不同病因心衰患者血浆脑钠素水平的影响

目的　观察不同病因心衰患者血浆脑钠素(BNP)水平的变化 ,探讨BNP在心衰发病机制中所起的作用以及 β -受体阻滞剂对心衰患者BNP水平的影响。 方法　采用酶联免疫吸附试验 (ELISA)法测定心衰患者血浆BNP水平。结果　心衰组BNP水平与正常对照组相比显著升高(P <0 0 1)。重度心衰心功能Ⅲ、Ⅳ级BNP水平明显高于心功能Ⅱ级。BNP变化的幅度在冠心病、扩张型心肌病不同病因心衰中有所不同 ,冠心病心衰BNP水平升高更明显 (P <0 0 1)。心衰患者中常规治疗组与非 β -受体阻滞剂治疗组相比 ,美托洛尔和卡维地洛治疗组BNP水平明显降低 (P <0 0 5 )。结论　心衰患者血浆BNP水平显著升高 ,BNP水平与心衰严重程度呈正相关 ,冠心病心衰BNP水平较扩张型心肌病组明显升高 ,提示冠心病心肌缺血损伤可能进一步促进BNP分泌。美托洛尔和卡维地洛均能下调心衰BNP水平 ,可能是不同β -受体阻滞剂逆转心衰神经激素过度激活的共同作用机制之一。     

The role of hyperglycaemia in the development of diabetic cardiomyopathy

1. Download : Download high-res image (140KB)
2. Download : Download full-size image

     

扩张型心肌病患者血浆氨基端脑钠素原的变化及其影响因素

目的:探讨扩张型心肌病(DCM)患者血浆氨基端脑钠素原(NT-proBNP)的变化及其影响因素.方法:用酶联免疫吸附方法,测定203例DCM组患者的血浆NT-proBNP浓度,并与203例对照组相比较.DCM组内再按下列不同的观察指标对NT-proBNP进行分析比较:按NYHA心功能分级进行Ⅱ级,Ⅲ级,Ⅳ级间比较;按体重指数进行超重者和不超重者间比较;按血清肌酐浓度进行肾功能异常者和肾功能正常者间比较;按是否合并心房颤动进行心房颤动者和无心房颤动者间比较.并用多元逐步回归分析,分析DCM患者中血浆NT-proBNP的影响因素.结果:与对照组比较,DCM组血浆NT-proBNP浓度显著升高(P＜0.01).DCM组血浆NT-proBNP浓度在各级NYHA心功能的DCM患者均显著高于对照组(P均＜0.01),且在不同NYHA心功能分级间亦逐级显著升高(P均＜0.01);在肾功能异常者血浆NT-proBNP浓度显著高于肾功能正常者(P＜0.01);超重者血浆NT-proBNP浓度显著低于不超重者(P＜0.01).多元逐步回归分析结果显示:只有NYHA心功能分级、体重指数、血清肌酐浓度、左心室射血分数、心率和左心房内径依次入选为血浆NT-proBNP浓度的独立预测因素(P＜0.05或0.01),其中NYHA心功能分级最强(P＜0.01).结论:DCM患者血浆NT-proBNP浓度显著升高,除取决于患者心功能外,还受体重指数、血清肌酐浓度等因素影响.     

Diltiazem reverses tissue Doppler velocity abnormalities in pre-clinical hypertrophic cardiomyopathy

BACKGROUND: Abnormalities in systolic and diastolic function shown by tissue Doppler imaging have been shown to be present in patients with hypertrophic cardiomyopathy who do not yet show clinical or echocardiographic evidence of the disease. These become more marked as left ventricular hypertrophy develops. We attempted to show that these abnormalities could be reversed by treatment with diltiazem. METHODS AND RESULTS: Six adults, who were carriers of a mutation involving the cardiac myosin binding, protein-C gene and who did not show clinical electrocardiographic or echocardiographic evidence of the disease were given a dose of 240mg of diltiazem daily. Tissue Doppler peak systolic and early diastolic velocities at the lateral mitral annulus were examined before treatment and at a mean of 8 weeks after starting treatment. Improvement in both parameters occurred with early diastolic velocities returning to normal and most systolic velocities also becoming normal. CONCLUSION: Diltiazem may have a role in helping to prevent abnormalities of function and perhaps the development of left ventricular hypertrophy in patients with pre-clinical hypertrophic cardiomyopathy.     

A case of arrhythmogenic right ventricular cardiomyopathy

The present report describes a 40-year-old woman with a long history of monomorphic ventricular tachycardia and left bundle branch block. She was treated with various antiarrhythmic agents; ventricular tachycardia ablation was attempted and an automatic implantable cardioverter defibrillator was implanted. Three-dimensional echocardiography clearly demonstrated features of arrhythmogenic right ventricular cardiomyopathy, including marked right ventricular (RV) dilation, decreased RV systolic function and thinning of the RV free wall. Other RV morphological abnormalities included excessive trabeculations and a localized apical aneurysm. Two years later, the patient developed symptoms of congestive heart failure. Despite maximal medical therapy, her clinical condition continued to deteriorate and she was referred for heart transplantation. Results of the pathology of her explanted heart confirmed this rare diagnosis. She presented with an unusual clinical course for arrhythmogenic right ventricular cardiomyopathy, which was complicated by progressive congestive heart failure and ultimately required heart transplantation. Three-dimensional echocardiography identified the structural abnormalities related to this rare disease.     

多巴酚丁胺在肥厚型心肌病激发试验的应用

目的 评价多巴酚丁胺激发试验在肥厚型心肌病激发试验中的安全性及有效性,比较潜在型肥厚型梗阻与静息型肥厚型梗阻性心肌病的临床特点. 方法 对22例确诊肥厚型心肌病患者(左心室流出道压力阶差正常或轻度增加)进行多巴酚丁胺激发试验,以5 μg·min-1·kg-1为起始剂量静脉泵人多巴酚丁胺,每隔5 min增加5 μg·min-1·kg-1,最大剂量20 μg·min-1·kg-1.每一次剂量泵入2 min后进行超声心动图检查,并对其临床特点与57例静息型肥厚型梗阻性心肌病患者进行比较. 结果 入选22例患者激发状态时左心室流出道流速峰值为(5.39±1.60)m/s,左心室流出道压力阶差(LVOTPG)峰值为(125.7±62.4)mm Hg(1 mm Hg=0.133 kPa);达到峰值时多巴酚丁胺给药平均速率为(13.9±6.85)μg·min-1·kg-1.16例(72.7%)患者达到阳性标准;6例(27.3%)患者虽达到阴性标准,但LVOTPG也有显著升高.潜在型梗阻患者的年龄、性别、各房室腔内径、左心室射血分数、室间隔厚度、LVOTPG等与静息型梗阻患者比较,差异均无统计学意义,但二尖瓣前向运动(SAM)现象发生率较低(62.5%比100%),Maron Ⅱ型较多[50.0%(8/16)比29.8(17/57)]. 结论 在肥厚型心肌病激发试验中,小剂量多巴酚丁胺负荷超声是一种较为安全和敏感性高的方法.潜在型较静息型肥厚型梗阻性心肌病患者的SAM现象发生率低,Maron Ⅱ型占优势.     

自体骨髓单个核细胞移植治疗扩张型心肌病的临床研究

目的研究自体骨髓单个核细胞(ABMMNCs)经冠状动脉(冠脉)移植对扩张型心肌病(DCM)患者心功能的影响及其安全性。方法16例扩张型心肌病患者,按患者的意愿分成两组移植组(n=10)在药物治疗的同时,通过冠脉转运将ABMMNCs移植入心肌组织内;对照组(n=6)只进行相关的药物治疗;两组在术前和术后6个月分别行超声心动图及动态心电图检查。结果超声心动图检查显示移植组的左心室射血分数(LVEF)较术前明显增高,左心室舒张末期内径(LVDd)、左心室收缩末期内径(LVSd)较术前明显降低,左心房内径(LAD)也较术前明显降低。而对照组的LVEF,LVDd及LVSd虽然较6个月前有所改善,但差异无统计学意义(P>0.05)。术中及术后随访6~12个月均无恶性心律失常和其他合并症发生。结论ABMMNCs经冠脉移植,可以治疗扩张型心肌病,改善心脏功能,而且较为安全。     

Myocardial injury following endogenous catecholamine release in rabbits

Catecholamines (CAT) given in large doses produce cardiomyopathic changes in several animal species. This study was designed to determine if endogenous release can also induce cardiac injury. Rabbits were infused with doses of tyramine (TYR), ranging from 200 to 500 micrograms/min/kg, i.v. for 90 min. Arterial pressure and heart rate were measured, as were total CAT concentrations, blood gases, pH and glucose. Two days later the animals were killed and cardiac injury assessed using a histological scoring system. All data were compared with controls given saline. Initial CAT averaged 452 pg/ml, rose to 2890 pg/ml after starting TYR, 500 micrograms/min/kg, and remained elevated for the duration of infusion. Circulating CAT levels were a function of TYR dose, and bore a linear relationship to the histological score (P less than 0.001). Development of lesions was unaltered by beta 1 blockade with practolol, but sharply reduced by alpha blockade with phentolamine (P less than 0.01). Pretreatment with insulin also reduced lesion formation, but diabetic (alloxan) rabbits showed no greater CAT injury. It is concluded that endogenous release of CAT induces myocardial injury in the rabbit in a dose-dependent manner. This is unrelated to myocardial O2 demand, and microvascular pathology was absent. Activation of alpha adrenergic pathways is likely the dominant or exclusive mechanism.