静脉注射胺碘酮治疗快速心房纤颤的临床观察

目的:观察静脉注射胺碘酮对心房纤颤并快速心室率(简称快速型房颤)患者的临床疗效。方法:对34例新发快速型房颤患者,10 min静脉推注胺碘酮150 mg,观察10 min,未转为窦性心律者再次于10 min内推注150 mg,仍未转复者则以0.5~1.0 mg/min静脉滴注24 h,转为窦性心律者则随时终止滴注。观察房颤转复、心室率控制情况及不良反应,同时比较老年组(18例)和非老年组(16例)有何不同。结果:34例患者在24 h内均转为窦性心律。两组患者用药后30 min,1 h,6 h,24 h心室率分别为(96.00±8.39)次/min与(98.00±8.35)次/min,(88.13±9.98)次/min与(86.47±8.68)次/min,(84.88±10.19)次/min与(82.88±8.25)次/min,(74.88±9.80)次/min与(78.88±7.80)次/min,较用药前的(138.58±9.15)次/min与(130.36±8.26)次/min明显下降(P<0.01),但两组间用药前、后无显著差异。无严重心律失常发生,未诱发或加重心功能不全。结论:静脉应用胺碘酮治疗快速型房颤安全有效,老年人用药剂量不减。     

眼针治疗阵发性室上性心动过速120例的即时疗效观察

目的:观察眼针对阵发性室上性心动过速的即时疗效。方法:选择符合诊断标准的门诊患者120例,针其眼针穴区:心区和上焦区。针后30分钟描记心电图,计算心率,观察眼针对阵发性室上性心动过速的影响。结果:显效103例,占85.83%;有效9例,占7.5%;无效8例,占6.66%;总有效率93.33%.结论:眼针对阵发性室上性心动过速有较好的即时疗效。     

可插入式循环心律监测仪的临床应用及护理(附一例报告)

目前,可插入式循环心律监测仪是一个高诊断率且寿命较长的皮下无电极心律监测仪.它可提供边续14个月的监测,由此大增加了捕获有显著症状的心律失常的机会.     

合并心律失常的心力衰竭56例治疗评价

目的探讨心力衰竭并发心律失常的发病规律及治疗方法。方法回顾性分析了93例慢性心力衰竭病人的临床资料，包括临床特点、诊断治疗方法以及预后。结果心律失常发生率为60．2％，以室性早搏发生率最高32．1％，其次是房性早搏26．8％，心房纤颤21．4％，其他19．7％，经治疗有效71例，总有效率76．3％。结论纠正心功能不全是治疗的关键，应根据具体情况选择性地应用抗心律失常药。     

不同浓度的金属硫蛋白对离体豚鼠乳头肌缺氧、复氧电生理特性的影响

为探讨金属硫蛋白（MT）对豚鼠乳头肌缺血再灌注损伤所致心律失常的影响，利用标准玻璃微电极技术，采用缺氧及复氧豚鼠乳头肌模型，模拟体内缺血再灌注损伤，观察不同浓度MT对豚鼠乳头肌电生理特性的影响。结果显示低浓度的MT（0．002mmol／L）对正常及缺氧和复氧豚鼠乳头肌的动作电位（AP）有关参数及自律性均无影响；中等浓度的MT（0．02mmol／L）仅使正常乳头肌的AP复极达50％时程（APD50）缩短24％（P＜0．05），但使缺氧乳头肌的AP复极达20％时程（APD20）、APD50和AP复极达90％时程（APD90）分别缩短68％、56％和43％（P均＜0．01），并使静息电位（RP）、AP幅值（APA）和0相最大上升速率（Vmax）分别增加30％、30％和45％（P均＜0．01）；高浓度的MT（0．1mmol／L）使正常豚鼠乳头肌的APD20、APD50和APD90分别缩短57％、54％和50％（P均＜0．01），并且RP、APA及Vmax分别下降22％（P＜0．05）、28％（P＜0．01）和29％（P＜0．05），而使缺氧豚鼠乳头肌的APD20、APD50和APD90分别延长92％、78％和50％（P均＜0．01），对RP、APA及Vmax无明显影响。在复氧期间，0．02mmol／L的MT可使自律性的发生率从77．8％降至55．6％（P＜0．05）；而0．1mmol／L的MT则使自律性的发生率从77.8％降至22．2％（P     

导管射频消融治疗飞行员快速心律失常临床分析

目的探讨导管射频消融（RFCA）在治疗飞行员多种快速性心律失常中的安全性及临床应用价值，探讨飞行员快速性心律失常的航空医学鉴定标准。方法对13例快速性心律失常的飞行员进行了电生理（EP）检查，特发性室性心动过速（VT）1例，频发室性期前收缩（VE）2例，阵发性心房纤颤（AF）1例，房室折返性心动过速（AVRT）5例，房室结折返性心动过速（AVNRT）3例，房性心动过速（AT）1例。对其中12例采用RFCA治疗。结果RFCA即刻成功率为100％，全组无并发症发生。1例房性心动过速未行导管射频消融治疗。所有飞行员术后地面观察6个月后，返院进行随访复查，同时进行飞行鉴定。12例导管射频消融治疗，术后6个月24h动态心电图、12导联心电图检查和食道电生理检查均未检测到术前的同型快速性心律失常发作，延迟成功率为100％，医学鉴定合格。1例AT仍有发作，飞行不合格。结论对于飞行员快速性心律失常进行导管射频消融治疗是一种安全、有效的治疗方法。心脏电生理检查应作为飞行员快速性心律失常医学鉴定的主要指标之一。     

美托洛尔对心肌梗死兔自主神经重构的影响

目的探讨β受体阻滞剂美托洛尔治疗对心肌梗死后心脏自主神经重构的改善作用。方法通过结扎新西兰大白兔冠状动脉前降支制作心肌梗死模型,随机分成心肌梗死 美托洛尔组[(10mg/(kg·d),治疗组)、心肌梗死组(模型组)和假手术组。8周后所有成活兔均进行统一的电生理检查,诱发室性心律失常。并处死实验动物,取心肌采用免疫组织化学的方法观察心室神经纤维的形态、密度及生长活性。结果模型组室性心律失常诱发率明显高于假手术组(58.3%比16.7%,P<0.001),而美托洛尔治疗后其诱发率降至8.3%。模型组梗死灶周S100及GAP43阳性神经纤维密度分别达到3889±521μm2/mm2和3090±622μm2/mm2,明显高于假手术组(1727±304μm2/mm2和718±177μm2/mm2;P均<0.01),且神经纤维空间分布紊乱;而治疗组梗死灶周S100及GAP43阳性神经纤维密度降至2725±283μm2/mm2和1922±508μm2/mm2,与模型组比差异均有统计学意义(P<0.05),且神经形态及分布更类似于假手术组,非梗死左心室游离壁心肌梗死后密度上调的S100及GAP43阳性神经纤维经美托洛尔治疗后也明显下降(P<0.05)。结论美托洛尔可改善心肌梗死动物模型的神经重构,从而可能预防心肌梗死后室性心律失常的发生。     

THE EFFECT OF ACUPUNCTURE ON PREVENTION AND TREATMENT OF ISCHEMIC ARRHYTHMIA AND THE RELATION BETWEEN EFFECT OF ACUPUNCTURE AND CHOLINERGIC MUSCARINE-LIKE RECEPTORS

For investigating the effect of acupuncture on ischemic arrhythmia and its mech-anism, adult albino rats with ligated anterior descending branch of coronary artery as experimentalmodel were treated with or without acupuncture, and others with imitative operation but without bothcoronary artery ligation and acupuncture treatment were used as control. It was found in acupuncturegroup that the fibrillation-liability of ischemic myocardium was efficiently decreased, the affinity ofAch-M receptors on membranes of ischemic myocardium was markedly increased, and the tolerance ofischemic myocardium to atropine was elevated in the experiment of atropine inducing fibrillation.These results indicate that acupuncture may play a therapeutic role on ischemic arrhythmia throughactivating the activity of muscarine-like receptors of cholinergic nervous system.     

KCNJ2 mutations in arrhythmia patients referred for LQT testing: A mutation T305A with novel effect on rectification properties

BACKGROUND: Loss-of-function mutations in the KCNJ2 cause approximately 50% of Andersen-Tawil Syndrome (ATS) characterized by a classic triad of periodic paralysis, ventricular arrhythmia, and dysmorphic features. Do KCNJ2 mutations occur in patients lacking this triad and lacking a family history of ATS? OBJECTIVES: The purpose of this study was to identify and characterize mutations in the KCNJ2-encoded inward rectifier potassium channel Kir2.1 from patients referred for genetic arrhythmia testing. METHODS: Mutational analysis of KCNJ2 was performed for 541 unrelated patients. The mutations were made in wild type (WT) and expressed in COS-1 cells and voltage clamped for ion currents. RESULTS: Three novel missense mutations (R67Q, R85W, and T305A) and one known mutation (T75M) were identified in 4/249 (1.6%) patients genotype-negative for other known arrhythmia genes with overall incidence 4/541 (0.74%). They had prominent U-waves, marked ventricular ectopy, and polymorphic ventricular tachycardia but no facial/skeletal abnormalities. Periodic paralysis was present in only one case. Outward current was decreased to less than 5% of WT for all mutants expressed alone. Co-expression with WT (simulating heterozygosity) caused a marked dominant negative effect for T75M and R82W, no dominant negative effect for R67Q, and a novel selective enhancement of inward rectification for T305A. CONCLUSIONS: KCNJ2 loss of function mutations were found in approximately 1% of patients referred for genetic arrhythmia testing that lacked criteria for ATS. Characterization of three new mutations identified a novel dominant negative effect selectively reducing outward current for T305A. These results extend the range of clinical phenotype and molecular phenotype associated with KCNJ2 mutations.