胺碘酮治疗急性心肌梗死后室性心动过速的临床观察

观察静脉注射胺碘酮对急性心肌梗死 (AMI)后持续性室性心动过速 (VT)的临床疗效及安全性。持续心电监护下证实的经利多卡因治疗无效的AMI后VT患者 16例 ,按常规方法静脉应用胺碘酮 ,72h内VT控制率累计达 93 .8%,未见明显副作用发生。结论 :静脉应用胺碘酮治疗AMI后早期VT安全、有效     

静脉胺碘酮治疗老年充血性心力衰竭并室性快速性心律失常

目的研究胺碘酮静脉应用治疗老年充血性心力衰竭患者并发的室性快速性心律失常疗效及安全性。方法对32例老年充血性心力衰竭并发的室性心动过速(VT)和(或)心室颤动(VF),首剂给予胺碘酮3~5mg/kg,10min内缓慢注入,15~30min若无效,再重复突击量1.5~3mg/kg,随后以1.0~1.5mg/min静脉滴注维持,依病情逐渐减量,静脉应用同时加用口服胺碘酮600mg/天。结果第1个24小时胺碘酮静脉平均用量为1690±499.4mg,维持静脉点滴平均4.3±1.7天,总有效率87.5%,静脉应用早期对PR、QRS、QTc间期均无影响。不良反应15.6%,用药期间无因胺碘酮导致或加重的心功能不全。结论大剂量胺碘酮静脉治疗老年心力衰竭并发的室性快速性心律失常安全、有效。     

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.     

充血性心力衰竭并有室性心律失常应用胺碘酮的经验

目的总结充血性心力衰竭(CHF)并有快速室性心律失常患者应用胺腆酮的疗效及安全性.方法26例有器质性心脏病,心功能(NYHA)Ⅱ～Ⅲ级,左心室射血分数(LVEF)0.24±0.07,伴有室性心动过速(VT)和(或)心室颤动(VF)的患者.应用静脉注射胺碘酮首剂3～5 mg/kg,稀释后10分内注入,继以0.75～1.00rmg/min维持注射,必要时可每隔30分追加胺碘酮75～150 mg,同时口服胺碘酮每日600～800mg.并逐步减至每日200mg维持.出院后随诊观察.结果第1个24小时,18/26例心律失常获控制占69%,静脉注射胺碘酮1248.0±135.4mg(1156～2184mg),56小时心律失常全部被控制,血液动力学稳定.患者心功能改善至LVEF 0.33±0.09.结论静脉注射胺碘酮治疗CHF伴VT和(或)VF安全有效,用药强调个体化,预防心律失常发作需长期口服胺碘酮.     

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。     

恶性室性心律失常的胺碘酮治疗

观察静脉与口服联合应用胺碘酮对恶性室性心律失常的作用。31例室性心动过速 (VT)和 /或心室颤动 (VF)患者 (男 21例,女 12例,年龄 48±14. 6岁),首剂静脉注射胺碘酮 150 ~300mg, 10min注入。继之以 0. 5~1. 0mg/min维持静脉泵入。静脉维持用药24~48h后给予口服胺碘酮 600mg/d,逐渐减量至 200mg/d维持。观察静脉用药期间的心率,QT间期,VT、VF的发作情况。结果: 22例于用药后 24h获得控制, 6例于 48h后获控制, 3例于 72h后获得控制。静脉用药期间,未见QT间期明显延长。结论:静脉用胺碘酮治疗恶性室性心律失常安全有效。静脉与口服联合给药起效快,可达到早期抢救生命的目的,又可稳定血药浓度,防止心律失常的复发。     

大剂量乙胺碘呋酮口服快速抑制复杂的室性心律失常

乙胺碘呋酮治疗室性心律失常的主要问题是产生疗效需时较长,用传统的治疗方法平均要9.5天。本文旨在探索口服大剂量乙胺碘呋酮快速抑制复杂的室性心律失常的有效性和安全性。18例研究对象中8例是难治的反复持续发作的室性心动过速(VT)或需要除颤和短期药物治疗者,并     

胺碘酮与利多卡因用于无脉性VF、VT院前急救效果比较

2005～2007年,我们分别将胺碘酮与利多卡因用于100例无脉性室性心动过速（VT）或心室纤颤（VF）患者的急救,发现胺碘酮在预防再次出现的快速室性心律失常方面优于利多卡因。现报告如下。     

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。     

静脉胺碘酮在危及生命的室性心律失常中的应用

介绍静脉应用胺碘酮对危及生命的室性心律失常的临床应用经验。 5 6例合并器质性心脏病的反复发作持续性室性心动过速 (VT) /心室颤动 (VF)患者 ,男 42例、女 14例 ,年龄 49.6± 13.8岁 ,其中冠心病心肌梗死 42例、心肌病13例、先天性心脏病 1例。静脉注射胺碘酮首剂 3～ 5mg/kg,10min注入 ,继之以 1.0～ 1.5mg/min维持静脉点滴 ,以后依病情渐减。静脉应用同时加用口服 6 0 0～ 12 0 0mg/2 4h。第 1次负荷量后 ,若心律失常控制不理想 ,可每隔 15～30min再给 1.5～ 3.0mg/kg的追加负荷量。以VT、VF消失为有效。第 1个 2 4h静脉用量 15 86 .5± 316 .8mg。维持静脉点滴 4.5± 2 .6天。总有效率 85 .7%。对持续性VT终止率 2 6 .9%。静脉用药早期对PR、QTc间期、QRS波时限无影响。静脉用药期间 ,3例出现窦性心动过缓 ,经减量后恢复 ;1例出现一过性Ⅱ度房室阻滞 ;12例出现静脉炎。静脉胺碘酮治疗危及生命的室性心律失常安全有效。 2 4h 10 0 0～ 15 0 0mg为较合适的初始静脉用量。     

Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.     

Development of congestive heart failure and alterations in left ventricular function in patients with sustained ventricular tachyarrhythmias treated with amiodarone

The interaction between the efficacy and tolerance of amiodarone and the degree of left ventricular (LV) dysfunction was assessed in 126 patients with sustained ventricular tachyarrhythmias. In all patients radionuclide angiographic LV ejection fraction (EF) was measured before and after 8 to 12 months of amiodarone therapy. At baseline mean EF was 25 +/- 13% and 86 patients had an EF of 30% or less. In patients receiving amiodarone at steady state, there was a small but significant increase in EF (23 to 26%, p less than 0.05). Congestive heart failure (CHF) was present in 43 patients before amiodarone therapy. In 16 patients new (9 patients) or worsened (7 patients) CHF developed during the first year of amiodarone therapy. Development of CHF was not consistently related to a change in EF or heart rate. The clinical efficacy and tolerance of amiodarone were affected by the baseline EF and development of CHF. Efficacy and tolerance was 80% in patients with an EF of more than 30% and 60% in those with an EF of 30% or less. Among the 16 patients in whom new or worsened CHF developed, 6 (38%) died and 9 (56%) had recurrent ventricular tachyarrhythmias. Both baseline EF and development of CHF during amiodarone treatment significantly affect the prognosis in patients with ventricular tachyarrhythmias.     

Amiodarone therapy in symptomatic,sustained refractory atrial and ventricular tachyarrhythmias

Amiodarone was utilized in 70 patients with symptomatic, sustained refractory tachyarrhythmias. Of these, 29 had atrial arrhythmia (20 recurrent atrial fibrillation and nine sustained supraventricular tachycardia). Control was achieved in eight with supraventricular tachycardia and in 16 with atrial fibrillation. Recurrence has been prevented in these 24 patients (83%) during an average follow-up of 13.4 months. An additional 41 patients had recurrent ventricular tachycardia. In 19 with symptoms consisting of dizziness or lightheadedness without syncope or clinically apparent hemodynamic compromise, treatment was limited to amiodarone. Of these, 14 responded (74%) and have been free of arrhythmia during an average follow-up of 13 months. In 22 who experienced either syncope or life-threatening hemodynamic impairment, amiodarone was added to those agents which had only partially suppressed advanced grades of ventricular premature beats. Fourteen of these patients (64%) have remained free of recurrent ventricular arrhythmia during an average follow-up of 12 months. After drug loading, maintenance therapy consisted of a daily dose ranging from 200 to 600 mg. Only mild side effects have been encountered in the 17 patients (23%) with any untoward responses. This experience confirms that oral amiodarone is an effective and safely applied agent against recurrent refractory atrial tachyarrhythmia and sustained intractable ventricular tachycardia with moderate symptoms. While also efficacious in refractory sustained life-threatening ventricular tachyarrhythmia, usage of the agent is often difficult in this condition owing in part to insufficient information concerning amiodarone pharmacokinetics.     

Usefulness of electrophysiologic testing in evaluation of amiodarone therapy for sustained ventricular tachyarrhythmias associated with coronary heart disease

The prognostic importance of electrophysiologic studies in patients with sustained ventricular tachyarrhythmias treated with amiodarone was prospectively studied in 100 consecutive patients. Sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) was inducible in all patients before amiodarone therapy. After amiodarone administration 2 groups of patients were identified. In group 1 patients the ventricular tachyarrhythmia was no longer inducible and in group 2 patients the arrhythmia remained inducible. In group 1, no recurrent arrhythmia occurred during a follow-up of 18 +/- 10 months. In group 2, 38 of 80 patients (48%) had arrhythmia recurrence during a follow-up of 12 +/- 9 months. The difference between group 1 and 2 could not be explained by clinical variables, amiodarone doses or plasma concentrations, or electrocardiographic variables. In patients in whom cardiovascular collapse or other severe symptoms where noted during electrophysiologic study after amiodarone treatment, recurrences caused sudden death (n = 12). However, in patients in whom the induced arrhythmia produced moderate symptoms, the recurrent arrhythmia was nonfatal VT (n = 26). Electrophysiologic testing provides clinical guidance and predicts prognosis in patients treated with amiodarone as it does for the evaluation of other antiarrhythmic agents.     

Electrophysiologically guided amiodarone therapy versus the implantable cardioverter-defibrillator for sustained ventricular tachyarrhythmias after myocardial infarction: results of long-term follow-up

OBJECTIVES: We sought to compare the long-term survival rates of patients with sustained ventricular tachyarrhythmia after myocardial infarction (MI) who were treated according to the results of electrophysiological (EP) study either with amiodarone or an implantable cardioverter-defibrillator (ICD). BACKGROUND: Patients with sustained ventricular tachyarrhythmias after MI are at high risk of sudden cardiac death (SCD). However, data comparing the long-term survival rates of patients treated with amiodarone or ICD, according to the results of EP testing, are lacking. METHODS: Patients underwent a first EP study at baseline and a second one after a loading dose of amiodarone of 14 +/- 2.9 g. According to the results of the second EP study, patients were classified either as responders or non-responders to amiodarone; non-responders were eventually treated with an ICD. RESULTS: Eighty-four consecutive patients with MI (78 men; 21-77 years old; mean left ventricular (LV) ejection fraction 36 +/- 11%) were consecutively included. Forty-three patients (51%) were responders, and 41 patients (49%) were non-responders to amiodarone therapy. During a mean follow-up period of 63 +/- 30 months, SCD and total mortality rates were significantly higher in the amiodarone-treated patients (p = 0.03 and 0.02, respectively). CONCLUSIONS: The long-term survival of patients with sustained ventricular tachyarrhythmias after MI, with depressed LV function, is significantly better with an ICD than with amiodarone therapy, even when stratified according to the results of the EP study. These patients should benefit from early ICD placement, and any previous amiodarone treatment seems to have no additional value.     

Control of refractory life-threatening ventricular tachyarrhythmias by amiodarone

The antiarrhythmic effects and dose-response relationship of amiodarone hydrochloride, 600 to 1200 mg daily, were studied in 22 patients with recurrent life-threatening symptomatic ventricular tachyarrhythmias refractory to two or more conventional antiarrhythmic agents. In all patients the presence of the arrhythmia was confirmed on ECG and/or 24-hour Holter readings. In 10 one or more episodes of cardiac arrest had been documented by ECG. Two patients died prior to initiation or stabilization of therapy; the goal of therapy was attained in all but one patient. Amiodarone abolished all complex premature ventricular contractions (PVCs) and paroxysmal or sustained episodes of ventricular tachycardia (VT) in all 19 remaining patients; In the 15 in whom predrug and serial 24-hour Holter recordings could be obtained and analyzed, the total PVC counts were reduced 90% to 98% by amiodarone. After a mean follow-up of 12 months on chronic amiodarone therapy, there have been no recurrences of VT or ventricular fibrillation and sustained antiarrhythmic response has been confirmed by Holter recordings. One patient died suddenly at home despite complete suppression of PVCs. Amiodarone prolonged the PR (+16.7%; P < 0.05) and QT_c (+22.7%; P < 0.01) intervals without effect on QRS duration. Side effects attributable to the drug were gastrointestinal discomfort, halo vision, proximal muscle weakness, transient elevations of hepatic enzymes, and skin photosensitivity, all being reversible on reduction in dosage which did not compromise antiarrhythmic efficacy. Amiodarone did not aggravate cardiac failure even in patients with low ventricular ejection fractions. This study indicates that amiodarone is an extremely potent and safe agent for the prophylactic control of life-threatening ventricular tachyarrhythmias.     

Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease.

AIM: To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias. METHODS: Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia. RESULTS: At 36 months. 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0.05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5.9 times higher (P=0.008) than that for patients on sotalol. CONCLUSION: Sotalol is superior to amiodarone for long-term treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly.     

Low dose amiodarone in refractory tachyarrhythmias.

Fifty patients with drug resistant tachyarrhythmias were treated with amiodarone for 6-22 months; 16 for recurrent ventricular tachycardia (VT), 2 for VT followed by ventricular fibrillation (VF), 14 for complex ventricular ectopics, and 18 for supraventricular tachyarrhythmias (SVT). Amiodarone was administered in a dose much lower than that used in western trials. The actual incidence of successful amiodarone therapy was 81.2% at 22 months for patients with VT. Among the patients with SVT, 88.6% patients were successfully treated for 22 months (range 3-22 months). Amiodarone toxicity appeared in 22 of 50 patients (44%) treated for more than 12 weeks. Withdrawal of therapy was required in 4 patients. Despite the lower dose, clinical efficacy and onset of action were comparable to the western experience.     

AMIODARONE THERAPY FOR LIFE THREATENING OR REFRACTORY CARDIAC ARRHYTHMIAS

Amiodarone was used in 40 patients with life-threatening or refractory tachyarrhythmias. Eighteen patients had recurrent ventricular tachycardia of whom 13 had suffered a cardiac arrest. Control has been excellent or good in 17 of these 18 patients during an average follow-up period of 10 months. A further 22 patients had supraventricular arrhythmias, including three with Wolff-Parkinson-White syndrome and paroxysmal atrial fibrillation. In 20 of these control has been excellent or good. The mean daily maintenance dose of amiodarone was 300 mg for patients with ventricular tachyarrhythmias and 200 mg for those with supraventricular tachyarrhythmias. Side-effects were common and included corneal microdeposits, skin rash and discolouration, alteration in thyroid function, and symptomatic bradycardia. Serious adverse effects were uncommon however and necessitated discontinuation of the drug in only two patients. Amiodarone did not appear to precipitate or exacerbate cardiac failure in any patient although many had severe left ventricular dysfunction. We conclude that amiodarone is effective in the therapy of life-threatening or refractory cardiac arrhythmias.     

Radioiodine ablation of the thyroid to prevent recurrence of amiodarone-induced thyrotoxicosis in patients with resistant tachyarrhythmias.

Amiodarone-induced thyrotoxicosis (AIT) is a common complication of amiodarone therapy. Although permanent withdrawal of amiodarone is recommended due notably to the risk of worsening of tachyarrhythmias, some patients may require the reintroduction of amiodarone several months after normalizing their thyroid function. We, retrospectively, assessed the effects of (131)I therapy to prevent recurrence of AIT in euthyroid patients requiring reintroduction of amiodarone. SUBJECTS AND METHODS: Amiodarone was required in 10 cases of recurrent symptomatic paroxysmal atrial fibrillation (AF) and in 5 cases of ventricular tachycardia (VT) (M = 12, F = 3, mean age: 63 +/- 14). The underlying heart disease was dilated cardiomyopathy (n = 4), ischaemic heart disease (n = 4), hypertensive heart disease (n = 2), arrhythmogenic right ventricular dysplasia (n = 27) and valvulopathy (n = 1). Two patients had idiopathic paroxysmal AF. RESULTS: A mean (131)I dose of 579 +/- 183 MBq was administered 34 +/- 37 after the episode of AIT. Amiodarone was reintroduced in 14 of 15 patients after a mean interval of 103 +/- 261 d. Fourteen patients developed definite hypothyroidism necessitating l-thyroxine but we observed no late recurrence of AIT. After a mean follow-up of 22 +/- 16 months, tachyarrhythmias were controlled in 12 of 14 patients. CONCLUSION: (131)I therapy appears to be an effective and safe approach to prevent the recurrence of AIT in a patient requiring the reintroduction of amiodarone for tachyarrhythmias.