病态窦房结综合征的诊治误区

病态窦房结综合征(简称SSS)是以缓慢窦性心律失常为基础(如窦性心动过缓、窦性停搏、窦房传导阻滞等)而产生头晕、晕厥等症状群组成的综合征，同时可表现出多种快速心律失常(如心房颤动、心房扑动、房性心动过速等)，所谓慢－快综合征，某些SSS患者常以快速心律失常就诊，易引起误诊误治。1 对象和方法 本组9例，男6例，女3例，年龄16～76岁，平均54岁，以快速心房颤动就诊者6例，心房扑动1例，房性心动过速2例，其中4例有心功能不全，心室率在120～170次/min。入院后治疗：1例心房扑动静脉注射心律平50 mg(8min)，2例心律平70 mg静脉注射，0.5h后口服150 mg，5例以地西兰0.4～0.6 mg静脉注射，其中1例因心率控制不满意，0.5h后静脉注射胺磺酮150 mg，1例静脉注射胺碘酮150 mg。2 结果 1例心房扑动静脉注射心律平约50 mg(8min)时扑动波消失，交界区逸搏心律，HR30次/min。以后表现窦房传导阻滞，Ⅰ度房室传导阻滞。其余8例患者用药后10min～6h，表现为严重窦缓2例，严重窦缓、窦性停搏4例，严重窦缓、窦房传导阻滞2例，同时出现交界区逸搏及交界区逸搏心律1例，HR28～45次/min。患者均出现明显头晕、胸闷，其中2例有晕厥，1例有黑朦。经阿托品、异丙肾上腺素治疗及临时起搏(4例)观察7～21d，不能恢复正常窦性心律，6例行永久起搏治疗，3例因经济困难未埋植起搏器，而行药物治疗。

系统认识人类心脏整体电活动

1903年,Einthoven发明了弦线型心电图描计器,并与1906年将其应用与临床,引起巨大轰动,这是人类对心电图活动进行整体研究的起始,至今仍具有重要意义.

Objective To investigate the molecular mechanism of human ether-a-go-go-related gene ( HERG) potassium channels regulated by protein kinase A (PKA) in a human cell lin e. Methods HERG channels were stably expressed in human embryonic kidney (HEK) 293 cells, a nd currents were measured with the patch clamp technique. The direct phosphoryl ation of HERG channel proteins expressed heterologously in Xenopus laevis oo cytes was examined by 32P labeling and immunoprecipitation with an a nti-HERG antibody. Results Elevation of the intracellular cAMP-concentration by incubation with the adenyl ate cyclase activator, forskolin (10μmol/L), and the broad range phosphodiest erase inhibitor, IBMX (100μmol/L), caused a HERG tail current reduction of 83 .2%. In addition, direct application of the membrane permeable cAMP analog, 8 -Br-cAMP (500μmol/L), reduced the tail current amplitude by 29.3%. Intrac ellular application of the catalytic subunit of protein kinase A (200 U/ml) led to a tail current decrease by 56.9% and shifted the activation curve by 15.4 m V towards more positive potentials. HERG WT proteins showed two phosphorylated bands, an upper band with a molecular mass of ≈155 kDa and a lower band with a molecular mass of ≈135 kDa, indicating that both the core- and the fully glyco sylated forms of the protein were phosphorylated.Conclusions PKA-mediated phosphorylation of HERG channels causes current reduction in a hum an cell line. The coupling between the repolarizing cardiac HERG potassium curr ent and the protein kinase A system could contribute to arrhythmogenesis under p athophysiological conditions.

The effect of U50488, a selective k-opioid receptor agonist, on cardiac rhythm in the isolated perfused rat heart and intracellular calcium ([Ca2+] i) in the single ventricular myocyte were studied. The results showed that U50488 can induce arrhythmias dose-dependently in the isolated perfused rat heart and increase [Ca2+] i in the single ventricular myocyte. The effect of U50488 can be blocked by a selectivek-receptor antagonist, nor-binaltorphimine.The arrhythmogenic effects and the increase of [ Ca2 + ] i induced by U50488 were blocked by U73122, neomycin and streptomycin, which are selective phospolipase C inhibitors, but not by U73433, the inactive structural analog of U73122. These results demonstrated that the arrhythmogenic effect of cardiac k-receptor is due to activation of phosphoinositol/Ca2+ pathway.