胺碘酮与β受体阻滞剂联合治疗急性顽固性室性心动过速

目的研究大剂量胺碘酮联合β受体阻滞剂治疗急重症顽固性室性心动过速(室速)病人的疗效及安全性.方法8例急重症器质性心脏病病人,左心室射血分数0.346±0.091.急性顽固性室速发作时予胺碘酮静脉负荷量后并静脉及口服维持,6例联合口服β受体阻滞剂,2例严重心功能不全病人联合静脉用艾司洛尔,在严密监测血压、心律下应用,从小剂量开始逐渐增量,稳定后换口服β受体阻滞剂治疗,调整至最大可耐受量即不影响血压亦不加重心力衰竭(心衰)的合适剂量.结果胺碘酮日最大静脉用量1500～2200 mg,艾司洛尔静脉负荷量5～40 mg后3～33 μg/(kg·min)维持.急性顽固性室速予大剂量胺碘酮联合β受体阻滞剂治疗,严重心功能不全者联合静脉用艾司洛尔,可迅速控制顽固性室速且无心衰加重和血压下降.未见严重毒副作用.结论大剂量胺碘酮联合β受体阻滞剂治疗可有效控制伴有心功能不全的顽固性室速.     

大剂量胺碘酮静脉注射在顽固性室性心动过速、心室颤动的临床应用

总结大剂量胺碘酮(Am)静脉注射治疗顽固室性心动过速(VT)和(或)心室颤动(VF)的用药经验.选择52例患者,男34例、女18例,年龄47.0±15.6(21～68)岁.对常规抗心律失常药物治疗无效,静脉注射负荷量Am,以3～5mg/kg稀释后10min内注入,随后以1.0～1.5mg/min泵入维持,若心律失常控制不满意,可每隔30min再注入75～150mg追加负荷量,同时口服Am,静脉用药平均7.5(6～12)天.第1个24hAm静脉用量为1865±272(I592～3120)mg,心律失常控制占56%(29/52),72h心律失常全部控制.1例96h后VT复发,追加Am负荷量后获控制,1例死于心源性休克.结论大剂量静脉注射Am对顽固VT和(或)VF安全有效,用药强调个体化.在用药过程中注意监测血压、心率、节律变化.预防心律失常复发需长期口服Am.     

胺碘酮治疗心室颤动和持续性室性心动过速临床观察

目的 观察胺碘酮(可达龙)静脉注射加口服治疗持续性室性心动过速、室颤的临床疗效.方法 对发生持续性室性心动过速(VT)、心室颤动(VF)的器质性心脏病患者38例除颤的同时静脉注射可达龙150 mg～300 mg,10 min静脉推注完毕(VT150 mg、VF300 mg)后继以1 mg/min泵入6 h,后18 h泵入0.5 mg/min,24 h静脉用量≤1 200 mg.结果 静脉平均用药2 d～4 d(3.9 d±1.8 d)第1天静脉用量900 mg～1 200 mg(1150mg±180mg),心律失常控制率24 h为27.7%,48 h为50%,72 h为22.3%.总病死率22.2%.结论 静脉注射加口服应用可达龙对持续性VT、VF控制安全、有效,但不能减少病人病死率.     

胺碘酮与β-受体阻滞剂联合治疗急性室性心动过速

目的观察胺碘酮与β-受体阻滞剂联合治疗急性室性心动过速的疗效及安全性。方法20例病人均在急性室性心动过速发作时采用胺碘酮负荷量后并静脉及口服维持,其中12例病人心律失常控制不满意时联合β-受体阻滞剂口服,调整β-受体阻滞剂至最大可耐受量,既不影响血压也不加重心力衰竭的合适剂量。结果胺碘酮最大量(1500±1800)mg,口服美托洛尔(倍他乐克)12.5mg~50.0mg,每日2次,可迅速控制室性心动过速而且无心力衰竭加重和血压下降。未见严重毒副反应。结论胺碘酮与β-受体阻滞剂联合治疗可有效控制伴或不伴有心功能不全的室性心动过速。     

胺碘酮联合应用β受体阻滞剂治疗顽固性室性心动过速2例

例 1　男 ,66岁。因心悸、胸闷就诊 ,外院心电图示室性心动过速 (室速 ) 1 60～ 1 80次 /ｍｉｎ ,经静脉应用利多卡因、普罗帕酮 ,心内程序电刺激及多次电复律均不能终止 ,伴血压下降而转入我院。临床诊断为陈旧性心肌梗死。体检 :血压 85 / 60ｍｍＨｇ( 1ｍｍＨｇ =0 .1 33ｋＰａ) ,双肺有湿口罗音 ,四肢凉。心电图示室速 1 5 0～ 1 60次 /ｍｉｎ ,超声心动图示左室射血分数 (ＬＶＥＦ) 2 0 %。予多巴胺维持血压 ,同时予胺碘酮 (ＳａｎｏｆｉＷｉｎｔｈｒｏｐＩｎｄｕｓｔｒｉｅ生产 ,杭州赛诺菲民生制药有限公司分装 ,商品名 :可达龙 ) 1 …     

胺碘酮并美托洛尔治疗顽固性室性心动过速的疗效及安全性

目的:观察胺碘酮联合β受体阻滞剂治疗顽固性室性心律失常的临床疗效及其安全性。方法:自2003年1月至2006年6月共观察治疗顽固性室速病人9例,其中冠心病急性心肌梗塞(AMI)4例,陈旧性心肌梗塞(OMI)3例,肥厚性心肌病1例,心肌炎1例。心功能(NYHA)Ⅱ、Ⅲ、Ⅳ级分别为3、5、1例。左室射血分数平均(0.35±0.72),在其他抗心律失常药无效情况下,应用胺碘酮150mg,静推,然后静点维持(1000～3000μg/min),室速控制或减少后,同时口服胺碘酮,如后室速仍未能快速有效控制,开始使用β受体阻滞剂,先静脉推注美托洛尔注射液5mg(稀释),每5～10min重复1次,共2～3次,然后口服美托洛尔12.5～25mg/次,2次/d,逐渐加至最大耐受量。结果:本组所有顽固性室速病人大剂量胺碘酮治疗后,室率均明显下降,2例血压下降者经同时配合小剂量多巴胺静点后维持正常。联合β受体阻滞剂后病人顽固性室速均得以控制。1例效果不佳者,行ICD(自动除颤起搏器)治疗。以口服胺碘酮和美托洛尔维持治疗后半年至2年未再有室速发作。死亡2例,死因为顽固性心衰1例,猝死1例。结论:胺碘酮联合β受体阻滞剂能安全、快速而有效控制顽固室速。     

胺碘酮联合美托洛尔治疗恶性室性心律失常疗效观察

2001年1月～2005年6月，我们应用胺碘酮和美托洛尔治疗恶性室性心律失常，疗效较好。现报告如下。     

胺碘酮联合美托洛尔治疗恶性室性心律失常疗效观察

将93例恶性室性心律失常合并严重血流动力学障碍患者随机分成两组．观察组给予胺碘酮及美托洛尔治疗,对照组给予利多卡因治疗。无效者改用胺碘酮治疗。观察组转复成功率为82．61％,维持率88.67％．总有效率77．78％,均明显高于对照组（61．11％、60．00％、54．50％）．且部分无效病例使用胺碘酮有效。     

胺碘酮联合美托洛尔治疗充血性心力衰竭合并室性心律失常疗效观察

目的观察胺碘酮联合美托洛尔治疗充血性心力衰竭合并室性心律失常的疗效及安全性。方法82例充血性心力衰竭合并室性心律失常患者,随机分治疗组42例和对照组40例;所有病例均给予基础治疗和常规抗心力衰竭治疗。对照组单用胺碘酮,第1周200mgTid,第2周200mgBid,第3周起维持量200mgQd。治疗组同时加用美托洛尔,从6.25mgBid起始,每周递增单次剂量6.25mg,目标剂量为25mgBid。结果治疗组12周有效率达95.24%,对照组80.00%(P0.05)。射血分数均有上升(P0.05),治疗组更显著,组间差异显著(P0.05)。QTc均有延长(P0.05),组间差异不显著(P0.05);QTcd均减少(P0.05),组间差异不显著(P0.05)。心功能改善率,治疗组88.10%,对照组75.00%,两组差异显著(P0.05)。结论胺碘酮联合洛美托洛尔治疗充血性心力衰竭合并室性心律失常疗效确切,不良反应较少。     

胺碘酮治疗顽固性室性心律失常临床分析

目的进一步了解顽固性持续性室性心律失常的易致因素及用胺碘酮治疗的效果和安全性。方法38例顽固性室性心律失常患者，首次静脉注入胺碘酮3～5mg／kg，随后以1．0～1．5mg／min维持24h，可同时口服胺碘酮600～1200mg／d，观察疗效。结果总有效率为89．5％，4例无效，未见严重致心律失常作用，心功能不全无加重。结论室壁瘤合并严重心功能不全是顽固性室速的主要原因，大剂量胺碘酮治疗顽固性持续性室性心律失常、有效。     

Intravenous amiodarone for short-term treatment of refractory ventricular tachycardia or fibrillation

Intravenous amiodarone was administered to 22 patients with recurrent ventricular tachycardia failing an average of 3.0 prior antiarrhythmic agents after a mean of 14.6 cardioversions per patient. Patients received a mean bolus of 239 mg amiodarone, and a constant infusion of 0.5 to 1.0 mg/ml was administered over a mean of 50.7 hours. Hypotension requiring pressor agents was seen in nine patients and temporary pacing was needed in five patients. In the hospital, arrhythmic deaths occurred in two (9%) patients and nonarrhythmic deaths occurred in six (27%) patients. There were three late sudden deaths and three additional patients with appropriate automatic defibrillator discharges in follow-up. Intravenous amiodarone is very effective in preventing arrhythmic deaths in patients with refractory ventricular tachycardia and fibrillation.     

硫酸镁协同胺碘酮转复室性心动过速的疗效分析

目的:分析硫酸镁协同胺碘酮转复室性心动过速的疗效。方法: 回顾性分析ICU中136例室性心动过速患者,按是否联用硫酸镁将患者分成联合用药组（n=72）和对照组（n=64）,分析硫酸镁协同胺碘酮的复律效果。结果: 两组患者基本情况、电转复能量、胺碘酮的负荷量及28 d病死率等比较均无统计学差别;联合用药组电转复次数［(1.4±0.9)次 vs.(3.0±2.2)次,P<0.01］和胺碘酮维持总剂量［(0.9±0.6) g vs.(2.3±1.2) g,P<0.01］显著低于对照组, 30 min转复率（33% vs. 9%,P<0.01）、24 h转复率（97% vs. 78%,P<0.01）及72 h维持成功率（97% vs. 84%,P<0.01）均显著高于对照组;联合用药组2h转复率高于对照组（81% vs. 62%,P<0.05）,住ICU时间短于对照组［(7.4±3.9) d vs.(9.1±5.2) d,P<0.05）。结论: 硫酸镁联合胺碘酮转复室性心动过速的疗效优于单用胺碘酮。     

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.     

Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation.

The clinical efficacy of intravenous amiodarone in terminating sustained ventricular tachycardia and in preventing recurrences of ventricular tachycardia and ventricular fibrillation was evaluated in 26 patients. All of them presented with organic heart disease accompanied by depressed left ventricular function. Intravenous amiodarone terminated spontaneous ventricular tachycardia in eight of 19 patients. Fifteen of the 26 patients had had at least one episode of ventricular tachycardia or ventricular fibrillation each day in the period immediately before the intravenous administration of amiodarone. Amiodarone controlled ventricular tachycardia or ventricular fibrillation in nine of these 15 patients; in three further cases it was successful when supplemented by additional administration of a previously ineffective antiarrhythmic drug and ventricular pacing. Two patients died despite these measures. In one, the amiodarone infusion had to be stopped because of an arrhythmogenic effect. Sustained deterioration of haemodynamic function or of pre-existing intraventricular conduction disturbances was never seen. Intravenous amiodarone was effective in terminating sustained ventricular tachycardia and in preventing frequent episodes of ventricular arrhythmia that were refractory to other antiarrhythmic drugs.     

Chronic effects of amiodarone in patients with refractory ventricular tachycardia

We examined the chronic electrophysiologic, systemic, and pharmacologic effects of chronic oral amiodarone therapy in 24 patients with refractory ventricular tachycardia and organic heart disease. Chronic amiodarone therapy resulted in significant increases in R-R interval (from 798 +/- 182 msec to 912 +/- 100 msec; P less than 0.01), P-R interval (from 205 +/- 66 msec to 221 +/- 87 msec; P less than 0.02), QRS duration (from 103 +/- 24 msec to 115 +/- 28 msec; P less than 0.001), and Q-Tc interval (from 413 +/- 48 msec to 470 +/- 46 msec; P less than 0.001). Significant increases were also noted in P-A interval (from 36 +/- 14 msec to 45 +/- 13 msec; P less than 0.05), A-H interval (from 119 +/- 61 msec to 141 +/- 87 msec; P less than 0.02), and H-V interval (from 52 +/- 12 msec to 64 +/- 11 msec; P less than 0.001). Electrophysiologic parameters showing changes included corrected sinus node recovery time (from 271 +/- 140 msec to 425 +/- 122 msec; P less than 0.01), the effective refractory period of the atrium (from 263 +/- 32 msec to 321 +/- 47 msec; P less than 0.01), the effective refractory period of the atrioventricular node (from 348 +/- 109 msec to 478 +/- 157 msec; P less than 0.001), the effective refractory period of the ventricle (from 253 +/- 21 msec to 291 +/- 28 msec; P less than 0.001), the atrial pacing cycle length producing A-V nodal Wenckebach (from 436 +/- 109 msec to 531 +/- 95 msec; P less than 0.001), and the functional refractory period of the A-V node (from 422 +/- 68 msec to 499 +/- 95 msec; P less than 0.001). Programmed electrical stimulation performed after 21-88 (mean 31) days of treatment was highly predictive of long-term results if suppression of arrhythmia induction was demonstrated (12 patients) or if the spontaneous arrhythmia was reinduced (5 patients). Induction of morphologically new ventricular tachyarrhythmias was frequent (42%) but had a low spontaneous recurrence rate (10%) during follow-up. Systemic parameters on chronic amiodarone therapy showed significant increases in total T4 and reverse T3, with no change in pulmonary function tests or left ventricular ejection fraction. Serum amiodarone levels at chronic electrophysiologic study ranged from 0.44-4.10 (mean 1.3) micrograms/ml. Long-term follow-up (2.5 to 20 months) demonstrated a marked improvement in clinical symptoms and mortality, but a significant recurrence rate of a well-tolerated slower arrhythmia persisted. Adverse effects on chronic amiodarone therapy were frequent (10 patients) and often disabling but required drug discontinuation in only 1 patient.     

Clinical efficacy and electropharmacology of continuous intravenous amiodarone infusion and chronic oral amiodarone in refractory ventricular tachycardia

The clinical efficacy and electropharmacologic effects of continuous intravenous (i.v.) amiodarone infusion (10 to 20 mg/kg/day for 4 to 7 days) followed by chronic oral amiodarone therapy (400 to 800 mg/day for 24 to 53 days) were evaluated in 17 patients with refractory sustained ventricular tachycardia (VT) or ventricular fibrillation. Intravenous amiodarone infusion prolonged the RR interval (from 754 +/- 85 to 860 +/- 157 ms, p less than 0.05), PR interval (from 192 +/- 53 to 212 +/- 54 ms, p less than 0.01) QRS duration (from 103 +/- 21 to 117 +/- 25 ms, p less than 0.001) and QTc interval (from 423 +/- 22 to 466 +/- 31 ms, p less than 0.001). Chronic oral amiodarone treatment had similar but more pronounced effects on electrocardiographic intervals. The ventricular effective refractory period tended to prolong after i.v. amiodarone infusion (p less than 0.1 to greater than 0.05) but prolonged significantly after chronic oral amiodarone (p = 0.025). Mean serum amiodarone concentration was 1.7 +/- 1.0 mg/liter with infusion and 1.5 +/- 0.6 mg/liter with oral therapy. Intravenous amiodarone infusion suppressed spontaneous VT in 5 of 9 patients with frequent VT recurrences, but had no effect on cycle length of spontaneous VT. Chronic amiodarone therapy either suppressed spontaneous VT recurrences or prolonged cycle length during VT recurrences. VT induction after i.v. amiodarone was not predictive of VT induction or spontaneous VT recurrences after chronic oral amiodarone treatment. Thus, i.v. amiodarone has limited value in acute control of VT and clinical or electrophysiologic response to it is not predictive of long term therapeutic results with amiodarone.     

Management of refractory sustained ventricular tachycardia with amiodarone: a reappraisal

We examined the value of clinical variables, chronic 24-hour ambulatory ECG monitoring, and chronic electrophysiologic (EP) testing in 49 patients with recurrent and refractory sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) treated with chronic oral amiodarone in order to develop a prospective approach to the management of these patients. All patients underwent control EP studies followed by continuous telemetric cardiac monitoring during oral amiodarone administration (mean duration 29 +/- 6 days, mean dose 739 +/- 230 mg). Follow-up 24-hour ambulatory ECG monitoring and EP studies were performed. Thirty VT recurrences occurred in the first 4 weeks of amiodarone therapy (total incidence, 61%), with the majority (55%) in the first 3 weeks of treatment. During long-term follow-up (1 to 42, mean 15 +/- 12 months), there were 12 symptomatic VT/VF recurrences (incidence 24%). There was a higher incidence of VT recurrences if patients had inducible sustained or nonsustained VT at chronic EP study (p less than 0.01), or complex ventricular arrhythmias on ambulatory ECG monitoring (p less than 0.05). The sensitivity, specificity, and predictive accuracy of chronic EP testing and 24-hour ambulatory ECG monitoring were 100%, 35%, and 51%, and 58%, 84%, and 78%, respectively. Chronic EP testing correctly identified all patients who had their arrhythmia suppressed by amiodarone on long-term follow-up, while 42% of all VT recurrences occurred in patients without complex ventricular arrhythmias on 24-hour ambulatory ECG monitor.(ABSTRACT TRUNCATED AT 250 WORDS)     

胺碘酮联合艾司洛尔静脉注射治疗室性心动过速的临床疗效研究

目的探讨胺碘酮联合艾司洛尔静脉注射治疗室性心动过速的临床疗效。方法选择2016年10月～2017年10月我院心血管内科收治的室性心动过速患者77例,按照住院号单双号法分为对照组39例和观察组38例。对照组给予胺碘酮治疗,观察组给予胺碘酮联合艾司洛尔治疗。比较2组患者治疗前后的心率、收缩压、舒张压等指标变化情况,评估2组临床疗效,并观察2组不良反应发生情况。结果与治疗前比较,2组治疗后心率、收缩压及舒张压明显降低,差异有统计学意义(P 0. 05)。且观察组治疗后心率[(71±14)次/min vs (101±16)次/min]、收缩压[(110±17) mm Hg(1 mm Hg=0. 133 k Pa) vs (139±12) mm Hg]及舒张压[(72±12) mm Hg vs (88±11) mm Hg]明显低于对照组,差异有统计学意义(P 0. 05)。观察组治疗后总有效率明显高于对照组,差异有统计学意义(97. 37%vs 76. 92%,P 0. 05)。对照组与观察组不良反应发生率比较,差异无统计学意义(P 0. 05)。结论室性心动过速采用胺碘酮联合艾司洛尔静脉注射治疗,疗效显著,能够显著改善患者心率、收缩压、舒张压指标,且不良反应少,安全性高。     

Long-term clinical outcome of ventricular tachycardia or fibrillation treated with amiodarone

The determinants of long-term clinical outcome were studied in 42 patients with recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) who were treated with amiodarone as the sole antiarrhythmic agent. Of the 42 patients, 11 (26%) either died suddenly or had recurrent, symptomatic, sustained VT during a mean follow-up period of 10 months (range 0.3 to 45). Of the 19 patients without inducible VT/VF during electrophysiologic study while receiving amiodarone, 1 patient died suddenly but no patient had recurrent VT/VF. Ten of the 23 patients (43%) with persistently inducible arrhythmia have died suddenly or have had recurrent VT/VF. Using survival and stepwise logistic regression analyses, 2 significant independent predictors of recurrent arrhythmia were identified; persistently inducible VT during electrophysiologic testing in patients receiving amiodarone therapy (p < 0.002) and the left ventricular ejection fraction at rest (p < 0.05). The predictive accuracy of the response to serial electrophysiologic testing during amiodarone therapy was 67%, the sensitivity was 58% and the specificity was 91%. Thus, serial electrophysiologic testing is useful for determining the prognosis in patients with inducible VT/VF treated with amiodarone.