Background: Heat shock protein beta 1 (HSPB1) is confirmed to be a ferroptosis-related gene and plays an important role in the progression of diabetic cardiomyopathy (DCM). However, the specific functions and underlying molecular mechanisms of HSPB1 in DCM progression remain to be revealed. Methods: Cardiomyocytes were exposed to high glucose (HG) to mimic DCM cell models. The levels of HSPB1, tripartite motif-containing 55 (TRIM55), upstream stimulating factor 1 (USF1) and fibrosis-related markers were detected using western blot. Cell viability, apoptosis, inflammation, ferroptosis and mitochondrial membrane potential depolarization were assessed by CCK8 assay, flow cytometry, ELISA, corresponding kit and JC-1 staining. The interaction between TRIM55 and HSPB1 or USF1 was confirmed by Co-IP assay, ubiquitination assay, and dual-luciferase reporter assay. Diabetic mouse models were constructed by streptozotocin to assess the role of HSPB1 in vivo. Results: Overexpression of HSPB1 suppressed HG-induced cardiomyocyte apoptosis, ferroptosis, inflammation, mitochondrial dysfunction and fibrosis. TRIM55 enhanced the protein degradation of HSPB1 through ubiquitination, and the inhibitory effect of TRIM55 knockdown on HG-induced cardiomyocyte injury could be reversed by HSPB1 silencing. USF1 bound to TRIM55 promoter to activate its transcription. USF1 knockdown inhibited HG-induced cardiomyocyte injury by mediating the TRIM55/HSPB1 axis. In animal study, HSPB1 overexpression could improve cardiac function, alleviate inflammation and fibrosis in diabetic mouse models. Conclusion: The USF1/TRIM55/HSPB1 axis proposed in this study provides a potential molecular target for the treatment of DCM.

Circular RNAs (circRNAs) have been identified as vital regulators in cardiovascular diseases, including acute myocardial infarction (AMI). In this study, the function and mechanism of circRNA heparan sulfate proteoglycan 2 (circHSPG2) in hypoxia-induced injury in AC16 cardiomyocytes were investigated. AC16 cells were stimulated with hypoxia to establish an AMI cell model in vitro. Real-time quantitative PCR and western blot assays were performed to quantify the expression levels of circHSPG2, microRNA-1184 (miR-1184), and mitogen-activated protein kinase kinase kinase 2 (MAP3K2). Counting Kit-8 (CCK-8) assay was used to measure cell viability. Flow cytometry was performed to detect cell cycle and apoptosis. Enzyme-linked immunosorbent assay (ELISA) was used to determine the expression of inflammatory factors. Dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were used to analyze the relationship between miR-1184 and circHSPG2 or MAP3K2. In AMI serum, circHSPG2 and MAP3K2 mRNA were highly expressed and miR-1184 was down-regulated. Hypoxia treatment elevated HIF1α expression and repressed cell growth and glycolysis. Moreover, hypoxia promoted cell apoptosis, inflammation, and oxidative stress in AC16 cells. Hypoxia-induced circHSPG2 expression in AC16 cells. CircHSPG2 knockdown alleviated hypoxia-induced AC16 cell injury. CircHSPG2 directly targeted miR-1184, and miR-1184 targeted and suppressed MAP3K2. Inhibition of miR-1184 or overexpression of MAP3K2 abolished the alleviated effect of circHSPG2 knockdown on hypoxia-induced AC16 cell injury. Overexpression of miR-1184 relieved hypoxia-induced impairment in AC16 cells by MAP3K2. CircHSPG2 could regulate MAP3K2 expression through miR-1184. CircHSPG2 knockdown protected AC16 cells from hypoxia-induced injury by regulating the miR-1184/MAP3K2 cascade.

目的 探究血清簇集蛋白(Clusterin)、组织激肽释放酶1(KLK1)与老年急性心力衰竭(AHF)病情关系及对患者预后的评估价值.方法 选取2019 年7 月—2021 年10 月河北医科大学第二医院心血管内四科收治老年AHF患者80 例为研究对象(AHF组),另选取同期在医院行健康体检者 80 例为健康对照组.根据心功能将AHF患者分为轻度亚组(n =37)和重度亚组(n =43),依据患者是否发生终点事件分为终点事件亚组(n =36)和非终点事件亚组(n =44).比较各组间的基本资料及血清Clusterin、KLK1 水平;Spearman相关性分析AHF患者血清Clusterin、KLK1 水平与病情程度之间的关系;Logistic 回归分析 AHF 患者发生终点事件的影响因素;受试者工作特征曲线(ROC)分析血清Clusterin、KLK1 对AHF患者预后的评估价值.结果 AHF组SCr、TnI、CK-MB、NT-proBNP、LVEDD、BNP、Clusterin水平显著高于健康对照组(t/P =8.439/<0.001、31.607/<0.001、5.212/<0.001、15.676/<0.001、11.106/<0.001、17.847/<0.001、12.792/<0.001),LVEF、KLK1 水平显著低于健康对照组(t/P =3.900/<0.001、8.963/<0.001);终点事件亚组 TnI、CK-MB、NT-proBNP、BNP、Clusterin 水平均显著高于非终点事件亚组(t/P = 8.389/<0.001、3.517/0.001、10.993/<0.001、5.626/<0.001、7.303/<0.001),LVEF、KLK1 水平显著低于非终点事件亚组(t/P =2.749/0.007、6.225/<0.001);与轻度亚组患者比较,重度亚组患者血清Clusterin水平显著升高,KLK1水平显著降低(t/P =8.236/<0.001、12.703/<0.001);Spearman相关性分析结果显示,AHF患者血清Clusterin水平与病情程度呈显著正相关(r =0.613,P<0.01),而血清KLK1 水平与病情程度呈显著负相关(r =-0.680,P<0.01);Logistic回归分析结果显示,BNP高、Clusterin高、KLK1 低是影响AHF患者发展为不良终点事件的危险因素[OR(95%CI)=1.401(1.132～1.735)、1.545(1.219～1.959)、1.624(1.246～2.116)];ROC曲线结果显示,血清 Clusterin、KLK1 及二者联合评估AHF患者预后的曲线下面积(AUC)分别为0.879、0.834、0.964,二者联合评估AHF患者预后的AUC大于单项预测(Z/P =2.001/0.045、2.712/0.007).结论 血清Clusterin、KLK1 对老年AHF病情及预后具有良好的评估价值.

目的 分析冠状动脉粥样硬化性心脏病(冠心病)患者外周血中CD14++CD16+单核细胞水平分析及其对内皮祖细胞体外功能的影响.方法 选取2018年10月至2019年3月于河北医科大学第二医院心血管内科冠心病患者和健康志愿者各20例,比较两组外周血中中间型单核细胞(intermediatemonocytes,IMs;CD14++CD16+)水平;使用流式细胞分选技术收集冠心病患者CD14++CD16+单核细胞,在体外与健康志愿者内皮祖细胞共培养,使用划痕实验检测细胞迁移能力;使用蛋白质印记法检测细胞黏附相关蛋白的表达评价细胞黏附能力;选取30只SD大鼠,采用随机数字表法分为健康组和冠心病组,每组各15只,建立心肌梗死大鼠模型,健康组移植未经共培养的内皮祖细胞,冠心病组移植CD14++CD16+单核细胞共培养后的内皮祖细胞,比较两组大鼠的心梗边缘区微血管数、微血管密度和心肌梗死率.结果 与健康志愿者外周血中CD14++CD16+水平相比,冠心病患者外周血中CD14++CD16+水平显著升高(P<0.05);冠心病患者CD14++CD16+单核细胞与健康志愿者内皮祖细胞共培养后期迁移能力显著降低,E-cadherin蛋白、Vimentin蛋白表达水平显著降低,N-cadherin蛋白表达水显著升高(P<0.05);相比健康组,冠心病组大鼠心肌梗死(心梗)边缘区微血管数、微血管密度和心肌梗死率显著升高(P<0.05).结论 冠心病患者外周血中CD14++CD16+含量水平显著高于健康志愿者,且CD14++CD16+可降低内皮祖细胞的迁移能力.

Objective:To investigate the electrocardiographic characteristics of left and right ventricles origin of premature ventricular contractions(PVCs) during V3 transition of precordial leads, right ventricular outflow tract (RVOT) anterior septum and right coronary sinus (RCC), and RVOT middle-posterior septum and left coronary sinus (LCC).Methods:From January 2017 to September 2019, 91 patients with ventricular extrasystole of outflow tract who had V3 transition in precordial lead and had successful radiofrequency ablation in RVOT anterior septum, middle posterior septum, LCC and RCC were selected for retrospective case control study.The electrocardiography measurements of PVCs were compared between the anteroseptal RVOT group and RCC group, as well as the middle-posterior septal RVOT group and the LCC group, respectively.The measurements included the R-wave amplitude in lead Ⅰ, Ⅱ, Ⅲ and aVF, R amplitude ratio in leads Ⅲ to Ⅱ, Q-wave amplitude in lead aVL and aVR, Q amplitude ratio in leads aVL to aVR, R-wave and S-wave amplitude from leads V1 to V3, the V2S/V3R index, the transition zone index, and the V2 transition ratio.Results:Thirty-six cases originated from the anteroseptal RVOT, and 11 from the LCC.Lead I R-wave amplitude in anterior septal RVOT was higher than LCC group((0.22±0.25) mV vs.(-0.17±0.33) mV; P=0.003). R-wave amplitude in lead Ⅱ was lower than that in the LCC group((1.59±0.35) mV vs.(1.76±0.27) mV; P=0.035). R-wave amplitude in lead aVF was lower compared with the LCC group((1.53±0.35) mV vs.(1.78±0.39) mV; P=0.050). The V2S/V3R index showed a significant difference between these two groups(1.99±0.66 vs.0.76±0.38; P<0.001). The V2 transition ratio also appeared a significant difference between the two groups(0.69±0.43 vs.1.05±0.35; P=0.005). PVCs arose from the middle-posterior septal RVOT in 32 cases, and from the RCC in 12 cases.Compared with RCC group, lead Ⅰ R-wave amplitude showed lower ((0.25±0.31) mV vs.(0.57±0.12) mV; P<0.001); R amplitude ratio in leads Ⅲ to Ⅱ higher (0.89±0.14 vs.0.72±0.18; P=0.002); Q amplitude in lead aVL((0.72±0.24) mV vs.(0.51±0.16) mV; P=0.002)higher, and Q amplitude ratio in leads aVL to aVR higher in the middle-posterior septal RVOT(0.76±0.23 vs.0.50±0.21; P=0.002). Conclusion:Among the cases with lead V3 transition, PVCs originated from the anteroseptal RVOT show significantly different R wave in lead Ⅰ, Ⅱ, aVF, V2S/V3R index, and the V2 transition ratio compared with those from the LCC.The PVCs from the middle-posterior septal RVOT and the RCC have different R wave in lead Ⅰ, R amplitude ratio in leads Ⅱ and Ⅲ, Q amplitude ratio in leads aVL and aVR.Combined with its different characteristics, it can help to identify the origin of left and right ventricles.

目的 探讨lncRNA PVT1对缺氧复氧(H/R)诱导的心肌细胞凋亡、氧化应激的影响及其对miR-761的调控作用.方法 采用H/R诱导大鼠心肌细胞H9c2建立细胞损伤模型,分别将si-NC、si-PVT1、miR-mimics-NC、miR-761 mimics、si-PVT1与miR-inhibitor-NC、si-PVT1与miR-761 inhibitor转染至H/R诱导的心肌细胞;采用qRT-PCR法检测PVT1、miR-761的表达量;采用流式细胞术检测细胞凋亡率;采用试剂盒检测丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的含量;双荧光素酶报告实验检测PVT1与miR-761的靶向关系;Western blot法检测B淋巴细胞瘤2(Bcl-2)、B淋巴细胞瘤2相关蛋白(Bax)的蛋白表达量.结果 与对照组比较,H-/R组PVT1的表达水平升高(P＜0.05),miR-761的表达水平降低(P＜0.05).与H/R+si-NC组比较,H/R+si-PVT1组凋亡率及Bax蛋白水平降低(P＜0.05),Bcl-2蛋白水平及SOD、CAT的活性升高(P＜0.05),MDA的含量降低(P＜0.05).与H/R+miR-mimics-NC组比较,H/R+miR-761 mimics组凋亡率及Bax蛋白水平降低(P＜0.05),Bcl-2蛋白水平及SOD、CAT的活性升高(P＜0.05),MDA的含量降低(P＜0.05).双荧光素酶报告实验证实PVT1可靶向结合miR-761;干扰miR-761可明显逆转沉默PVT1对H/R诱导的心肌细胞氧化应激及凋亡的作用.结论 沉默PVT1可通过上调miR-761而抑制细胞凋亡及氧化应激从而减轻H/R诱导的心肌细胞损伤.

目的 探讨重组人脑利钠肽治疗急性失代偿性心力衰竭的疗效及其对血清可溶性生长刺激表达基因2 (sST2)、心肌营养素1 (CT-1)水平的影响.方法 选取2018年3月-2020年1月在河北医科大学第二医院治疗的急性失代偿性心力衰竭患者90例作为研究对象,将患者随机分为对照组(n=45)和观察组(n=45).对照组患者给予常规抗心力衰竭治疗.观察组在常规抗心力衰竭治疗的基础上给予注射用重组人脑利钠肽治疗,前3 min以负荷量为1.5 μg/kg进行静脉冲击,接下来72 h使用0.007 5 μg/ (kg·min)进行静脉滴注,两组均连续治疗2周.观察两组患者的临床疗效,同时比较两组患者的心、肾功能指标,血清可溶性生长刺激表达基因2 (sST2)、心肌营养素1(CT-1)水平.结果 治疗后,观察组患者总有效率为88.89％,显著高于对照组的64.44％,两组比较差异有统计学意义(P＜0.05).治疗后,两组患者左心室收缩末期内径(LVESD)、左心室收缩末期容积(LVESV)显著降低,左室射血分数(LVEF)显著升高(P＜0.05);且观察组LVESD、LVESV低于对照组,LVEF高于对照组(P＜0.05).治疗后,两组胱抑素C(Cys-C)、血肌酐(Scr)水平显著降低,肾小球滤过率(GFR)水平显著升高(P＜0.05);且观察组Cys-C、Scr水平显著低于对照组,GFR水平高于对照组(P＜0.05).治疗后,两组血清sST2、CT-1水平较治疗前显著降低(P＜0.05),且观察组血清sST2、CTo1水平低于对照组(P＜0.05).结论 重组人脑利钠肽治疗可降低急性失代偿性心力衰竭患者血清sST2、CT-1水平,提高患者的心、肾功能,提高临床疗效,改善患者预后,具有重要临床价值.

目的 分析急性脑梗死(ACI)后脑心综合征(CCS)的临床特点,探讨其发病机制及预后.方法 分析2017年6月-2019年10月收治的ACI合并CCS患者85例,为观察组.选取同期出现ACI无心功能改变的患者70例,作为对照组,对上述患者行心电图、超声心动图及心肌酶谱和肌钙蛋白-T等检查.结果 ACI出现CCS患者中心电图改变主要表现心律失常和心肌缺血.观察组患者中LDH、AST、CK、CK-MB和cTnT水平较对照组均升高(P<0.05).85例ACI患者合并CCS患者中死亡52例(61.18％),70例无CCS的ACI患者中死亡15例(21.43％),两组比较差异有统计学意义(P<0.05).结论 ACI患者发生CCS时,常会加重患者病情,并影响预后,临床上应提高警惕.

Reperfusion therapy after acute myocardial infarction (AMI) can effectively restore the blood supply and nutritional support of ischemic myocardium and save the dying myocardium. However, myocardial ischaemia-reperfusion (I/R) injury has become a new threat to reperfusion therapy for AMI. Many long-chain noncoding RNAs (lncRNAs) are dysregulated by I/R damage. Of these dysregulated lncRNAs, Gpr19 was selected as a potential gene of interest based on its high expression change. We aimed to explore the functional role and molecular mechanism of Gpr19 in I/R injury of AMI. C57BL/6 mice underwent I/R injury as in vivo models. Neonatal rat ventricular cardiomyocytes (NRCMs) exposed to an oxygen glucose deprivation/recovery (OGD/R) system were used as an in vitro model. A TUNEL assay, western blot, and oxidative stress analysis were conducted in this study to determine apoptosis and oxidative stress levels. Our results indicated that inhibition of Gpr19 improves cardiac function and reduces apoptosis and myocardial fibrosis scar formation in vivo. Suppression of Gpr19 attenuates oxidative stress and apoptosis in NRCMs exposed to OGD/R. We further demonstrated that inhibition of Gpr19 decreases oxidative stress and apoptosis in OGD/R-induced NRCMs by regulating miR-324-5p and mitochondrial fission regulator 1 (Mtfr1). We elucidated the functional role and potential molecular mechanism of Gpr19 in I/R injury of AMI, provided a theoretical basis for the importance of Gpr9 in I/R injury, and provided a new perspective for the clinical treatment of I/R injury of AMI.

目的 探索RhoA激酶信号通路介导的自噬障碍在2型糖尿病大鼠(T2DM)心肌纤维化中的作用.方法将60只SD大鼠随机分为对照组、模型组、法舒地尔组(10 mg/kg/d)、3-甲基腺嘌呤(3-MA)组(15 mg/kg/d)和法舒地尔+3-MA组各12只.除对照组的所有大鼠均采用高脂饮食法联合小剂量链脲佐菌素诱导T2DM大鼠模型,均给予相应药物干预4周.RT-PCR检测心肌组织ROCK1、ROCK2、PCⅠ、PCⅢmRNA的表达;Western Blot检测心肌组织肌球蛋白磷酸酶靶向蛋白1(MYPT1)、p-MYPT1、LC3-I、LC3-Ⅱ、Beclin 1、p62、UNC-51样激酶1(ULK1)、p-ULK1的表达;MTT法检测心肌成纤维细胞的增殖;ELISA和RT-PCR检测成纤维细胞培养液和细胞内PCⅠ和PCⅢ水平.结果与模型组相比,法舒地尔组大鼠成纤维细胞的增殖活性明显降低(P<0.05),ROCK1、ROCK2、PCⅠ和PCⅢmRNA的表达均明显上调(P<0.05),p-MYPT1/MYPT1和p62的表达明显下调(P<0.05),LC3-Ⅱ/LC3-Ⅰ、Beclin 1和p-ULK1/ULK1的表达明显上调(P<0.05),成纤维细胞PCⅠ和PCⅢ的水平均明显下降(P<0.05);与法舒地尔组相比,法舒地尔+3-MA组大鼠成纤维细胞的增殖活性明显增加(P<0.05),ROCK1、ROCK2、PCⅠ和PCⅢmRNA的表达均明显下调(P<0.05),p-MYPT1/MYPT1和p62的表达均明显上调(P<0.05),LC3-Ⅱ/LC3-Ⅰ、Beclin 1和p-ULK1/ULK1的表达均明显下调(P<0.05),成纤维细胞PCⅠ和PCⅢ的水平均明显升高(P<0.05).结论RhoA激酶信号通路介导的自噬障碍可以诱导T2DM大鼠的心肌组织纤维化.

OBJECTIVE To study the effect of telmisartan on protection of myocardia of mice with viral myocarditis and its mechanism so as to alleviate the myocardial injury and avoid the development of dilated cardiomyopathy . METHODS A total of 70 mice were recruited as the experiment objects and randomly divided into the observation group with 30 mice ,the control group with 30 mice ,and the blank group with 10 mice .The observation group and the control group were treated with abdominal injection of coxsackie B3 virus so as to establish the myocarditis mice model ,the mice in the observation group were fed with telmisartan from the date when they had the viral in-fection ,for 7 consecutive days ;the control group was not given any drug intervention ;the mice in the blank group were treated with abdominal injection of equal amount of phosphate buffer but were not given drug intervention . The myocardial pathologic histology integral ,concentrations of serum adiponectin ,cardiac troponin I (cTn I) ,and BNP as well as concentrations of tumor necrosis factor alpha and interleukin-6 in myocardial homogenates were ob-served and compared among the three groups .RESULTS The level of serum adiponectin of the observation group was significantly higher than that of the control group ,however ,the levels of tumor necrosis factor alpha and in-terleukin-6 in myocardial homogenates ,the levels of serum cardiac troponin Ⅰ and BNP ,and pathologic integral were lower in the observation group than in the control group ,and there was significant difference (P < 0 .05) ;as compared with the blank group ,the level of serum adiponectin of the control group was reduced ,while the levels of interleukin-6 ,tumor necrosis factor alpha ,troponin Ⅰ and BNP ,and pathologic integral were significantly ele-vated ,and there was significant difference (P < 0 .05) .CONCLUSION Telmisartan can alleviate myocardial injury-induced by the viral myocarditis and has certain effect on protection of hearts ,and its mechanism may be associated with the elevated level of serum adiponectin , or the reduced levels of inflammatory factors such as interleukin-6 and tumor necrosis factor alpha .

Objective To investigate effect of different doses of rosuvastatin on brachial artery endothelium-dependent vasodilation and carotid intima-media thickness in patients with coronary heart disease.Methods 92 patients with coronary heart disease in our hospital were admitted and divided into four groups according to randomly digital method, including 23 cases in control group were treated with lipid nitrate, antiplatelet aggregation, anticoagulant, lowering blood sugar, blood pressure control and other of conventional therapy;23 cases in group A, on the basis of conventional therapy, were treated with rosuvastatin 5 mg/d, orally, once daily;23 cases in group B were treated with rosuvastatin 10 mg/d, orally, once daily based on the conventional therapy;23 cases in group C were treated with rosuvastatin 20 mg/d, orally, once daily based on conventional treatment, each group was treated for 8 weeks.Brachial artery endothelium-dependent vasodilation (FMD) and carotid intima-media thickness (IMT) of patients before and after treatment were collected by color ultrasonic doppler, while observed lipid levels changes of 4 groups.Results Control group was treated for eight weeks, FMD, ITM, blood lipid levels and each index values were not significantly changed, the difference was not statistically significant;After treatment, total cholesterol ( TC) , low-density lipoprotein cholesterol C ( LDL-C) of A, B, C groups were significantly better than that before treatment, the difference was statistically significant (P<0.05), and decrease amplitude with dose of rosuvastatin increased became grearer, but the total cholesterol (TC), high density lipoprotein cholesterol C( HDL-C) there was no significant difference compared with before treatment; Compared with before treatment, ITM of A, B, C groups decreased, and the difference was statistically significant (P<0.05), decrease amplitude with dose of rosuvastatin increased became greater.Conclusion Rosuvastatin can significantly improve brachial artery endothelium-dependent vasodilation and carotid intima-media thickness in&nbsp;patients with coronary heart disease, and there is a clear dose-response relationship, which may be associated with rosuvastatin decrease total cholesterol and low-density lipoprotein cholesterol C in patients with coronary heart disease.It has guide significance to clinical.

Objective To investigate the effect of metoprolol combined dexmedetomide on NADPH oxidase subunit,MCP-1,MMP and apoptosis related protein in ischemic reperfusion rats. Methods SD rats were divided into 4 groups: sham operation group( SO),ischemic perfusion group( IP),apocynin treatment group( AT) and metoprolol combined dexmedetomide group( MD). Myocardial ischemia-reperfusion injuny model was established by ligation of left anterior descending coronary artery( LAD) method. The expression of NAPDH,MCP-1,MMP-2 and MMP-9 were detected by Western blot or Real-time PCR. The apoptosis related protein Caspase-3 and Caspase-9 were also assayed in each group. Results The expression of NADPH oxidease subunit,MCP-1,MMP-2,MMP-9 was increased greatly in IP group when compared with SO group( P < 0. 01),as well as apoptosis related protein Caspase-3 and Caspase-9 were up-regulated dramatically in IP group when compared with SO group( P < 0. 01),while AT group and MD group could recover these parameters greatly. Conclusion Metoprolol combined dexmedetomide alleviates ischemic perfusion injury mediated by the way of increasing MCP-1 expression by inhibiting activated NADPH oxidase in heart and inhibiting extracellular matrix recombination.

患者,男,29岁,主因反复口腔溃疡8年,间断发热2年余,间断胸闷、喘憋1年余于2010年3月15日入院.患者缘于8年前开始反复口腔溃疡,1年超过10次,未予诊治,次年略有好转,1～2次/年.6年前曾有不明原因出现全身脓疱疹,抗过敏治疗后好转.3年前再次加重,口腔溃疡发作5～10次/年.受凉后出现后背肌肉痛、左侧胸痛及双侧肩周疼痛.

患者,女,64岁,主因间断胸闷、气短6年,加重10天于2010年4月7日入院.患者6年前无明显诱因出现活动后胸闷、气短,无胸痛及放射痛,休息后可缓解,此后上述症状间断发作,多于活动后发作,活动耐量逐渐减低.10天前患者无明显诱因出现胸闷、气短加重,伴夜间阵发性呼吸困难,为求进一步诊治入我院.既往高血压病史3年,血压(Bp)最高达220/105 mmHg(1 mmHg=0.133 kPa).查体:意识清楚,Bp 200/100 mmHg,双肺呼吸音粗,两肺底可闻及少许湿啰音,心界向左扩大,心率90次/min,律齐,肺动脉瓣听诊区可闻及3/6级收缩期杂音,P2>A2.腹平软,肝脾未触及,双下肢无水肿.心电图示:窦性心律,I、aVL、V4-6 ST段压低,T波双向倒置,aVR导联ST段抬高.

经皮腔内冠状动脉介入治疗(PCI)已经成为冠状动脉疾病血运重建的最佳手段之一。但是,PCI本身可能会引起血管壁的损伤和炎症反应,进而引起心肌损伤。近年来他汀类药物在PCI围手术期的应用受到普遍重视,许多循证医学证据表明,他汀类药物可以减轻冠脉介入治疗中的心肌损伤,改善预后,拓展了该类药物在冠脉介入治疗中的应用范围。本文就他汀类药物在此方面的应用进展作一综述。

患者,男,52岁,主因间断腰酸、腰痛1月余,于2009年6月5日入院.患者缘于1月余前出现活动后腰酸、腰痛,休息后可缓解,伴乏力、倦怠、食欲减退、记忆力下降、言语迟钝、体质量增加、颈肌强直感、双下肢轻度水肿,且活动耐量逐渐下降;查心肌酶示:肌酸激酶(CK)2 560.0 U/L.

药物支架的出现开创了冠状动脉介入治疗(PCI)的新纪元.对简单冠状动脉病变而言,PCI治疗效果明确,优势显著,成为首选的治疗方法.近年来对于冠状动脉复杂病变,尤其是左主干(LM)病变、三支病变的PCI治疗一直是争论、研究的焦点.

他汀类药物在心血管疾病的治疗中应用越来越广,地位越来越高.近年来,关于他汀类药物在冠状动脉介入治疗(PCI)中的应用积累了许多循证医学证据.