48例室性心动过速的治疗体会

目的：探讨室性心动过速（室速）的治疗方法与疗效。方法经心电图诊断为室性心动过速48例患者给予病因治疗和抗心律失常药物治疗并进行效果分析。结果48例室性心动过速的治疗，治疗有效率为83.33%以上。结论对室性心动过速采取病因治疗、药物治疗、同步直流电复律、人工调搏法效果满意，用于治愈持续性室性心动过速和防止复发。     

胺碘酮联合β受体阻滞剂治疗恶性室性心律失常疗效观察

目的 探讨胺碘酮联合β受体阻滞剂治疗恶性室性快速心律失常,尤其＂电风暴＂ 的疗效.方法 回顾性分析23例恶性室性心律失常患者病历资料,11例胺碘酮联合β受体阻滞剂治疗的患者为试验组,12例应用胺碘酮治疗的患者为对照组,2组患者用药方法 及其它治疗措施均以王吉耀等编著的〈内科学〉及中华医学会心血管病分会编写的〈2008抗心律失常药物治疗指南〉中的方法 为准,2组无差异;观察用药前后患者心律变化情况,以心律转为窦性心律、室颤转为室速、持续性室速或（和）多形性室速变为非持续性或（和）单形性室速为治疗有效.结果 试验组转为窦性心律4例,由室颤转为室速1例,持续性室速变为非持续性室速2例,多形性室速变为单形性室速1例,有效率72.7%（8/11）;对照组转为窦性心律4例,由室颤转为室速2例,多形性持续性室速变为非持续性室速1例,有效率58.3%（7/12）.试验组符合＂电风暴＂诊断标准的4例患者,3例治疗效果显著,有效率达75%（3/4）;对照组符合＂电风暴＂诊断标准的3例患者,1例治疗有效,有效率33.3%（1/3）.结论 胺碘酮联合β受体阻滞剂治疗恶性快速室性心律失常效果显著,尤其是治疗＂电风暴＂最有效的方法 .     

新生儿心律失常的临床特征及病因探讨

目的探讨新生儿心律失常的病因及临床特征。方法对98例新生儿心律失常的病因、临床特征、心律失常类型及治疗情况进行分析。结果感染68例（36．7％）、窒息缺氧32例（32．7％）、先天心脏病10例（10．2％）、电解质紊乱8例（8．2％）、感染性心肌炎6例（6．1％）。期前收缩42例（42．9％）;快速心律失常28例（28．6％）：室上性心动过速21例,其中阵发性室上性心动过速（PSVT）8例、紊乱性房性心动过速（MAT）4例;室性心动过速（VT）7例;房室传导阻滞16例（16．3％）。42例期前收缩中有38例经治疗原发病、营养心肌后消失;8例PSVT：1例经刺激迷走神经后复律,2例静推三磷酸腺苷（ATP）后复律,4例给普罗铂酮后复律,4例紊乱性房性心动过速：3例经给洋地黄药物和美托洛尔后复律,1例死亡。7例VT：2例给利多卡因后复律,1例给普罗帕酮后复律,1例给胺碘酮后复律,1例口服维拉帕米后纠正,2例死亡。结论新生儿心律失常病因以感染和缺血缺氧为主,临床上以期前收缩和快速心律失常、房室传导阻滞多见,无器质性病变的心律失常大多预后良好,有器质性病变的危重心律失常预后较差,死亡率高。     

抗心律失常药物致心律失常的诊断与处理

抗心律失常药物治疗时导致新的心律失常或原有心律失常加重,称为抗心律失常药物致心律失常作用,其发生率在5%￣10%,尤其左室功能不佳者发生率高。其发生机制与复极延长,早期后除极导致尖端扭转型室性心动过速(室速)等有关。大多发生在开始治疗后数天或改变剂量时,通常表现为持续性室速、长QT间期与尖端扭转型室速[1]。严重者可致死,故应高度警惕其发生。1抗心律失常药物致心律失常的诊断1.1Morganroth诊断标准1.1.1凡出现以往未发生的新的室速,又无其他原因可查者。1.1.2原有室性心律失常加重①基础状态期前收缩(早搏)1～50次/小时者增加1…     

伊布利特转复房颤的效果及不良反应分析

目的 观察新一代Ⅲ类抗心律失常药伊布利特转复阵发性房颤的效果、不良反应。方法 选择2019年1月-2023年3月本科室治疗的68例阵发性房颤患者,10min一次性静脉注射伊布利特1mg,观察转复率、转复时间、严重不良反应。结果 伊布利特对阵发性房颤转复成功55例,成功率80.8%,平均转复时间26.7min,最快转律时间为3min,最长转律时间138min。无器质性心脏病患者,发生1例非持续性单型性室速,4h内自行消失。合并冠心病、慢性心力衰竭患者,发生持续性单型性室速、阿斯综合征1例,电复律终止;发生非持续性单型性室速1例,4h内自行终止。未发生尖端扭转性室速,未发生严重心动过缓、加重、低血压,无死亡病例。结论 无器质性心脏病的阵发性房颤患者,使用伊布利特转律快速、有效、安全;合并冠心病、慢性心力衰竭、急性心肌梗死的患者,在急救完备的情况下,可谨慎使用。     

心律平治疗阵发性室上性心动过速临床观察(附102例分析)

目的评价心律平抗心律失常的效果及安全性。方法102例阵发性室上速患者均为静脉注射给药:心律平70 m g加入生理盐水稀释后静脉注射,必要时15 m in重复1次,不超过3次。结果阵发性室上速患者102例96例有效,有效率为94.1%;出现窦性停搏3例,经抢救后很快恢复窦性心律。结论静脉注射心律平治疗阵发性室上速的疗效显著,是相对安全的。     

28例预激综合征并室上性心律失常不同药物复律对比分析

２８例预激综合征并室上性心律失常不同药物复律对比分析福州市第一医院杨挺陈玉华预激综合征（ＷＰＷ）常并室上性快速心律失常，其中以阵发性室上速最常见（约占８５％），房颤１０＋％，如心率大于２００次／分，处理不及时易导致室颤猝死。本文就２８例预激综合征并室...     

86例阵发性室上速药物治疗体会

８６例阵发性室上速药物治疗体会莆田市涵江医院林永刚，林永廉阵发性室上速（以下称ＰＳＶＴ）是常见心律失常之一。药物治疗是主要措施，笔者近年对８６例ＰＳＶＴ分型施治，转复率高。现报告如下。一、一般资料８６例中，男２６例，女６０例，男：女＝１：２．３；年龄...     

同步电复律治疗心脏瓣膜术后室上性心动过速56例观察与护理

室上性心动过速(室上速)是体外循环心脏瓣膜成形或替换术后一种较为常见的需要治疗的心律失常,终止室上速发作的方法有刺激迷走神经方法、药物治疗、导管消融治疗、直流电转复等。刺激迷走神经很难奏效;导管消融属有创治疗,不作为首选方法;大多数抗心律失常药对循环功能均有不同程度的抑制作用,甚至有导致心脏停搏的严重后果。电复律自问世以来,已广泛应用于临床,室上速是同步直流电复律最常见的适应证,     

急性心肌梗死后顽固性持续室速抢救成功8例分析

目的　通过对 8例急性心肌梗死后顽固性持续室速抢救的资料分析 ,旨在认识此种类型的室速 ,总结抢救顽固性持续室速的经验。方法　 8例均为急性心肌梗死演变期或恢复期的患者 ,各种抗心律失常药物治疗无效 ,8例均行同步直流电复律 ,7例转复成功 ,1例 2次电击可转复但不能维持 ,经补充电解质 ,改善心肌缺血之后联合抗心律失常治疗转为窦性心律 ,转复后长期口服胺碘酮维持。结果　 8例抢救成功。门诊随访 ,2例存活 4年因心力衰竭而死亡 ,其余 6例长期存活。服用胺碘酮无 1例出现甲状腺功能紊乱 ,肺纤维化 ,尖端扭转型室速等副作用。结论　急性心肌梗死后顽固性持续室速同步直流电复律安全有效 ,但要注意基础病因治疗及维持心肌细胞的极化状态 ,转复后可长期口服胺碘酮维持     

Vernakalant. Too dangerous in atrial fibrillation

The usual aim of treatment for patients with symptomatic paroxysmal or recent-onset atrial fibrillation, including after cardiac surgery, is to slow the heart rate. Electrical and drug (amiodarone) cardioversion are other options. Vernakalant, an antiarrhythmic drug, has been authorised in the European Union for rapid reduction of recent-onset atrial fibrillation. It is only available in an injectable form. Vernakalant has not been compared in clinical trials with treatments slowing the heart rate, or with electrical cardioversion. The only available comparison with another antiarrhythmic agent is a clinical pharmacology study versus amiodarone, a slow-acting drug, based on the rate of cardioversion at 90 minutes in 240 patients. As expected, given the brief observation period, the rate was significantly higher with vernakalant (51.7% versus 5.2%). During clinical evaluation, 6 deaths occurred in the vernakalant groups versus none in the other groups (placebo or amiodarone). The main adverse effects of vernakalant are cardiac arrhythmias (ventricular arrhythmia, torsades de pointes, bradycardia) and severe hypotension. Altered taste, sneezing, paraesthesia, nausea and pruritus were frequent, and respiratory and neuropsychological effects were also reported. A trial in atrial flutter was interrupted when cases of cardiogenic shock occurred. Interactions are to be expected with drugs that prolong the QT interval, and also with drugs that lower the heart rate or the blood potassium concentration. In practice, it is better to continue to use amiodarone for drug cardioversion and to avoid using vernakalant.     

Ibutilide in rapid conversion of atrial flutter in octogenarians

INTRODUCTION: Atrial flutter is a common sustained atrial tachyarrhythmia for which frequency increases with age. Ibutilide is a novel class III antiarrhythmic agent used for the rapid cardioversion of atrial fibrillation or atrial flutter. AIM: The aim of our study was to assess the use of ibutilide in a selected population of very elderly patients (octogenarians) with recent-onset atrial flutter. METHOD: Twenty-nine consecutive elderly patients (11 male, 18 female; mean age 83 +/- 3 years; interquartile range of 10) with recent-onset atrial flutter were included in the study; none of them had signs or symptoms of severe heart failure, angina or impaired renal or hepatic function. All patients underwent a 10-minute intravenous infusion of ibutilide (0.87 mg in 10 ml). RESULTS: The rate of successful arrhythmia termination was 75.9% within a mean time of 31 +/- 20 minutes. No clinical variables were shown to be associated with successful cardioversion, although there was a tendency towards higher efficacy in patients with a shorter duration of arrhythmia. Two female patients (6.9%) developed torsade de pointes, requiring direct current cardioversion under general anaesthesia. Episodes of nonsustained ventricular tachycardia occurred in two other patients. CONCLUSION: Ibutilide appears to be an effective and well tolerated drug for rapid conversion of recent-onset atrial flutter in octogenarian patients, and may represent a valid approach in the acute management of atrial flutter in this particular set of patients.     

Class III antiarrhythmic action in experimental atrial fibrillation and flutter in dogs

Progress in the pharmacological treatment of atrial fibrillation and flutter has been achieved by the introduction of the class III antiarrhythmic drug amiodarone. In the present study we tested amiodarone and a new class III antiarrhythmic drug, melperone, in experimentally induced atrial fibrillation and flutter in pentobarbital-anesthetized dogs. By high-rate stimulation in the right atrium, atrial fibrillation was induced in 4, and atrial flutter in 10 out of 22 dogs. Atrial flutter rate was 496 +/- 13 min-1 (median +/- 95% confidence interval). Both drugs converted the arrhythmias at doses from 2.5 to 10 mg . kg-1 and reduced that atrial flutter rate before conversion. Average ventricular rate during arrhythmias (261 +/- 16 min-1) decreased after amiodarone, and was unchanged or, in three out of nine dogs, increased after melperone. The doses of amiodarone converting the arrhythmias increased atrial refractoriness, whereas the effects on AV nodal conduction and refractoriness were variable. The results support the concept that atrial flutter is due to circus movement where the flutter rate is dependent upon atrial refractoriness. The class III antiarrhythmic drugs amiodarone and melperone seem to be equally potent in converting atrial arrhythmias.     

Ibutilide – recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation

Ibutilide is a ‘pure’ class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. At a cellular level it exerts two main actions: induction of a persistent Na+ current sensitive to dihydropyridine Ca2+ channel blockers and potent inhibition of the cardiac rapid delayed rectifier K⁺ current, by binding within the channel pore cavity upon channel gating. Ibutilide has been shown to terminate atrial flutter and fibrillation in animal studies, with some risk of ventricular pro-arrhythmia. Experimental models of hypertrophy/heart failure show altered sensitivity to ibutilide, with increased dispersion of repolarisation and incidence of pro-arrhythmia. Patient trials show that ibutilide is effective at terminating atrial arrhythmias when given alone, and that it can increase effectiveness and reduce energy requirements of electrical cardioversion. The risk to patients of polymorphic ventricular tachycardia necessitates careful patient selection and monitoring during and after treatment. An ibutilide analogue, trecetilide, requires further investigation but may offer a less readily metabolised and pro-arrhythmic alternative to ibutilide.     

经食道心房调搏诊治快速型室上性心律失常的临床分析

目的讨论快速型室上性心律失常经食道心房调搏术（TEAP）进行诊断的临床价值。方法采用经食道心房调搏术对快速型心律失常患者共139例进行诊断。结果 78例患者为阵发性室上性心动过速（PSVT）、7例室性心动过速、32例心房扑动、22例心房颤动。PSVT患者中,46例AVRT,17例AVNRT,15例PAT。采用TEAP对PSVT发作进行诱发及终止,72例成功,6例失败,终止成功率为92.3%。采用TEAP对心房扑动进行终止,28例成功,4例失败,终止成功率为87.5%。采用药物终止心律失常,能够对患者心脏生理相关参数造成影响,而电刺激治疗不会对心脏造成影响。结论快速型室上性心律失常采用经食道心房调搏术进行诊断,操作简便、准确性高、安全可靠,值得推广应用。     

Ibutilide--recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation

Ibutilide is a 'pure' class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. At a cellular level it exerts two main actions: induction of a persistent Na+ current sensitive to dihydropyridine Ca2+ channel blockers and potent inhibition of the cardiac rapid delayed rectifier K+ current, by binding within the channel pore cavity upon channel gating. Ibutilide has been shown to terminate atrial flutter and fibrillation in animal studies, with some risk of ventricular pro-arrhythmia. Experimental models of hypertrophy/heart failure show altered sensitivity to ibutilide, with increased dispersion of repolarisation and incidence of pro-arrhythmia. Patient trials show that ibutilide is effective at terminating atrial arrhythmias when given alone, and that it can increase effectiveness and reduce energy requirements of electrical cardioversion. The risk to patients of polymorphic ventricular tachycardia necessitates careful patient selection and monitoring during and after treatment. An ibutilide analogue, trecetilide, requires further investigation but may offer a less readily metabolised and pro-arrhythmic alternative to ibutilide.     

抗心律失常药及心律失常持续时间对心房扑动、心房颤动转复效果的影响

目的 探讨抗心律失常药及持续时间对心房颤动、心房扑动转复效果的影响.方法 回顾分析180例房扑及180例房颤患者的临床资料,并按选择的药物伊布利特、普罗帕酮及胺碘酮治疗各分为三组,每组患者再分为持续时间≤3 d和＞3d,每组各30例,比较各组患者治疗1.5h后的转复率,采用SPSS 16.0进行统计分析.结果伊布利特组≤3 d和＞3d的房扑的转复率为90.00％和83.33％,普罗帕酮的≤3 d和＞3d的房扑的转复率为76.67％和36.67％,胺碘酮的房扑的转复率为73.33％和33.33％,对于房扑持续时间≤3 d,伊布利特、普罗帕酮、胺碘酮的房扑的转复率差异没有统计学意义(P＞0.05);对于房扑持续时间＞3d,伊布利特的转复率明显高于普罗帕酮、胺碘酮的(P＜0.05);三种药物房颤的转复效果比较:伊布利特的≤3 d和＞3d的房颤的转复率为80％和73.33％,普罗帕酮的≤3 d和＞3d的房颤的转复率为43.33％和26.67％,胺碘酮的房颤的转复率为50％和36.67％,对于房颤持续时间＜3d,伊布利特的转复率明显高于普罗帕酮、胺碘酮(P＜0.05);对于房颤持续时间＞3d,伊布利特的转复率明显高于普罗帕酮、胺碘酮的(P＜0.05);三组药物房扑、房颤总转复率分别为81.67％、45.83％、48.33％,伊布利特明显高于普罗帕酮、胺碘酮(P＜0.05);伊布利特对房扑的转复率明显高于房颤的转复率(P＜0.05).结论 对于持续时间≤3 d的患者,伊布利特、普罗帕酮及胺碘酮房扑转复成功率没有明显差异,但伊布利特房颤转复率明显增高;对于持续时间＞3d的患者,伊布利特房扑、房颤转复的成功率均高于普罗帕酮及胺碘酮,应根据心律失常具体情况灵活选用伊布利特、普罗帕酮及胺碘酮进行治疗.     

心律失常的药物治疗

摘要： 心律失常种类繁多, 十分常见, 临床中常将其分为缓慢和快速心律失常两大类, 每类各有其共同的治疗原则。对于缓慢心律失常, 迄今尚无可长期应用的有效口服药, 起搏器依然是唯一有效的治疗措施。目前, 导管消融已经应用到几乎每种类型的快速心律失常。由于治疗效果满意, 导管消融是室上性心动过速和心房扑动的首选治疗措施。而对于其他类型的快速心律失常, 特别是心房颤动和各种类型的过早搏动 （早搏）, 大部分患者仍然接受药物治疗。胺碘酮、 普罗帕酮、 索他洛尔和美西律是我国常用的抗心律失常药。本文概述了这些常见抗心律失常药物的治疗原则及注意事项。     

Calcium antagonists. Clinical use in the treatment of arrhythmias

Calcium antagonists have recently emerged as a class of drugs for the treatment of angina, hypertension and certain cardiac arrhythmias. Verapamil is the prototype calcium antagonist and has the most clearly defined antiarrhythmic properties. Other agents in the class include D-600 (gallopamil), tiapamil, nifedipine, and diltiazem. The antiarrhythmic effects of these compounds can be correlated with their electrophysiological properties which may differ significantly among different compounds and also between isolated tissues in intact animals and man. As a class they do not increase the effective refractory period of the atria, ventricle, His-Purkinje fibres or the accessory pathways in the heart. The dominant effect is slowing of conduction in the AV node with the prolongation of the AV nodal refractory period. The most marked changes are produced by verapamil, the least with nifedipine which is devoid of antiarrhythmic actions. Verapamil and its congeners as well as diltiazem terminate paroxysmal supraventricular tachycardia and slow the ventricular response in atrial flutter and fibrillation. They are also of prophylactic value in preventing recurrences of paroxysmal supraventricular tachycardia and controlling the ventricular response in atrial flutter and fibrillation during long term oral therapy. Their value in ventricular arrhythmias is uncertain but they are unlikely to be effective except in those complicating coronary artery spasms. The relative merits and potencies of various calcium antagonists in different arrhythmias need further studies.     

Dofetilide: a review of its use in atrial fibrillation and atrial flutter

Dofetilide is a 'pure' class III antiarrhythmic agent which has demonstrated efficacy in the conversion of atrial fibrillation or flutter to sinus rhythm and the maintenance of sinus rhythm. By blocking the rapid component of the cardiac delayed rectifier potassium current (I(Kr)), dofetilide prolongs the cardiac action potential duration and the effective refractory period. This is thought to increase the likelihood of a re-entrant wavefront encountering refractory tissue and terminating the arrhythmia. Preliminary findings from the EMERALD (European and Australian Multicenter Evaluative Research on Atrial Fibrillation Dofetilide) and SAFIRE-D (Symptomatic Atrial Fibrillation Investigation and Randomized Evaluation of Dofetilide) studies suggest that oral dofetilide is effective in the conversion of atrial fibrillation or flutter to sinus rhythm. Both studies have yet to be published in full. In SAFIRE-D, dofetilide 500microg twice daily for 3 days achieved a conversion rate of 32% compared with a 1% rate for placebo. A similar conversion rate was achieved after 3 days in EMERALD with dofetilide 500microg twice daily (29%) which was significantly greater than that achieved with sotalol 80mg twice daily (6%; p < 0.05). Oral dofetilide also appears to be effective in the maintenance of sinus rhythm. An abstract report of EMERALD participants who had been converted to sinus rhythm showed that 71% of patients who received oral dofetilide remained in sinus rhythm after 6 months (compared with 26% of placebo and 59% of sotalol recipients: both p < 0.05). Restoration of sinus rhythm using intravenous dofetilide is more likely in patients with recent-onset versus prolonged-duration arrhythmia, and in those with atrial flutter rather than atrial fibrillation. Limitations of comparative data for intravenous dofetilide are such that few conclusions can be drawn. Although generally well tolerated in clinical trials, dofetilide has proarrhythmic potential. Torsade de pointes ventricular tachycardia was reported in up to 3.3% of patients who received oral dofetilide in the DIAMOND (Diamond Investigations of Arrhythmia and Mortality on Dofetilide) studies, although only a small proportion of patients in these studies had atrial fibrillation; most episodes occurred within the first 3 days. Whether the propensity of dofetilide for this life-threatening arrhythmia is similar to that of other class III antiarrhythmic agents has yet to be determined. Importantly, the long term use of oral dofetilide in patients at high risk for sudden cardiac death is not associated with an increased risk of mortality, although these DIAMOND findings cannot necessarily be extrapolated to patients with atrial fibrillation. CONCLUSIONS: Dofetilide offers an alternative to currently available antiarrhythmic agents for the pharmacological conversion of atrial fibrillation or atrial flutter to sinus rhythm and for the maintenance of sinus rhythm after cardioversion. However, further comparative data are necessary before its definitive place can be determined.