QT Dispersion Level and Its Clinical Significance.in Dilated Cardiomyopathy

［1］Richardson CP, Mckenna RM, Bristow CM, et al.Report of the 1995 Word Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation, 1996,93: 841 ［2］Barr CS, Naas A, Freeman M, et al. QT dispersion and sudden unexpected death in chronic heart failure. Lancet, 1994,343:327 ［3］Martin AB, Garson A, Perry JC, et al. Prolonged QT interval in hypertropic and dilated cardiomyopathy in children. Am Heart J, 1994,127(1):64 ［4］Pye M, Quinn AC, Cobble SM. QT dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?Br Heart J, 1994,71(5):51 ［5］Berger RD, Kasper EK, Baughman KL, et al. Beat to beat QT interval variability: novel evidence for repolarization lability in ischemic and non ischemic dilated cardiomyopathy. Circulation, 1997, 96 (5):1557 ［6］Wolfram G, Ulrike S, Volker M, et al. QT dispersion and arrhythmic events in idiopathic dilated cardiomyopathy. Am J Cardiol, 1997,78: 458 ［7］Fei L, Goldman JH, Prasal K, et al. QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy. Eur Heart J, 1996,17: 258 ［8］Pan YZ, Guo NS, Xing ZF, et al. The relation between QT dispersion and ventricular arrhythmia of dilated cardiomyopathy. Chin J Inter Medi, 1996,35(11):73 ［9］Galinier M, Vialette JC, Fourcade J, et al. QT interval dispersion as a predictor of arrhythmic events in congestive heart failure. Importance of aetiology. Eur Heart J, 1998,19(7) :1054     

正常及突变MyBPC与肌凝蛋白结合功能的对比研究

目的　比较正常及突变 My BPC与肌凝蛋白的结合功能 .方法　重叠 PCR法制备正常及突变 My BPC的表达载体 ,大肠杆菌 BL- 2 1中表达并提纯蛋白 . 10 0 μL 含 2 .2 μmol· L- 1肌凝蛋白溶液中 ,分别加入不同浓度 My BPC蛋白 ,经离心、 SDS- PAGE,密度法测定两者的结合率 .结果　3774D1 8,32 2 3S1 4 0 结合率分别为 (6 8.2 0± 1.72 ) % ,(2 4.41±2 .10 ) % ,较正常 My BPC (82 .70± 2 .44 ) %显著降低 (n=5 ,P<0 .0 1) .结论　为家族性肥厚型心肌病突变基因的“肽类毒剂”致病学说提供了依据     

Dramatic improvement of severe dilated cardiomyopathy in an acromegalic patient after treatment with octreotide and trans-sphenoidal surgery

Severe congestive heart failure developed in an acromegalicpatient, and was successfully treated with octreotide followedby trans-sphenoidal surgery. Clinical, hormonal echocardiographicand haemodynamic findings as well as histological heart examinationbefore and after treatment revealed tliat over-production ofgrowth hormone may induce the myocardial cell degeneration responsiblefor mechanical heart dysfunction. In addition, this unique exampledemonstrates the reversibility of myocardial damage followingoctreotide and trans-sphenoidal surgery, leading to significantimprovement in cardiac function with minimal diastolic dysfunctionand moderate interstitial fibrosis.     

单电极VDD心脏起搏治疗肥厚性梗阻型心肌病(附1例报告)

目的：用ＶＤＤ心脏起搏治疗１ 例肥厚性梗阻型心肌病（ＨＯＣＭ）,并观察其临床及血流动力学效果。　方法：常规方法植入ＶＤＤ型心脏起搏系统,设置房室起搏间期１２０ ｍ ｓ,心房感知０．１５ ｍ Ｖ,起搏前后进行左室流出道压力阶差等血液动力学对比观察。　结果：术后房室同步起搏率为１００％ ,左室流出道压力阶差从６．８ ｋＰａ（５１．４ｍ ｍ Ｈｇ）降至２．８１３ ｋＰａ（２１．１ ｍ ｍ Ｈｇ）,二尖瓣前移现象消失,临床症状明显改善,随访期间未再出现晕厥。　结论：ＶＤＤ起搏植入简便、房室同步功能稳定,对ＨＯＣＭ 患者不失为一种新的有效的治疗方法。     

超声心动图对扩张性心肌病患者左室舒张功能的评价

为评价超声心动图对扩张性心肌病（ＤＣＭ）患者左室舒张功能的诊断价值。方法：用超声心动图 和放射性核素显像（ＲＮＶ）对２０例ＤＣＭ患者和２０例同龄正常人的左室舒张功能进行对照分析。结果：ＤＣＭ组左室 舒张功能ＲＮＶ指标峰充盈率（ＰＦＲ）明显降低,同对照组比较差异有显著性（Ｐ＜０．０５）;超声指标二尖瓣血流频谱早 期充盈峰速度（νＥ）、晚期充盈峰速度（νＡ）、νＡ／νＥ等参数同对照组比较无明显差异（Ｐ＞０．０５）,表现为“正常”。结 论：超声心动图舒张功能指标νＥ、νＡ、νＡ／νＥ不能真实反映ＤＣＭ患者的左室舒张功能。     

52例扩张型心肌病的X线、超声及心电图综合研究评价

目的：为了解扩张型心肌病（ＤＣＭ）的临床,Ｘ线,Ｂ超与心电图之间的规律性联系。方法：一分析了５２例被临床证实的ＤＣＭ患。结果：心脏Ｘ线检查;（１）肺淤２血占７０％（３７／５２）;（２）５９．６％心脏扩大呈”普大“或”主动脉”型;（３）心胸比率：０．５３４占２８．８％,０．５７－０．６５占６１％,０．７１有５例,且全部死亡;（４）心搏：正常有１５例,减弱有３７例;（５）２例５０岁以上患行冠状     

Acute clinical deterioration in a patient with end-stage dilated cardiomyopathy and left ventricular thrombus formation

The case of a 17-year-old male patient with severe end-stage dilated cardiomyopathy and a large thrombus formation within the cavum of the left ventricle is reported. After an acute thrombectomia combined with a partial left ventriculectomy (Batista procedure), the patient was successfully treated with an appropriate left ventricular assist device (LVAD) system using a centrifugal nonocclusive pump (Biomedicus, Medtronic, Anaheim, CA, U.S.A.). Mechanical support was removed on Day 9, and the patient was discharged from the hospital on Day 19. The effectiveness of emergency mechanical support in patients with very unfavorable prognoses is discussed.     

E. coli endotoxin enhances cardiomyopathy in rats with chronic alcohol consumption

The purpose of the study was to show whether it was possible to produce alcoholic cardiomyopathy by short-term alcohol ingestion combined with an infinitesimally low endotoxin injection. Wistar rats were fed an alcoholic liquid diet according to the formula of Lieber and Decarli, and challenged with an injection ofE. coli lipopolysaccharide (LPS) endotoxin (1.0 g/g body weight per day for ten weeks). After ten weeks alcohol diet combined with LPS challenge, light microscopical examination showed changes commonly seen in alcoholic cardiomyopathy such as hypertrophy, oedema and disarray of myofibers. By electron microscopy, degeneration of mitochondria and degeneration of myocardial fibers were observed, the latter showing disturbance of the myofibrilla arrangement and interstitial fibrosis. Rats on an alcoholic liquid diet and rats challenged with a single identical doses of LPS did not show characteristic histological findings of alcoholic cardiomyopathy. These results suggest that short-term alcohol ingestion combined with an infinitesimally low endotoxin injection experimentally produces alcoholic cardiomyopathy, and may support the idea that endotoxin plays an important role in the aetiology of alcoholic cardiomyopathy.     

The acute response of left ventricular filling dynamics to intravenous verapamil predicts the changes in exercise tolerance after oral verapamil therapy in patients with hypertrophic cardiomyopathy

We studied the correlation between changes in left ventricularfilling dynamics induced by acute intravenous administrationof verapamil and the changes in exercise tolerance induced byoral administration of the agent in 30 patients with hypertrophiccardiomyopathy. Diastolic cardiac function was measured by meansof a nuclear stethoscope before and 10 min after intravenousadministration of verapamil, 0.15mg. kg^–1 over 2 min.Treadmill exercise tests using a modified Bruce protocol wereperformed before the initiation of oral verapamil treatmentand after 4 weeks of oral therapy at a dose of 320–360mg. day^–1 (mean±SD 332±17mg. day^–1). Peak filling rate (PFR) increased in 21 patients, 18 of whom(86%) also had an increase in exercise duration. PFR showedno increase in nine patients, eight of whom (89%) had no changein exercise duration (sensitivity 95%, specificity 73%, predictivevalue of the positive result 86%, predictive value of the negativeresult 89%). Acute changes in time from the beginning of rapidfilling to PFR (t-PFR) and in left ventricular end-diastolicvolume (EDV) were less useful in predicting improvement in exercisetolerance. In 19 patients the changes in PFR and EDV parallelled.Twelve of the 13 patients (92%) will an increase in both parametersalso had an increase in exercise duration, whereas all six inwhom these parameters were reduced showed no increase in exerciseduration (sensitivity 100%, specificity 86%, predictive valueof positive results 92%, and predictive value of negative results100%). In conclusion, the response of PFR, and even more so the combinedresponse of PFR and EDV to intravenous verapamil, accuratelyidentify patients with hypertrophic cardiomyopathy who are likelyto show improvement in exercise tolerance after oral verapamiltherapy.     

The relationship of myocarditis to dilated cardiomyopathy

Three patients with congestive cardiomyopathy are reported inwhom high neutralizing antibody titres to Coxsackie B viruseswere detected. At post-mortem examination, all three had histologicallydemonstrable chronic inflammation of the myocardium. The heartsof ten patients dying in cardiac failure due to other causesshowed no comparable inflammatory infiltration. This providesfurther evidence that Coxsackie B viral myocarditis is involvedin the pathogenesis of some cases of dilated cardiomyopathy. One patient also had pulmonary veno-occlusive disease. Thishas been reported in association with myocarditis once previouslyin an infant. A viral aetiology has been postulated. It seemslikely in this patient to have also been due to a CoxsackieB virus.