable after symptomatic treatment. Outcomes: After discharging from hospital, the patients continued to take ambrisentan. No epistaxis or gastrointestinal bleeding was found in one month of follow-up, but the symptoms of chest tightness were not significantly alleviated. Lessons: BMPR2 with a nonsense mutation is more likely to cause HPAH with HHT and are more likely to be life-threatening.

目的:观察ACS(急性冠状动脉综合征)患者社会支持程度对其死亡率及MACE(不良心血管事件)的影响.方法:纳入本院2017年4月-12月间诊疗ACS患者90例为研究对象,用简单随机化手段将其分为对照组 、实验组,每组45例,对应常规ACS对症治疗 、联合社会支持模式干预.比较两种干预模式下ACS患者社会支持度 、发生死亡和MACE概率等数据并以此归纳之间的联系性.结果:通过MSPSS量表对两组患者社会支持度情况进行评估,提示实验组患者高社会支持例数显著高于对照组且有统计学意义(P<0.05);分别于患者出院后的1、3、6、12个月通过随访掌握死亡和MACE事件,实验组患者显著低于对照组且有统计学意义(P<0.05).结论:对ACS患者应该重视社会支持程度,有利于提高其出院后生存质量,保障治疗的延续性和依从性.

目的:探讨心内科多重耐药菌感染的危险因素,为预防和控制MDRB感染提供依据.方法:用回顾性调查的方法,对我院心内科病房2015年1月至2017年2月46例经病原学及药敏试验证实MDRB临床感染病例进行分析总结.用SPSS24.0软件进行统计分析.结果:心内科MDRB中前3位分别为肺炎克雷伯菌、大肠杆菌、鲍曼不动杆菌.Logistics分析提示使用第三代头孢、合并慢性心力衰竭、合并急性心肌梗死、合并糖尿病与MDRB感染密切相关.结论:使用第三代头孢、合并CHF、合并AMI、合并糖尿病与MDRB感染密切相关.

We read with interest the case reported by García-Izquierdo et al. 1 García-Izquierdo E. Parra-Esteban C. Mirelis J.G. Fernández-Lozano I. The de Winter ECG pattern in the absence of acute coronary artery occlusion. Can J Cardiol. 2018; 34: 209.e1-209.e3 Abstract Full Text Full Text PDF Scopus (8) Google Scholar in an issue of the Canadian Journal of Cardiology. The authors present a very interesting case of a patient with chest pain and electrocardiograhic (ECG) changes compatible with the de Winter ECG pattern, in which the diagnosis of myocarditis was ultimately confirmed by cardiac magnetic resonance and coronary angiography. Unfortunately, we think that the ECG (Fig. 1) that the authors analyzed does not represent the “de Winter ECG pattern” described by de Winter and colleagues. 2 Verouden N.J. Koch K.T. Peters R.J. et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart. 2009; 95: 1701-1706 Crossref PubMed Scopus (103) Google Scholar The de Winter ECG Pattern in the Absence of Acute Coronary Artery OcclusionCanadian Journal of CardiologyVol. 34Issue 2PreviewA 26-year-old man presented to the emergency department with chest pain and electrocardiogram (ECG) changes compatible with the de Winter pattern. Emergent coronary angiography was used to rule out the presence of significant stenosis. Cardiac magnetic resonance imaging confirmed the diagnosis of myocarditis. This case underlines the lack of data regarding the positive predictive value of this ECG pattern for the diagnosis of acute myocardial infarction. Until further prospective studies are available, we believe that the de Winter ECG pattern should be considered as an “ST-elevation equivalent” when myocardial ischemia is suspected. Full-Text PDF

A 54-year-old man presented to the emergency department with chest pain and electrocardiogram (ECG) changes of acute ST-segment elevation myocardial infarction (STEMI) and junctional ST-depression with tall symmetrical T-waves (de Winter T-wave) in the lateral and inferior leads. Emergent coronary angiography revealed a culprit lesion in the gigantic obtuse marginal artery (OM). This case demonstrates the de Winter T-wave can occur in a patient with an acute occlusion of OM. Emergency physicians, ambulance staff, cardiologists and all involved in STEMI networks should familiarize themselves with this unusual ECG pattern and consider transferring patients for urgent angiography and reperfusion therapy.

The de Winter electrocardiogram (ECG) pattern may signify proximal left anterior descending artery (LAD) occlusion and was suggested to be managed as ST-segment elevation myocardial infarction (STEMI) equivalent for urgent angiography and reperfusion therapy. However, cardiac catheter laboratory is not readily or timely available in every hospital. When timely percutaneous coronary intervention (PCI) is not available, thrombolytic therapy can be considered in patients with ongoing ischemia symptoms. Here, we present a case of a successful thrombolytic therapy with de Winter ECG pattern occurred after ST-segment elevation in a scenario which the catheter laboratory was unavailable.