Do antiarrhythmic drugs work? some reflections on the implications of the cardiac arrhythmia suppression trial

Despite major advances in our understanding of the mechanisms of cardiac arrhythmias and how antiarrhythmic drugs appear to work, there remains much doubt whether these agents reduce arrhythmic mortality except in certain subsets of patients. The results of the Cardiac Arrhythmia Suppression Trial (CAST) have indicated that certain antiarrhythmic drugs not only "fail to work" but may substantially increase mortality. The effects of Class Ic agents in CAST and the meta-analysis of randomized antiarrhythmic trials in the survivors of acute infarction suggest that drugs that act primarily by delaying conduction are particularly deleterious in the survivors of acute infarction. Whether these data have a wide applicability in terms of all ventricular arrhythmias is unclear, but beta-blockers remain the only class of agents that in control trials have been shown to reduce sudden death. The effect appears to be related to beta-blockade and not to suppression of premature ventricular contractions (PVCs). Beta blockers appear to act by preventing ventricular fibrillation. It is reasonable to assume that PVC suppression per se is unlikely to produce a reduction in sudden death. Uncontrolled data with amiodarone suggests that it has the potential to prolong survival by controlling arrhythmias. The effects of amiodarone and beta blockers, both significantly attenuating adrenergic stimulation, provide pharmacologic probes to define the crucial determinants of efficacy of a compound for mortality reduction in high risk survivors of myocardial infarction. The focus must now shift from antiectopic and antiarrhythmic agents that delay conduction to those that exert antifibrillatory actions by sympathetic antagonism and those that exhibit the added property of lengthening myocardial refractoriness.     

小脑和脑干梗塞致突发性耳聋

目的:了解小脑和脑干梗塞引起的突发性耳聋的临床特点.探讨其发病机制.方法:回顾性分析12例小脑和脑干梗塞所致突发性耳聋的临床资料.结果:该组患者主要临床表现为耳聋、眩晕、耳鸣、眼震、同侧颜面麻木感.头颅CT或MRI发现小脑或脑干有小于2 cm的梗塞灶.结论:发病机制主要为小脑前下动脉(AlCA)供血不足使小脑脑桥角或脑干缺血,损伤该区域的耳蜗神经和听神经传导通路,导致耳聋.小脑和脑干梗塞的诊断主要依据临床表现、CT或MRI检查.     

Study on Pulmonary Surfactant of Sudden Death of Infant

Objective To find the pathogenesis of sudden infant death syndrome (S IDS) from changes of pulmonurry surfactant. Methods By means of thin-layer ckromatography technique, surfactant in whole lung specimens of 10 infants with SIDS and 10 control infants without SIDS (dead of nonrespiratory diseases ) were examined qualitatively and quantitatively. Results Eleven components in pulmonary surfactant were examined qualitatively, including lysophosphatidylcholine , sphingomyelin , phosphatidylcholine , phosphatidylserine , phosphatidylinositol , phos phatidylethanolamine , phosphatidylglycerol , diphosphatidylylycerol , phosphatidic acid, cholesterol and neutral lipids. Quantitative examination showed that the amount of surfactant of whole lung specimens in sudden death group [-(8.9±1.0) rng/g wet lung weight] was significantly less than that in control group [-(12. 6±1.4) mg/g uet lung weight, P＜0. 01]. Qualitative variance showed that the percentages of phosphatidylcholine (49. 4 % ± 2. 0 % ) and phosphatidylylycerol ( 2. 6 % ± 0. 7 % ) decreased markedly in sudden death group compared with those in control group (61.5 % ± 3. 0 % and 4.3 % ±1. 5%, P ＜ 0. 01 ). Conclusion Before death there is serions defect on metabolism of pulmonary surfactant in sudden death infants, with the amount decreasing and the ratio of its components being disturbed, which is one of the important pathogenies of SIDS.     

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     

Synthetic Evolution of a Supramolecular Harpooning Mechanism to Immobilize Vesicles at Antifouling Interfaces

The immobilization of vesicles has been conceptualized as a method to functionalize biointerfaces. However, the preservation of their integrity post immobilization remains a considerable challenge. Interfacial interactions can cause vesicle rupture upon close surface contact and non-specific protein adsorption impairing surface functions. To date, immobilization of vesicles has relied solely on either entrapment or prior modification of vesicles, both of which require laborious preparation and limit their applications. This work develops a bioinspired strategy to pin vesicles without prior modification while preserving their intact shape. This work introduces antifouling diblock copolymers and ultrathin surface-attached hydrogels containing a brush-like interface consisting of a bottle brush copolymer of N-(2-hydroxypropyl) methacrylamide (HPMA) and N-(3-methacrylamidopropyl)-N,N-dimethyldodecan-1-aminiumiodide (C12+). The presence of positive charges generates an attractive force that pulls vesicles toward the surface. At the surface, the amphiphilic properties of the combs facilitate their insertion into the membrane, mimicking the harpooning mechanism observed in antimicrobial peptides. Importantly, the antifouling poly(HPMA) backdrop serves to safeguard the vesicles by preventing deformation and breakage. Using a combination of thermodynamic analysis, surface plasmon resonance, and confocal laser scanning microscopy, this work demonstrates the efficiency of this biomimetic system to capture vesicles while maintaining an antifouling interface necessary for bioapplications.     

Value of ambulatory electrocardiographic monitoring to identify increased risk of sudden death in patients with left ventricular dysfunction and heart failure

To examine the predictive value of ventricular arrhythmias onambulatory electrocardiographic (ECG) monitoring, 211 patientswith left ventricular dysfunction and congestive heart failure(76% men, age 63±4 years, left ventricular ejection fraction0.26 ± 0.10) were studied. During a follow-up of 21 ±11 months, there were 45 cardiac deaths: 22 were due to progressivepump failure and 23 were sudden. Patients with a low left ventricularejection fraction ( 0.27) and ventricular tachycardia on 24h ECG were at higher risk of dying suddenly and from progressivepump failure (both P<0.0001). Patients who died suddenlywere found to have significantly longer (P=0.003) and faster(P=0.029) ventricular tachycardias on their baseline ambulatoryECG, than survivors. This association was not observed in patientswho died of progressive pump failure. Therefore, low left ventricularejection fraction and ventricular tachycardia on 24 h ECG recordingpredict an increased risk of cardiac mortality. Our resultsalso suggest that longer and faster ventricular tachycardiarecorded by 24 h ECG may identify patients at risk of suddendeath, a finding which has not been described before.     

异丙酚复合芬太尼维持麻醉对脑代谢的影响

观察异丙酚复合芬太尼维持麻醉对脑代谢的影响。方法： 择期手术病人８ 例, 芬太尼、硫贲妥钠、维库溴铵诱导插管, 静脉联接Ｇｒａｓｅｂｙ 微泵异丙酚８ ｍｇ／ （ｋｇ·ｈ） , 芬太尼１ μｇ／ （ｋｇ·ｈ）维持麻醉。连续监测ＭＡＰ、心电图、脉搏氧饱和度和呼气末二氧化碳分压, 同步采集动脉血和颈内静脉血作血气分析, 计算动－ 静脉氧含量差（Ｄａ － ｖＯ２） 和脑氧摄取率（ＥＲＯ２） 。结果： 异丙酚麻醉维持平稳, Ｄａ － ｖＯ２ 和ＥＲＯ２ 在给药３０ ｍｉｎ 、６０ ｍｉｎ 较气管插管后５ ｍｉｎ 无明显改变, 有平均动脉压下降和心动过缓。结论： 异丙酚复合芬太尼维持麻醉可保持脑氧供需平衡稳定。     

Cerebral reperfusion in brain death of a newborn. Case report

A case of sudden infant death after 15 minutes of successful resusciation of cardiovascular function is presented. While apnoic cranial nerve areflexia and electrocerebral silence persisted, angiography and transcranial Doppler sonography demonstrated nearly normal cerebral perfusion, which even increased day by day inspite of the persistence of other signs of brain death. The phenomenon cerebral reperfusion is concluded to be compatible with the diagnosis of brain death.     

突发性聋患者血浆一氧化氮和内皮素含量的测定

目的 :探讨血浆一氧化氮 (NO)和内皮素 (ET)水平在突发性聋 (突聋 )发病过程中的作用。方法 :对32例突聋患者用硝酸还原酶法测定血浆NO ,用放射免疫法测定血浆ET。结果 :突聋组血浆NO显著降低 ,ET显著升高 ,与正常对照组相比较 ,突聋组血浆NO显著降低 (P <0 .0 1) ,ET显著升高 (P <0 .0 1) ;突聋治疗前与治疗后血浆NO、ET之间差异有显著性意义 (P <0 .0 1) ;治疗有效者与无效者血清NO、ET水平的差异也有显著性意义 (P <0 .0 1)。结论 :在突聋发作过程中 ,血浆NO和ET的含量显著变化 ,可能促进了疾病的发生和发展     

鼓室置管治疗儿童分泌性中耳炎疗效观察

目的 探讨鼓室置管治疗儿童分泌性中耳炎(SOM)的疗效和并发症。方法 回顾性分析了我科1997年～2001年经鼓室置管治疗的45例(78耳)儿童SOM的临床资料。结果 45例随访1-2年，85％耳(35例，66耳)听力明显改善，鼓室导抗图恢复成A型。结论 积极改善咽鼓管功能并适当延长留管时间，防止过早脱管对提高儿童SOM的治愈率有着积极的意义。