静脉胺碘酮转复左室特发性室性心动过速的疗效观察

14例左室特发性室性心动过速(ILVT)患者静脉注射胺碘酮,首剂3~5mg/kg,若未能转复,可于30min后再追加负荷量150mg,20min内注入,继之以0.75~1.5mg/min静脉泵维持。结果:8例第1次负荷量后即刻转复。4例在追加1次负荷量后成功转复。2例反复发作者经静脉泵滴注后2h内均能转复。结论:静脉胺碘酮转复ILVT安全有效。     

心律平和胺碘酮治疗室性心动过速1例

患者秦某,女,50岁,因劳累后心慌气短、胸闷,反复发作2年,在省级医院确诊为心脏病,频发室性早搏,随住院治疗.出院后停服抗心律失常药物,病情平稳.2004年3月20日晚9时突然意识丧失,大小便失禁,口吐白沫,面色发绀,急来我院就诊,测血压为零,脉搏消失,双肺痰鸣音,心音微弱,心率150/min,律不齐,腹软,肝肋下未触及,双下肢无浮肿,心电图示室性心动过速,立即给予吸氧、吸痰,静脉输注2%利多卡因100 mg,连续3次无效,改为心律平150 mg静脉推注效果不佳,换用胺碘酮0.4加10%葡萄糖150 mL静脉输注,15 min后,病人意识转清,呼吸平稳,心电图显示窦性心律,心律80/min,律齐,血压恢复为90/60 mmHg,病情平稳,直至第二天上午8时左右,再次出现晕厥,室性心动过速,心律平150 mg、胺磺酮0.4静脉输注,约10 min后,上述症状消失,窦性心律,心率70/min,律齐,后持续口服心律平50 mg,每天3次,胺碘酮0.2,每天1次,维持治疗.     

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。     

大剂量胺碘酮对持续性室性心动过速的纠治

目的 :观察大剂量胺碘酮治疗持续性室性心动过速 ( SVT)的临床疗效及副作用。方法 :初始以胺碘酮 15 0 m g静脉注射 (静注 ) ,5～ 10 min注射完毕 ,必要时重复 1～ 2个初始量 ,继以 0 .5～ 5 m g/ min静脉维持 3～ 8d。结果 :6例 SVT均在静脉用药 2 h内得到控制 ,2 h内静脉胺碘酮用量 3 90～ 5 4 0 ( 4 68.4± 5 4 .7) m g;2 4 h内静脉平均用量 10 0 0～ 180 0 ( 14 10 .3± 3 5 6.5 ) m g,除注射局部均发生不同程度的静脉炎外 ,未见低血压、心功能恶化及致心律失常作用。结论 :短期内经静脉大剂量应用胺碘酮安全有效     

再负荷胺碘酮治疗复发性、持续性室性心动过速的临床疗效及安全性观察

目的评价再负荷胺碘酮治疗复发性、持续性室性心动过速的临床疗效及安全性。 方法12例初次负荷量胺碘酮治疗后正在口服维持量或停药不超过3个月的复发性、持续性室性心动过速(VT)和(或)心室颤动(VF)患者,男11例,女1例,平均60.75±4.58岁。分别给予静脉并口服胺碘酮(10例),单用口服胺碘酮800mg/d(2例)再负荷治疗。 结果12例复发性持续性VT和(或)VF均得到有效控制,未见明显副作用。再负荷胺碘酮治疗获满意疗效所需剂量约为初次负荷剂量的60%。 结论再负荷胺碘酮治疗复发性、持续性VT有良好的临床疗效及安全性。     

过量口服胺碘酮致尖端扭转型室性心动过速1例

1　临床资料患者女性 ,6 7岁 ,农民 ,因反复头昏近三个月 ,伴胸闷、气促一月 ,晕厥二次于 2 0 0 0年 1月 2 7日转诊我院。既往高血压病史多年 ,未服用利尿剂。入院前因“心律失常 (频发室性期前收缩 )”在外院就诊 ,口服胺碘酮片 2 0 0 mg每日三次 ,连续服用至第 35天 ,在家休息时无明显诱因突发晕厥二次。急诊入院时一般情况尚可 ,神清 ,血压 12 0 / 80 mm Hg,心界不大 ,心率 5 3次 / min,律不齐 ,各瓣膜区未闻杂音 ,肺无罗音 ,腹部及神经系统未发现异常。实验室检查血钾 4 .0 mmol/ L ,血镁 0 .9m mol/ L,心肌酶未见异常 ;超声心动图示…     

胺碘酮治疗充血性心力衰竭并发室性心动过速50例疗效观察

充血性心力衰竭(CHF)是临床常见危重病症,一旦并发室性心动过速(VT),可加重心肌损害,明显增加病死率。1996年9月至2003年1月,我们采用胺碘酮治疗CHF合并VT患者50例。现报告如下。     

静脉应用胺碘酮治疗充血性心力衰竭并发的室性心动过速

目的　观察静脉注射胺碘酮治疗充血性心力衰竭并发的室性心动过速的有效性及安全性。方法　对 5 1例充血性心力衰竭并发持续性室性心动过速的患者首剂给予胺碘酮突击量 3～ 5mg/kg ,15min无效再重复突击量。维持量为 6 0 0mg胺碘酮稀释于 5 0 0ml生理盐水中静脉点滴 2 4h。结果　本组 0 5h内平均负荷量 (2 71 5± 82 8)mg ,第 1个 2 4h胺碘酮静脉用量平均 (916 5± 15 3 4)mg。总有效率 88 2 % ,不良反应发生率 15 9% ,无心功能恶化。结论　静脉注射胺碘酮治疗充血性心力衰竭并发的室性心动过速有效 ,也较安全     

胺碘酮治疗心房颤动心律转复后维持窦性心律疗效观察

心房颤动 (房颤 )是临床上一种常见病 ,发作时多伴明显心悸症状和血流动力学改变 ,持续时间过长还可形成心房内附壁血栓 [1] ,故应积极治疗。持续性房颤可由阵发性房颤 ( PAF)发展而来 ,PAF患者心律转复后如何安全、长期、有效地维持窦性心律 ,是临床上广泛关注的问题。而某些传统治疗心律失常药物如洋地黄类 ,维拉帕米等 ,对预防房颤复发无效 ,奎尼丁可能增加死亡风险 ,而胺碘酮可能是安全有效药物[2 ] 。因此 ,本文对 3 1例具有明显症状的 PAF口服小剂量胺碘酮心律转复后维持窦性心律患者进行临床疗效观察 ,现报告于下。1　资料与方法…     

胺碘酮治疗冠心病持续性室性心动过速的临床观察

分析胺碘酮在控制冠心病并发持续性室性心动过速(简称室速)的临床特点。选择冠心病合并持续性室速患者30例,年龄59.78±10.2岁,给与静脉和口服胺碘酮负荷量后计算室速控制率;分析胺碘酮总负荷量与患者的左室舒张期末径(LVEDV)、左室射血分数(LVEF)、有无室壁瘤的关系;观察血药浓度、用药前后(包括合并用药)心率、血压、QTc等的变化及副作用。结果:①胺碘酮对冠心病持续性室速的控制率为90%;②胺碘酮总负荷量14.81±8.89(4.14～48.79)g,静脉负荷时间158±155.79(26～648)h;③胺碘酮负荷用量与LVEF和有无室壁瘤相关,与LVEDV无关;④胺碘酮的有效血药浓度个体差异性大;⑤在治疗期间总副作用发生率16.67%。结论:胺碘酮控制冠心病室速安全有效,胺碘酮负荷总量及有效血药浓度个体差异性大。     

胺碘酮与美托洛尔联合治疗在室性心动过速/心室颤动中的临床应用

对于顽固性室性心律失常，尤其是对于交感神经张力明显增高的患者，如单用胺碘酮无效，适量加用静脉或口服β受体阻滞剂有时可显奇效。因为高交感神经张力除了使室性心律失常不易终止和易复发外，还可削弱胺碘酮的延迟复极作用，在应用β受体阻滞剂后胺碘酮的药理作用方能充分发挥，且可与β受体阻滞剂对多种离子通道的阻滞作用相互增强。但在临床应用中，一定要结合患者的不同病理生理状态进行个体化给药，同时密切监测患者的心率、血压变化，做好临时起搏等抢救准备。要有全局观念，切忌只对心律失常、不对病人的教条化治疗。     

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.     

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.     

Efficacy and tolerance of high-dose intravenous amiodarone for recurrent, refractory ventricular tachycardia

High-dose intravenous amiodarone was given to 35 patients with recurrent life-threatening ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents. Intravenous amiodarone was given as a 5 mg/kg dose over 30 minutes followed by 20 to 30 mg/kg/day as a constant infusion for 5 days. Twenty-two (63%) patients responded to intravenous amiodarone. All 22 responders received oral amiodarone. Thirteen (59%) continue to receive oral amiodarone after an average follow-up of 19 months, 4 (18%) had sudden cardiac death on oral amiodarone, 2 (9%) died while receiving amiodarone, secondary to left ventricular failure, and 3 (14%) discontinued amiodarone because of side effects. Of the 13 (37%) nonresponders, 10 died in the hospital while receiving intravenous amiodarone, secondary to lethal arrhythmia. Three nonresponders were discharged from the hospital; 2 with automatic cardioverter/defibrillators and 1 receiving a combination of antiarrhythmic agents. Serious adverse events occurred in 13 (37%) patients during intravenous amiodarone therapy. These included hypotension in 8 patients, symptomatic bradycardia in 4 patients and sinus arrest with bradycardia and hypotension in 1 patient. Minor side effects occurred in 23 (66%) patients. In conclusion, high dose intravenous amiodarone is effective in most patients with recurrent, sustained VT but is associated with an unacceptably high incidence of serious adverse events. The optimal dose and duration of intravenous amiodarone for patients with recurrent, refractory sustained VT remain unknown.     

Efficacy of the combination of low doses of beta-blockers and amiodarone in the treatment of refractory ventricular tachycardia

Thirty one patients aged 56 +/- 16 years with chronic ventricular tachycardias (VT) refractory to 4.4 +/- 1.8 antiarrhythmic drugs, used alone or in combination, were managed by low doses of beta-blocker agents combined with oral amiodarone, either after loading (1.2 g for 7 days, n : 7) or reloading (1.2 g for 4 days, n : 24) of amiodarone. All patients proved refractory to amiodarone alone. Nine VT were also refractory to endocardial catheter fulguration in 8 patients. Twenty one patients had coronary artery disease, 4 had arrhythmogenic right ventricular dysplasia, 4 had dilated cardiomyopathy, 1 had valvular disease, and 1 had no structural heart disease. Twelve patients had an ejection fraction less than 30 p. 100. Ten patients were in NYHA functional class 3. VT was permanent in 3 patients, daily in 5, weekly in 7, paroxysmal in 16. In 14 patients, VT occurred both at day and night. Oral administration of a daily low dose of a beta-blocker agent (acebutolol 100 mg, betaxolol 5-10 mg, metoprolol 50-100 mg, nadolol 20-40 mg, pindolol 2.5 mg, propranolol 30 mg, sotalol 80-160 mg, tertatolol 2.5 mg) combined with 400 mg per day of amiodarone suppressed VT episodes in all patients. None presented heart failure or collapse. The mean reduction of the heart rate was about 17 p. 100. One patient need a definite pacemaker to correct sinus bradycardia. At discharge, exercise ECG (n: 20) induced non sustained VT in 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

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.     

Successful treatment of stress-induced therapy refractory ventricular tachycardia with verapamil

A 51-year-old woman was admitted to the hospital for further elucidation of a syncope of unknown origin and exercise-induced tachycardias with broad QRS-complex. The tachycardia was induced by bicycle exercise stress testing, had a frequency of 165/min, showed an inferior axis and left bundle branch block. Organic heart disease was excluded by right and left heart catheterization and selective coronary angiography. A nodoventricular bundle or an atrio-ventricular bundle was excluded by an extensive electrophysiologic study, therefore the documented tachycardia was probably of ventricular origin. However, it was not possible to induce a ventricular tachycardia by programmed ventricular stimulation with up to three extrastimuli even after the infusion of isoprenaline. Sotalol (2 x 160 mg/die) and the combined treatment with mexiletine (2 x 360 mg/die) and disopyramide (2 x 250 mg/die) did not prevent the induction of the tachycardia by exercise testing. The combination of sotalol and flecainide (2 x 100 mg/die) evoked complex ventricular arrhythmias at rest not noted before, and it was therefore withdrawn as well. After all antiarrhythmic drugs were withdrawn verapamil was given in a dose of 3 x 120 mg and this therapy reproduceably prevented the induction of ventricular tachycardia by exercise testing.