DILATED CARDIOMYOPATHY WITH HYPERTENSION: PREVALENCE AND RESPONSE TO HIGH-DOSE β1-ADRENOCEPTOR ANTAGONIST THERAPY

• 1 The aim of the present study was to investigate the prevalence of hypertension in patients with dilated cardiomyopathy (DCM) and to determine the tolerance and efficacy of a high dose of the β₁‐adrenoceptor antagonist metoprolol in the long‐term treatment of DCM patients.
• 2 The prevalence of hypertension in DCM patients (n = 362) and age‐matched controls (n = 401) was evaluated and compared. To investigate the effects of metoprolol, DCM patients were divided into hypertensive (DCM‐H) or normotensive (DCM‐N) subgroups. Metoprolol was administered at a starting dosage of 6.25 mg/day and increased gradually to 250 mg/day or the maximum tolerable dose. Blood pressure (BP), heart rate (HR), left ventricular (LV) end‐diastolic dimension (LVEDD), left atrial end‐diastolic dimension (LAEDD), LV ejection fraction (LVEF), LV posterior wall thickness (LVPWT) and ventricular septal thickness (VST) were determined at baseline and 6 and 12 months after metoprolol treatment.
• 3 The prevalence of hypertension was significantly higher in DCM patients than in age‐matched controls (32.8 vs 20.1%, respectively; P < 0.01). Resting HR and a family history of hypertension were highest in the DCM‐H group. There were no significant differences in age, gender and occupation between the DCM‐H, DCM‐N and age‐matched control groups.
• 4 The tolerable dose for metoprolol was significantly higher in the DCM‐H group than the DCM‐N group (189.6 ± 14.8 vs 133.9 ± 12.0 mg/day, respectively; P < 0.05). Metoprolol significantly reduced BP and HR in the DCM‐H group and improved LVEDD, LAEDD and LVEF in all DCM patients, with a greater effect seen in the DCM‐H group.
• 5 In conclusion, DCM patients have a higher prevalence of hypertension than the general population. Patients in the DCM‐H subgroup were characterized by a higher resting HR and a family history of hypertension and were more tolerant of and more responsive to metoprolol treatment. These data suggest that this subgroup of DCM patients could have higher sympathetic nerve activity and is suitable for treatment with a higher dose of metoprolol.

     

卡托普利对心肌梗死后左室重塑的影响

目的 探讨卡托普利(开搏通)与急性心肌梗死(AMI)后左室重塑的关系.方法 选择首次AMI患者70例,在发病后给予卡托普利治疗,应用彩色多普勒超声显像仪,于发病第4周和52周行超声心动图检查,观察左室形态、大小、室壁运动并记录左室收缩末期内径(LVDs)、舒张末期内径(LVDd)、左室收缩末期容积(LVESV)、左室舒张末期容积(LVEDV)、左室射血分数(LVEF)、左房内径(LAD)和二尖瓣血流频谱图中快速充盈E波最大流速(VE)和心房充盈A波最大流速(VA)等指标并计算VE/VA等指标.其中8例退出研究,将不规律应用卡托普利(n=29)和规律服用卡托普利(n=33)患者分为A、B 2组,比较52周时2组超声心动图观察指标.结果 B组的LVDs、LVDd、LVESV、LVEDV和LAD比A组降低,但LVEF和VE/VA比A组升高(P＜0.05).结论 卡托普利可以干预AMI后左室重塑,明显改善左室舒缩功能.     

急性前壁心肌梗死患者急诊经皮冠状动脉介入治疗术后早期应用重组人脑利钠肽对心脏近期保护作用的研究

目的 研究急性前壁心肌梗死患者急诊经皮冠状动脉介入治疗(PCI)后早期应用重组人脑利钠肽(rhBNP)对心脏的近期保护作用.方法 60例急性前壁心肌梗死患者入院后行急诊PCI,术后随机分为rhBNP组和对照组,前者即刻持续静脉微量泵入rhBNP 72 h,后者不予泵入rhBNP.分别记录2组患者术前、术后的呼吸频率、心...     

比伐卢定对急性冠状动脉综合征患者介入术后内皮损伤和炎性反应的影响

目的 探究比伐卢定对急性冠状动脉综合征（ACS）患者介入术后内皮损伤和炎性反应的影响。方法 选取2015年2月至2016年3月南阳市中心医院收治的90例行PCI患者,随机数表法分为观察组与对照组各45例。对照组采用常规肝素治疗,观察组则采用比伐卢定治疗。对比两组手术前后内皮损伤指标[血浆内皮素1（ET-1）、一氧化氮（NO）、血浆血管性假血友病因子（vWF）]、炎性指标[白介素-18（IL-18）、白介素-10（IL-10）、超敏C反应蛋白（hs-CRP）]、心功能指标[左心室舒张末期容积（LVEDV）、左心室收缩末期容积（LVESV）、左心室射血分数（LVEF）、脑钠肽（BNP）]变化及心脑血管不良事件发生率。结果 术前,两组患者内皮指标比较,差异无统计学意义（P>0.05）,术后24 h,观察组ET-1及vWF水平均低于对照组[（68.37±6.17）ng/L vs（101.83±10.24）ng/L、（514.33±86.57）U/L vs（588.92±98.46）U/L],观察组NO水平高于对照组[（72.42±7.06）mmol/L vs（58.26±6.49）mmol/L],差异均有统计学意义（P<0.05）。观察组IL-18水平（53.84±23.67）pg/mL、hs-CRP水平（7.22±2.74）mg/L、LVEDV水平（88.63±10.24）mL、LVESV水平（32.47±4.26）mL及BNP水平（74.82±7.94）ng/L均低于对照组IL-18水平（73.58±26.79）pg/mL、hs-CRP水平（8.67±3.56）mg/L、LVEDV水平（95.16±9.58）mL、LVESV水平（44.83±5.72）mL及BNP水平（163.51±15.44）ng/L,IL-10水平（43.61±6.08）pg/mL及LVEF水平（51.82±10.19）%高于对照组IL-10水平（33.56±4.18）pg/mL及LVEF水平（39.14±9.28）%,差异有统计学意义（P<0.05）。两组患者术后1个月心脑血管不良事件发生率比较,差异无统计学意义（P>0.05）。结论 ACS患者术后采用比伐卢定治疗可有效缓解内皮损伤,同时可降低炎性反应,恢复心功能,治疗安全性高。     

复合超声心动图在检测淋巴瘤化疗所致心脏毒性中的应用价值

目的　探讨超声复合技术在动态监测淋巴瘤化疗所致心脏毒性中的应用价值。方法　选择2020年1月至2021年12月河南科技大学第一附属医院就诊的非霍奇金淋巴瘤化疗患者28例（化疗组）,其中男12例、女16例,年龄（51.22±10.17）岁;同期选择健康志愿者30例为对照组,其中男12例、女18岁,年龄（50.19±12.06）岁。所有患者在化疗后2周期、4周期、6周期采用实时二维超声心动图（RT-2DE）、组织多普勒成像（TDI）、二维斑点追踪成像（2D-STI）检测各心功能指标。观察两组左心室射血分数（LVEF）、左心室前后径（LV）、左心房前后径（LA）、E峰、A峰、E/A值、二尖瓣E峰减速时间（DT）、血流频谱舒张早期速度（E）与二尖瓣环舒张早期运动峰速度（e’）比值、左心室整体圆周应变（LVGCS）、左心室整体径向应变（LVGRS）、左心室整体纵向应变（LVGLS）、左心室扭转角度峰值（LVPtw）。计量资料采用独立样本t检验或单因素方差分析,计数资料采用卡方检验。结果　化疗组化疗后2周期、4周期LVEF、LV、LA、E峰、A峰、E/A与对照组比较,差异均无统计学意义（均P>0.05）;化疗2周期化疗组DT与对照组比较,差异无统计学意义（P>0.05）,化疗4周期化疗组DT为（213.16±21.23）ms,与对照组（181.26±20.23）ms比较,差异有统计学意义（P<0.05）。化疗组化疗后6周期LVEF为（49.01±4.12）%、LV为（56.68±4.32）mm、LA为（43.64±4.02）mm、E峰为（78.36±12.20）cm/s、A峰为（90.96±12.61）cm/s、E/A为（0.76±0.21）、DT为（256.23±32.14）ms,与对照组比较差异均有统计学意义（均P<0.05）。化疗组化疗后2周期e’、E/e’与对照组比较,差异均无统计学意义（均P>0.05）;化疗组化疗后4周期e’为（8.22±1.27）cm/s、E/e’为（18.17±3.12）,化疗6周期e’为（4.29±2.17）cm/s、E/e’为（20.17±4.06）,与对照组比较差异均有统计学意义（均P<0.05）。化疗组化疗后2周期、4周期、6周期LVGRS、LVGCS、LVGLS、LVPtw与对照组比较,差异均有统计学意义（均P<0.05）。结论　接受蒽环类药物化疗的肿瘤患者会导致心脏毒性,RT-2DE联合TDI及2D-STI能更早期更敏感地检测到化疗所致的心脏毒性,对指导临床具有重要意义。     

三维斑点追踪技术评价冠心病患者左心室心肌特性改变

目的 应用三维斑点追踪技术(three dimensional speckle tracking imaging,3D-STI)分析冠心病患者左心室整体应变特性,探讨该技术评价冠心病患者左心室心肌特性改变的临床价值.方法 选取经冠状动脉造影证实的冠心病患者40例(心肌梗死患者不纳入研究)作为研究对象,并随机选取年龄、性别相匹配的经冠状动脉造影证实的正常人32例做对照组.所有受试者行二维及三维超声心动图检查.采用二维双平面Simpson法测量受试者的左心室每搏量(SV)及左心室射血分数(LVEF),应用三维斑点追踪技术测量2组的左心室整体长轴应变值(GLS)、圆周应变值(GCS)、径向应变值(GRS)、面积应变值(GAS)以及三维应变(3D-Strain),对2组间参数进行比较,并对各参数与LVEF之间的相关性进行分析.结果 冠心病组患者与正常对照组[(46.23±7.37)ml VS(49.67±8.37)ml,P=0.096]、LVEF[(57.17±3.41)% VS(58.87±3.69)%,P=0.069]差异无统计学意义(P>0.05).与正常对照组相比,冠心病患者GLS[(-14.95±2.61 )% VS(-18.37±3.09)%,P<0.01]及GRS[(39.42±4.95 )% VS(44.11±6.10)%,P=0.002]均明显减小(P<0.05);GCS[(-15.53±3.63 )% VS(-17.21±3.60)%,P=0.076]略微减小,但差异无统计学意义(P>0.05);GAS[(-26.43±3.01)% VS (-30.27±3.29)%,P<0.01]、3D-Strain[(42.92±3.86)% VS (45.90±3.52)%,P=0.003]均显著减小(P<0.05).相关性分析表明GLS、GCS、GAS与LVEF之间呈负相关(r分别为-0.667、-0.651、-0.685,P<0.01),GRS、3D-Strain与LVEF之间呈正相关(r分别为0.640、0.646,P<0.01).结论 实时三维斑点追踪技术能够更加便捷、准确的反映冠心病患者的左心室心肌特性的变化.     

实时三维超声斑点追踪成像在冠心病诊断中的应用价值

目的 探讨实时三维超声斑点追踪成像(3D-STI)在冠心病诊断中的应用价值.方法 选取2018年1月至2019年3月在郑州市第七人民医院治疗的冠心病病人110例(冠心病组),采用冠状动脉(冠脉)病变评分(Gensini评分)标准进行评分,其中轻度病人32例,中度病人56例,重度病人22例,同时选取健康志愿者110例作为...     

二尖瓣环位移自动追踪技术评价蒽环类药物对乳腺癌病人左室收缩功能的影响

目的 应用二尖瓣环位移自动追踪技术评价蒽环类药物对乳腺癌病人左室收缩功能的影响,探讨反映左室功能受损较为准确和敏感的参数.方法 收集2018年10月至2019年12月于山西医科大学第二医院乳腺外科诊断为乳腺癌的女性病人50例,均行以表柔比星为主的化疗方案,分别于化疗前、化疗2及4周期后,行常规超声心动图、二维斑点追踪技术(2D-STI)及二尖瓣环位移自动追踪技术(TMAD)检查,获得左室射血分数(LVEF)、左室整体纵向峰值应变(LVGLS)及二尖瓣环连线中点最大位移与左心室舒张期末最大纵径比值(Mid％).比较化疗前后以上各参数的差异.结果 与化疗前比较,化疗4周期后LVEF降低,化疗前(67.85±4.16)％,化疗4周期后(63.35±4.49)％;与化疗前比较,化疗2、4周期后LVGLS降低,化疗前(?22.78±1.93)％,化疗2周期后(-18.85±1.02)％,化疗4周期后(-16.97±1.07)％;与化疗前比较,化疗2、4周期后Mid％均值降低,化疗前(17.52±0.96)mm,化疗2周期后(14.92±0.76)mm,化疗4周期后(12.99±0.98)mm;化疗前后各周期Mid％均值与LVEF呈弱相关(r=0.452,0.505,0.435,P<0.05),与LVGLS呈强相关(r=0.815,0.802,0.857,P<0.05);ROC曲线分析显示化疗4周期后LVGLS和Mid％均值预测蒽环类药物心脏毒性的ROC曲线下面积分别为0.962及0.912;重复性检验结果显示LVGLS和Mid％均值的观察者内ICC值分别为0.885、0.912,观察者间ICC值分别0.841、0.900;LVEF、LVGLS及Mid％均值与药物剂量均呈负相关(r=-0.398,-0.876,-0.906,P<0.05).结论 TMAD技术可早期识别化疗病人左心室整体收缩功能障碍,Mid％均值较LVGLS测量简便易行且重复性好,可作为敏感参数.     

3D-STI评价老年急性NSTEMI合并慢性肾功能不全的临床研究#br#

目的　探讨三维斑点追踪技术（3D-STI）评价老年急性非ST段抬高型心肌梗死（NSTEMI）合并慢性肾功能不全患者冠状动脉病变的严重程度及左室壁运动、左室功能受损程度的价值。方法　收集明确诊断急性NSTEMI的老年患者128例,根据肾功能情况分为肾功能不全组（不全组）和肾功能正常组（对照组）,对比患者一般临床特点、心脏超声三维斑点整体纵向应变（GLS）、整体径向应变（GRS）、整体圆周应变（GCS）、整体面积应变（GAS）及左室射血分数（LVEF）与冠状动脉病变SYNTAX评分情况。结果　与对照组比较,肾功能不全组的心脏GLS、GCS、GRS、GAS的绝对值及LVEF均明显降低;冠状动脉病变SYNTAX评分明显升高,以三支病变为主;B型钠尿肽前体（NT-proBNP）、超敏C反应蛋白（hs-CRP）明显升高;以上差异均有统计学意义（P＜0.01）。冠状动脉SYNTAX评分与GLS、GCS、GRS、GAS绝对值及LVEF呈负相关（r分别为-0.472、-0.477、-0.528、-0.580、-0.306,均P＜0.01）;LVEF与GLS、GCS、GRS、GAS绝对值呈正相关（r分别为0.423、0.316、0.413、0.403,均P＜0.01）。结论　3D-STI可作为一种评价老年急性NSTEMI合并慢性肾功能不全的患者冠脉病变程度、左室壁运动及左室功能的新技术,为临床早期治疗及疗效的评估提供参考依据。     

Cholinergic stimulation with pyridostigmine improves autonomic function in infarcted rats

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超声应变和应变率显像技术对肥厚型心肌病患者左室收缩功能的评价

应用超声应变及应变率显像技术评价肥厚型心肌病（HCM）患者左室局部心肌收缩功能。方法选取38例HCM患者作为观察组,选取健康志愿者36例作为对照组,分别进行组织多普勒超声检查,应用应变和应变率显像技术对局部心肌进行定量分析和评价。结果观察组患者左房内径、左室内径、左室收缩期末内径、室间隔厚度、左室后壁厚度均明显增加,左室射血分数明显减少（均P〈0．05）。观察组患者左室下壁、侧壁、后壁、前壁及室问隔心肌收缩期峰值应变、应变率均明显低于对照组（均P〈0．05）。结论应变和应变率显像技术能准确反映HCM患者左心室局部心肌收缩功能减退及特性的改变。     

CLORICROMENE REDUCES INFARCT SIZE AND ALTERS POSTISCHAEMIC BLOOD FLOW DEFECTS IN DOG MYOCARDIUM

1. The aim of the present investigation was to evaluate the effect of cloricromene on myocardial infarct size, regional myocardial blood flow and neutrophil accumulation in a canine model of ischaemia-reperfusion. 2. Dogs were instrumented to measure blood pressure, left anterior descending (LAD) coronary flow (flow probe) and regional myocardial blood flow (coloured microspheres). Two groups were studied: (i) CLO (n= 8) received an infusion of cloricromene (15 μg/kg per min); and (ii) VEH (n= 8) received saline. Infusions began at the onset of ischaemia (60 min) and continued through reperfusion (180 min). 3. Haemodynamic responses were not different between groups. Cloricromene reduced the area of necrosis expressed as a percentage of the area at risk from 35 ± 3% in the VEH group to 23 ± 4% in the CLO group (P<0.05). Regional myocardial blood flow in the ischaemic region was different between groups; VEH dogs showed an early reperfusion hyperaemia followed by a progressive reduction in flow, while CLO dogs exhibited a gradual increase in reflow in the absence of an early hyperaemie response (P<0.05). Left anterior descending flow was enhanced during the reperfusion period in the CLO group compared with VEH (P<0.05). Cloricromene reduced polymorphonuclear neutrophil (PMN) infiltration (myeloperoxidase activity) in all myocardial regions when compared with VEH (non-ischaemic zone, 0.34 ± 0.54 vs 0.05 ± 0.01 IU/l00 mg; ischaemic zone, 2.03 ± 0.80 vs 0.24 ± 0.08 IU/100 mg; and necrotic zone, 0.56 ± 0.04 vs 3.59 ± 1.09 IU/100 mg for VEH vs CLO groups, respectively; P<0.01). In a separate in vitro preparation, cloricromene reduced adherence of platelet-activating factor (PAF)-stimulated PMN to canine coronary endothelium. Stimulation of PMN by 100 nmol/L PAF resulted in adherence of 176 ± 36 compared with 48 ± 12 cells/mm² in PAF-stimulated PMN treated with 100 p. mol cloricromene (P<0.001). 4. These data indicate that cloricromene reduces myocardial infarct size in a canine model of ischaemia-reperfusion injury. Postischaemic blood flow patterns are significantly different in cloricromene-treated dogs. Cloricromene-mediated reductions in infarct size, neutrophil accumulation and adherence may play a role in this effect.     

Arrhythmogenic effects by local left ventricular stretch: effects of flecainide and streptomycin

Mechanical stretch has been shown to provoke arrhythmia. We wanted to analyze ventricular arrhythmia induced by local left ventricular stretch in order to find out, where arrhythmias originate and whether they can be prevented pharmacologically. Isolated rabbit hearts (Langendorff technique) were submitted to increased left ventricular stretch at the left wall by insertion of an additional intraventricular balloon and adjusting the end-diastolic pressure (EDP) to 25 mmHg for 10 min followed by 20 min recovery at normal EDP of 5–8 mmHg. Activation and repolarization processes were investigated by ventricular 256 electrode epicardial mapping. The hearts were treated during the whole procedure either with vehicle, 0.5 μM flecainide (sodium channel blocker) or 100 μM streptomycin (here used as stretch-activated ion-channel blocker). In addition, we performed a series of experiments, in which we enhanced EDP to 30 mmHg (global stretch instead of local stretch) by inflating the left ventricular pressure balloon (strain, 0.148?±?0.034). Each series was performed with n?=?6. Stretch resulted in local strain of 25 % at the left wall together with a local slowing of the activation process at the left wall, in a change in the activation pattern, and in ventricular arrhythmia. Coronary flow was not affected. Ventricular arrhythmias originated from the border between the stretched area and the non-stretched region. Flecainide and streptomycin reduced the prolongation of the activation process at the stretched left wall and mitigated the difference in total activation time between left and front wall but only partially prevented arrhythmia. In the additional global stretch experiments relative coronary flow and the other parameters remained unchanged, in particular TAT. Thus, in contrast to the local stretch series, there was no difference in the change in TAT between left and front wall. Only rare single ventricular extrasystoles (<1/min; originating from LV (front and left wall) i.e. from within the stretched region) were seen during stretch (but not at the beginning) and during recovery. Local left ventricular stretch can elicit ventricular arrhythmias. Local slowing of electrical activation seems involved so that the difference in total activation time of the stretched free left wall and the non-stretched increased.     

ANGIOTENSIN CONVERTING ENZYME INHIBITOR, CAPTOPRIL, INHIBITS CARDIAC HYPERTROPHY WITHOUT CHANGING COLLAGEN TYPES AND CONCENTRATION IN SPONTANEOUSLY HYPERTENSIVE RATS

1. The effects of the ACE inhibitor, captopril, on collagen metabolism in spontaneously hypertensive rats (SHR) with cardiac hypertrophy was examined. Captopril (100 mg/kg per day) was administered in drinking water to 20 week old male SHR for 12 weeks. Collagen concentration was calculated from hydroxyproline content, and relative proportions of types I, III and V collagen were determined by non-interrupted SDS-polyacrylamide gel electrophoresis (SDS-PAGE). These parameters were examined in age and sex matched Wistar-Kyoto (WKY) rats, as well as in non-treated SHR, and compared with those of captopril-treated SHR. 2. Captopril significantly reduced both blood pressure (191 ± 12.1 vs 146 ± 11.2 mmHg, P < 0.01), and the ratio of left ventricular (LV) weight to bodyweight (BW; 2.38 ± 0.17 vs 2.05 ± 0.12 mg/g, P < 0.01). There were no significant differences in collagen concentration among WKY rats, captopril-treated SHR and non-treated 32 week old SHR. However, total collagen content in captopril-treated SHR reduced significantly compared with non-treated 32 week old SHR (16.8 ± 2.0 vs 21.3 ± 0.8 mg, P < 0.01). The relative proportion of type V collagen was significantly higher in both captopril-treated (58.6 ± 3.4 vs 46.8 ± 1.3%, P < 0.01) and non-treated 32 week old SHR (59.9 ± 3.1 vs 46.8 ± 1.3%, P < 0.01) compared with WKY rats. However, there were no significant differences between captopril-treated SHR and non-treated 32 week old SHR. 3. The data from this study showed that captopril reduced cardiac hypertrophy, as reported previously, but did not change collagen types and concentration of the hypertrophied myocardium in SHR.     

Association of inflammation,myocardial fibrosis and cardiac remodelling in patients with mild aortic stenosis as assessed by biomarkers and echocardiography

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