QT间期与小剂量胺碘酮治疗室性心律失常疗效的相关性研究

目的:探讨小剂量胺碘酮治疗室性心律失常时QT间期与疗效的相关性。方法:50例采用小剂量胺碘酮治疗室性心律失常的患者,观察患者治疗4个月,室性心律失常QT间期延长与有效控制率的关系及其不良反应。结果:50例患者治疗有效率高达90%,且维持量小[(140±37)mg/d]。QT间期延长者较未延长者治疗效果更满意;QT间期未延长者延长负荷期后,部分患者QT间期延长而取得满意疗效无明显不良反应。结论:小剂量胺碘酮治疗室性心律失常时QT间期延长者疗效更满意。     

胺碘酮治疗室性心律失常的临床疗效与QT间期的关系

目的 观察胺碘酮治疗室性心律失常的临床疗效与QT间期的关系.方法 选取室性心律失常患者50例,采用常规治疗基础上口服胺碘酮,全程、负荷、维持治疗,观察相关指标.结果 通过治疗后,患者的QT间期显著延长、室性早搏、短阵室速均有显著改善,总有效率为96％,为发生心功能降低,肝功能异常,甲状腺功能异常及皮肤、神经、眼角膜损伤、恶性心律失常等不良反应.结论 采用胺碘酮治疗室性心律失常疗效显著,不良反应较少,治疗后QT间期延长情况与个体有关,对部分QT间期不延长患者可适当增大剂量,可达到治疗效果,因此,口服胺碘酮治疗室性心律失常疗效显著,用药途径方便、安全、QT延长情况有个体化差异.     

胺碘酮对恶性室性心律失常QT离散度的影响

目的观察胺碘酮对恶性室性心律失常QT离散度的影响。方法观察60例恶性室性心律失常患者服用胺碘酮治疗前后校正的QT离散度（QTcd）的变化。结果应用胺碘酮治疗恶性室性心律失常（LownⅢ级以上）后与治疗前相比较，显著减少（P〈0．05），QTcd亦有显著性下降（P〈0．01），并未发现该药具有严重毒副作用。结论胺碘酮治疗恶性室性心律失常安全有效，能缩小QT离散度，从而减少室颤的发生，可降低恶性严重室性心律失常和心源性猝死。     

胺碘酮治疗室性心律失常对TpTe的影响

目的:观察胺碘酮治疗室性心律失常治疗时程对心电图T波顶点至T波终点的宽度(T-peak to T-end interval,TpTe)的影响。方法: 85例室性心律失常患者,胺碘酮150 mg静脉注射,继以1 mg/kg,持续6 h,后减量至0.5 mg/kg,持续48 h后停用,静脉胺碘酮24 h后,开始同时加用口服胺碘酮,每次0.2 g ,1日3次,1周;每次0.2 g,每日2次,1周; 0.2 g每日1次维持,观察用药后1、3、7、10、14、17、21 d心率、TpPe、QT、TpPe-c、QTc变化。结果: 心律失常控制率达92%（78/85）。治疗有效组自治疗后第1天心率明显减慢,QT间期明显延长（P≤0.01）,14 d时达最大值,后趋于平稳,但未见统计学意义差异。但整个治疗时程中胺碘酮对TpTe、TpTe-c及QTc未见有统计学意义的改变。结论: 胺碘酮治疗室性心律失常不影响TpTe,TpPe独立于心率,不需要心率校正。     

小剂量胺碘酮长期治疗室性和室上性心律失常

目的：观察小剂量胺碘酮长期治疗室性和室上性心律失常的疗效和实用性。方法：回顾性分析对124倒药物治疗无效的或致命性心律失常患者用胺碘酮治疗10年的结果。其中，室性心律失常45例(36％)，房性心律失常52例(42%)．房室折返性心动过速27例(22%)。治疗室上性和室性心律失常的负荷剂量分别为600rag／日共7天和600～1200mg／日共14天，每日维持剂量分别为194±48和206±55mg。平均用药时间32±28个月，总共治疗326．3患者·年。结果：39例持续性室性快速心律失常的保险统计的满意控制率(无猝死和非致命性心律失常复发)在第1年为78%，第2年71％。室上性心律失常满意控制率(持续性房性心律失常的心室率<100bpm伴症状明显改善，阵发性房性心律失常和房室折返性心动过速的发作<1次／年)在第1、2、3年分别为73%、65%和62％。与胺碘酮有关的不良反应累积发生率为5．8／100人·年，需停药的12例(9．7％)。15例发生甲状腺功能异常，2例发生肝脏毒性反应，另1例发生非致命性肺纤维化。胺碘酮总的治疗成功率(心律失常满意控制且无不良反应)在第1、2、3年分别为67%、50%和53%。结论：小剂量胺碘酮治疗室性和室上性心律失常与大剂量用药用样有效而副作用较少。     

胺碘酮长疗程个体化治疗室性心律失常的临床疗效和安全性

为探讨胺碘酮长疗程个体化治疗室性心律失常 (VA)的临床疗效和安全性 ,31例室性心律失常 (VA)患者给予胺碘酮个体化治疗 ,疗程 1年以上 ,观察治疗前和治疗后 1年患者室性心律失常的有效控制率、QT间期变化以及不良反应。结果 :31例患者胺碘酮的维持量为 15 5± 37mg/天 ,比推荐的用量 (2 0 0～ 40 0mg/天 )要小 ,而胺碘酮治疗室性心律失常 (VA)的有效率仍高达 90 .3% ;QT间期轻度延长 (396± 5 1msvs 438± 5 3ms ,P <0 .0 5 )。不良反应方面 ,有一例患者出现一过性FT3、FT4 升高 ;未出现扭转型室速和室颤发作 ;无肺毒性和肝肾损害等副作用。不良反应也比文献报道的非个体化治疗方案要少 (3 .2 %vs 5 %～ 15 % )。结论 :胺碘酮长疗程个体化治疗室性心律失常(VA)的临床疗效确切 ,维持用量较小 ,相关的不良反应也减少。     

稳心颗粒联合胺碘酮治疗室性心律失常疗效观察

室性心律失常在器质性心脏病患者中非常常见,易使病情恶化,发生猝死,有效地控制室性心律失常对改善症状、改善心功能、改善预后十分重要.我院应用稳心颗粒和胺碘酮联合治疗室性心律失常取得较满意疗效,现报道如下.     

胺碘酮和美托洛尔联合治疗室性心律失常并慢性心力衰竭的疗效观察

将36例合并慢性心力衰竭（CHF）的频发、复杂室性早搏或非持续性室性心动过速患者，随机分为胺碘酮、美托洛尔联合治疗组（治疗组17例）和胺碘酮单独治疗组（对照组19例）。治疗组给予胺碘酮负荷量600mg/d，维持量200mg/d，美托洛尔25－50mg/d；对照组单用胺碘酮，方法同治疗组。两组同时给予利尿剂、血管紧张素转换酶抑制剂等常规药物治疗，观察5个月。结果治疗组心功能及室性心律失常的治疗有效率明显高于对照组，两组比较有显著性差异（P＜0．05）。治疗后两组LVEF、LVEDV、LVESV和6min步行试验均明显改善，治疗组优于对照组，均有显著性差异（P＜0．05）；治疗组再住院率、心脏事件发生率低于对照组，有显著性差异（P＜0．05）。两组不良反应发生率无显著性差异（P＞0．05）。认为胺碘酮和美托洛尔联合治疗室性心律失常合并慢性心力衰竭优于单用胺碘酮，不良反应无增加。     

胺碘酮对室性心律失常患者QT离散度的影响

要：目的观察胺碘酮对室性心律失常患叩离散度的影响。方at400例室性心律失常患应用口服或静脉注射胺碘酮治疗,其中18例持续性室性心动过速患静脉应用胺碘酮治疗,负荷量为24h总量900～1500mg,同时口服胺碘酮600mg/d。382例频发室早伴或不伴短阵室速的患口服胺碘酮治疗,负荷量为第1周600mg/d,并根据病情逐渐减量。结果400例室性心律失常患应用胺碘酮治疗均有效,并发现该药能减少叽离散度,未见严重毒副作用．结论胺碘酮治疗室性心律失常安全有效．能影响患的QT离散度．且能减少室颤的发生。     

胺碘酮治疗室性心律失常临床观察

胺碘酮为广谱抗心律失常药,主要通过抑制电压依赖性钾通道,使外向钾电流受抑,动作电位和有效不应期延长,从而起到抗心律失常的作用,多用于室上性和室性快速心律失常的治疗。现归纳总结我院应用胺碘酮治疗室性心律失常的经验。     

Relationship between QT interval duration and exercise-induced ventricular arrhythmias

This study was performed to determine if QT prolongation beforeand during early exercise is related to the occurrence of exercise-inducedventricular arrhythmias (EIVA). EIVA occurred in 47 of 142 patientswith angiographic evidence of coronary artery disease (CAD);no EIVA occurred among the 22 patients without CAD (OV). RestingQTc and QT intervals during early exercise were similar in patientswithout EIVA, irrespective of the presence or absence of CAD;however resting QTc was significantly longer in CAD patientswho showed EIVA (443±40ms; ?<0·01) than inCAD patients without EIVA (424 ± 37 ms) and in OV patients(421 ±32 ms). During early exercise, the QT intervalremained significantly longer in patients with than in thosewithout EIVA. There was a trend toward increasing resting QTc in patients who exhibited EIVA more severe than grade 3.When resting QTc was longer than 440 ms, subsequent EIVA werecorrectly predicted in CAD patients with a sensitivity of 43%,a specificity of 72% and a predictive accuracy of 63%. Thus, a trend toward longer resting QTc values exists in CADpatients who develop EIVA; however, a long resting QTc (>440 ms) appears to be only a weak predictor of subsequent EIVA.     

The relationship between left ventricular shape and QT interval dispersion

Left ventricular geometry is suspected to affect heterogeneity of myocardial repolarization; therefore, it is plausible but unproven that increased sphericity of the left ventricle is associated with greater QT interval dispersion. In 60 patients with dilated cardiomyopathy with left ventricular ejection fraction < or = 30%, we found that spherical distortion of the left ventricle was associated with increased QT dispersion, implying increased heterogeneity of myocardial repolarization.     

高血压病左室肥厚QT离散度与心率变异性分析

目的；探讨高血压病左室肥厚（LVH）与QT离散度（QTd）、心率变异性（HRV）的关系。方法：测量70例高血压非LVH（组Ⅰ）、62例高血压病LVH患者（组Ⅱ）和80例健康人（组Ⅲ）的QTd与校正的QTd（QTcd）及心率变异指数（HRVI），并对各组进行比较分析。结果：组ⅡQTd、QTcd较组Ⅰ、Ⅲ显著延长（均P＜0．01），组ⅠHRVI较组Ⅲ显著减低（P＜0．01），组Ⅱ较组Ⅰ、Ⅲ的HRVI显著减低（均P＜0.01）。结论：高血压病LVH的发生及其易出现各种并发症的原因可能与其QTd、QTcd的延长及HRVI的减低有关。     

Characterization of the non-linear rate-dependency of QT interval in humans.

AIMS: Repolarization has rate-dependent and rate-independent components. A function considering such components separately was validated in canine Purkinje fibres and applied to the QT/RR relation in humans. METHODS AND RESULTS: Action potential duration (APD) was measured in Purkinje fibres during steady-state pacing at different cycle lengths (CL) and after prolonged quiescence (APD(0)). The APD/CL relationship was expressed by this function: APD=APD(max)(*)CL(S)/(CL(50)(S)+CL(S)), where APD(max) (APD extrapolated at infinite CL) is a rate-independent measure of repolarization, CL(50) (CL at which 50% of APD(max) is achieved) and S evaluates the rate dependency of APD. The same function was used to fit the QT/RR relation in 46 normal subjects (20 males, 26 females) and in 7 amiodarone-treated subjects undergoing a bicycle stress test. RR and QT (V(5)) were measured at the end of each load step; QT(c) (Bazett's formula) was obtained at rest. The APD/CL and QT/RR relations were equally well expressed by the function with high correlation coefficients (R>or=0.90). In Purkinje fibres, APD(max) was 461+/-37 ms, CL(50) was 394+/-54 ms and S was 0.98+/-0.11. APD(max) and APD(0) correlated (R=0.96) and were similar. The corresponding values in humans were: QT(max) 432+/-63 ms, RR(50) 345+/-60 ms and S 2.6+/-0.8. While QT(c) and QT(max) were longer in females, RR(50) and S were similar between genders. Amiodarone increased QT(c), QT(max) and RR(50) and decreased S. In QT(max) and QT(c) distributions generated by pooling data from treated and untreated subjects, 86% of treated subjects were correctly identified by QT(max) and 28% by QT(c). CONCLUSIONS: Canine and human repolarization showed a saturating dependency on cycle length, described by the proposed function. Gender and amiodarone independently affected QT(max), RR(50) and S: therefore they might reflect specific ionic mechanisms. Finally, QT(max) identified drug-induced repolarization abnormalities in individual subjects better than QT(c).     

Diagnostic performance of QT interval variables from 24-h electrocardiography in the long QT syndrome

Aims The long QT syndrome is mainly defined by QT interval prolongation(QTc >0·44s). However, data obtained in genotyped patientsshowed that resting QTc measurement alone may be inaccuratefor ascertaining the phenotype. The aim of this study was toevaluate the diagnostic performance of QT interval rate-dependencein untreated chromosome 11-linked patients. Methods The study population consisted of 25 untreated longQT patients linked to chromosome 11 and 25 age- and gender-matchedcontrols. QTc intervals were measured on 12-lead resting ECGrecordings. From 24-h Holter recordings, the slope of the relationshipbetween ventricular repolarization and heart rate was studiedseparately day and night to assess neural modulation. Mean heartrates and rate-dependences of QT and Q-maximum of T (QTm) intervalswere compared between long QT patients and controls for bothtime periods. Results In both groups, the rate-dependences were modulatedby day–night influences. When compared to controls, longQT patients showed a significant increase at night in QT/RRslopes (0·158±0·05 vs 0·117±0·03,P=0·002)and QTm/RR slopes (0·163±0·05 vs 0·116±0·04,P=0·0006).Multivariate analysis, adjusting QTc interval on age and gender,discriminated between long QT patients and controls with a 76%sensitivity and a 84% specificity. A 96% sensitivity and a 96%specificity were reached by taking into account the QTm/RR slopeat night, the QTc interval and the mean heart rate during theday. Conclusion QT interval variables obtained from 24-h ECG recordingsimprove long QT syndrome diagnosis by showing an increased nocturnalventricular repolarization rate-dependence in genotyped chromosome11-linked patients.     

The prognostic value of the QT interval and QT interval dispersion in all-cause and cardiac mortality and morbidity in a population of Danish citizens

Aims. To evaluate the prognostic value of the QT interval and QT intervaldispersion in total and in cardiovascular mortality, as wellas in cardiac morbidity, in a general population. Methods and results. The QT interval was measured in all leads from a standard 12-leadECG in a random sample of 1658 women and 1797 men aged 30–60years. QT interval dispersion was calculated from the maximaldifference between QT intervals in any two leads. All causemortality over 13 years, and cardiovascular mortality as wellas cardiac morbidity over 11 years, were the main outcome parameters.Subjects with a prolonged QT interval (430ms or more) or prolongedQT interval dispersion (80ms or more) were at higher risk ofcardiovascular death and cardiac morbidity than subjects whoseQT interval was less than 360ms, or whose QT interval dispersionwas less than 30ms. Cardiovascular death relative risk ratios,adjusted for age, gender, myocardial infarct, angina pectoris,diabetes mellitus, arterial hypertension, smoking habits, serumcholesterol level, and heart rate were 2·9 for the QTinterval (95% confidence interval 1·1–7·8)and 4·4 for QT interval dispersion (95% confidence interval1·0–19·1). Fatal and non-fatal cardiac morbidityrelative risk ratios were similar, at 2·7 (95% confidenceinterval 1·4–5·5) for the QT interval and2·2 (95% confidence interval 1·1–4·0)for QT interval dispersion. Conclusion. Prolongation of the QT interval and QT interval dispersion independentlyaffected the prognosis of cardiovascular mortality and cardiacfatal and non-fatal morbidity in a general population over 11years.     

高血压左心室肥厚患者心电图QT离散度改变

目的　探讨原发性高血压左心室肥厚患者心电图QT离散度 (简称QTd)变化。　方法　用美国超九 ATL(XO16 3)彩色多谱勒诊断仪二维超声测量其舒张期左心室室间隔厚度和左心室后壁厚度 ,以≥ 1 2cm作为左心室肥厚诊断标准 ,对高血压左心室肥厚组 (n =36 ,男 女 =2 0 16例 ,平均年龄 6 0岁± 12岁 )、高血压左心室非肥厚组(n =5 0 ,男 女 =30 2 0例 ,平均年龄 6 2岁± 12岁 )进行测量 ,再用心电图ECG 8110P( 0 180 8A3)描记其常规 12导联心电图 ,手工测量其最大QT间期 (QTmax)、最小QT间期 (QTmin)和心动周期RR间期 ,计算QTd和心率校正的QTcd ,并随机匹配正常人群组 (n =4 0 ,男 女 =2 4 16例 ,平均年龄 5 8岁± 13岁 )。　结果　高血压左心室肥厚组QTd为6 0ms± 17ms ,QTcd为 6 8ms± 2 4ms,高血压左心室非肥厚组QTd为 4 1ms± 13ms,QTcd为 4 3ms± 17ms ,正常人群组QTd为 4 3ms± 11ms ,QTcd为 4 4ms± 16ms,前两组比较有显著性差异 ,P <0 0 1,后两组比较无显著性差异 ,P >0 0 5。　结论　原发性高血压左心室肥厚患者QT间期离散度增大。