异搏定治疗有效的室性心动过速9例分析

对异搏定治疗有效的室性心动过速（室速）9例进行分析，其中5例为短联律间距室速，另4例为非短联律间距室速；呈短联律间距室速者对Ⅰ、Ⅱ、Ⅲ类抗心律失常药物治疗效果不佳，而异搏定可很快终止其发作，故宜首选异搏定；非短联律间距室速部分对利多卡因、心律平的治疗也有效，对于此类患者宜先用Ⅰ、Ⅲ类抗心律失常药物治疗，无效时才可试用异搏定。根据本组资料并结合文献复习，认为本病的发病机理可能与触发活动以及钙、钾离子流折返和植物神经功能异常等因素有关。     

短联律间距室性早搏引发的多形性室性心动过速或/和心室颤动五例临床分析

报道5例短联律间距室早引发的多形性室速或/和室颤,临床表现与常见的QT间期延长综合征引起的扭转室速不同,其特点有:单一或触发室速的室早联律间距极短(240～320ms);窦律时QT间期及T/U波形态正常;无明显心脏病证据;利多卡因对此治疗无效,而异搏定、心律平、硫酸镁有效。     

维拉帕米终止特殊类型室性心动过速的使用特点

目的：探讨维拉帕米终止特殊类型室性心动过速（室速）的临床使用特点。方法：总结２０例分支型室速和短联律间距室性早搏引发的多形性室速，静脉应用维拉帕米终止室速发作的经验。结果：维拉帕米静脉注射可终止此两种特殊类型室速发作，维持静脉滴注能预防急性复发，终止室速发作的有效剂量平均总量０．３ｍｇ／ｋｇ（平均２１ｍｇ，范围５～５５ｍｇ）。结论：维拉帕米在特殊类型室速中的应用剂量宜个体化     

伴短联律间期多形性室速的单相动作电位表现1例

伴短联律间期多形性室速的单相动作电位表现１例刘伏元，童步高，浦寿月我们观察到１例ＱＴ间期正常，以短联律间期室性早搏（室早）、多形性室性心动过速（室速）为主，伴有非短联律间期室早的患者，在右心室单相动作电位检查发现短联律间期室早是由于延迟后去极（ＤＡＤ...     

超大剂量的维拉帕米治疗伴极短联律间距的多形性室速

伴极短联律间距的多形性室性心动过速 (室速 )是一种特殊类型的高度致命性室性心律失常 ,由Ｂｅｌｈａｓｓｅｎ首先报道[1] 。随着人们对此类室速的认识和治疗的进步 ,大大降低了其病死率。此类室速通常对Ⅰ、Ⅱ、Ⅲ类抗心律失常药无效 ,而静脉应用或口服维拉帕米 (Ｖｅｒａｐａｍｉｌ)对终止及预防发作十分有效。临床上通常用量 ,静脉注射首次以 5ｍｇ为宜 ,无效时再追加 ,总量一般为 2 0～ 2 5ｍｇ[2 ,3 ] ;口服剂量为 2 4 0～ 4 80ｍｇ/ｄ。本文报道 1例伴极短联律间距的多形性室速 ,常规剂量无效 ,需用超大剂量的维拉帕米 (12 0 0ｍｇ/…     

极短联律间距的多形性室速四例诊治体会

室速是常见的心律失常,易导致黑蒙、晕厥,甚至猝死。而据Belhassen[1]首先报道:极短联律间距的多形性室速是一种原因不明,特殊类型的高度致命性的室性心律失常,临床易忽视其特点而丧失抢救时机。本文收集4例此类患者的诊治,以供交流,现报道如下。1临床资料患者1,男,36岁,既往体健。以反复无明显诱因晕厥1年就诊。发病前无先兆,一般持续数秒,不伴抽搐等症状,恢复后无特殊不适,多次体检均未见异常。口服普萘洛尔无效。于2次24h动态心电图检查后发现频发多形性室早,RonT,短阵室速,服用可达龙2个月无效,观察其心电图后发现室早、室速的联律间…     

多形性室性心动过速伴发于极短联律间距致反复晕厥一例

多形性室性心动过速伴发于极短联律间距致反复晕厥一例秦南屏，黄兆铨，叶武患者女，３２岁。反复发作胸闷、心悸、眩晕、晕厥４年，１天来症状加重入院。曾在外院以频发室性早搏（室早）（Ｒ－ｏｎ－Ｔ）、短串室性心动过速（室速）、经利多卡因、美西律、维拉帕米治疗、...     

室早指数及临床意义的探讨

目的探讨室早指数对器质性病变患者发生恶性室性心律失常的预测价值。方法106例经动态心电图诊断为窦性心律伴发室性心律失常的患者,分为器质性与非器质性病变两组,统计室早个数、室速和室颤的发作阵次及诱发室速、室颤的室早联律间期、室早前次心搏的QT间期。结果106例患者中,平均24h室早总数12066±1105个;阵发室速662±79次,53例由RonT室早诱发,其中器质性病变46例(86.85%);阵发室颤39±5次,均发生于器质性病变者,其中11例(68.8%)由快速多形性室速诱发;器质性与非器质性病患者中诱发室速和(或)室颤的室早联律间期分别为340±15ms和420±20ms,室早前次心搏的QT间期分别为420±10ms和410±25ms,室早指数分别为0.90±0.10和1.00±0.15,两组比较有显著性差异(p<0.05)。结论当室早指数在0.78～0.83之间时,易诱发阵发性室速和室颤,尤其是器质性病变者,临床应给予足够的重视和治疗。     

多形性室性心动过速2例的治疗

例1 男,63岁。因发作性胸痛、心悸2年,突发晕厥5小时入院。有冠心病、陈旧性心梗病史2年。入院后即给予扩冠,极化液及对症治疗。次日有心绞痛发作,下午5时患者突感头晕,急查EKG示为多形性室性心动过速(PVT)。给予心律平70mg静注,转为窦性心律,但仍有频发室早,短阵室速,Q—T间期0.40s;继而静注利多卡因50mg,同时以1.6mg/min静滴维持,早搏减少(图1—A)。第三天上午8时患者突然意识丧失,心电监护示多形性室性心动过速,后转为室颤(图1—B)。即予电除颤,恢复窦性心律。为治疗及预防多形性室速,给予普鲁卡因胺0.1g静注,每4h一次,口服胺碘酮、美多心安,当胺碘酮发挥作用时停用普鲁卡因胺,同时静注25％硫酸镁4g/d,早搏及短阵室速消失,未再发生多形性室速,病情稳定,继续治疗半月出院。 例2 男,70岁,以冠心病,陈旧性前壁、下壁心肌梗塞,不稳定型心绞痛,心功能Ⅲ级入院。血生化正常,EKG示陈旧性前壁、下壁心梗,胸前导联广泛性心肌缺     

早复极患儿高通气试验诱发恶性室性心律失常

患儿男、12岁,因睡眠中发生一过性意识丧失伴抽搐、小便失禁而行脑电图检查,结果为阴性,患儿姐姐也有同样情况。两周后,患儿睡眠中再发晕厥并再行脑电图检查。检查中行通气试验60秒时,出现短联律间期的室早(<200ms)、心电图短长短现象,并发生多形性室速。心电图可见长RR间期后J波幅度增高(图1)。复习前次脑电图检查高通气试验时,也有短联律间期的室早,但未诱发室速。本图为多通道脑电图和单导联心电图同步记录,患儿高通气1min后,短联律间期的室早诱发室速、室颤。而高通气试验前无室早,长RR间期后可见J波幅度增加(箭头指示)。     

Hazards of intravenous verapamil for sustained ventricular tachycardia

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.     

Efficacy of verapamil in exercise-induced ventricular tachycardia

The antiarrhythmic efficacy of verapamil was determined by serial treadmill testing in 16 patients with reproducible exercise-induced ventricular tachycardia (VT). Twelve of the 16 patients responded to verapamil, 0.2 mg/kg intravenously; in 8 of these 12 responders, an oral verapamil regimen of 160 to 320 mg given every 8 hours also prevented exercise-induced VT. Plasma verapamil concentration was significantly higher in the responders than in the nonresponders to intravenous verapamil, but levels were similar in responders and nonresponders to oral therapy. The 8 responders to the oral drug were followed up while receiving verapamil therapy for 6 to 22 months (mean 15), and exercise-induced VT did not recur in any patient. Five of the 8 responders also had concomitant spontaneous VT unrelated to exercise which verapamil suppressed initially as well: 4 remained free of spontaneous VT, while 1 patient had recurrence of spontaneous VT. Thus, in patients with exercise-induced VT, verapamil is a promising alternative therapy to beta-adrenergic blocking agents. The effectiveness of verapamil is consistent with a mechanism of arrhythmogenesis involving calcium channels.     

Differentiation and mechanisms of prevention and termination of verapamil-sensitive sustained ventricular tachycardia

The purpose of this study was to differentiate by means of electrophysiologic study, a drug's ability to terminate or to prevent ventricular tachycardia (VT). Differences between the 2 effects were examined in patients with VT and the underlying mechanisms were studied in verapamil-responsive idiopathic sustained VT. The clinical significance of the distinction for chronic oral drug therapy is discussed.

Thirty-five cases of inducible sustained VT were studied. A drug was considered “preventative” if it prevented VT induction and repetitive ventricular response, and “terminating” if it stopped induced VT within 15 complexes or could stop VT after its intravenous administration.

Prevention and termination occurred together in 13 of 19 cases (68%) with disopyramide, in 10 of 19 cases (53%) with procainamide, in 8 of 12 cases (67%) with lidocaine, in 11 of 15 cases (73%) with mexiledne, and in 10 of 16 cases (63%) with verapamil. In the 16 in which verapamil terminated VT, VT rate immediately before termination slowed markedly from 167 ± 33 to 134 ± 28 beats/min. In the 6 cases without preventative effects, minimal and maximal premature intervals for VT induction increased significantly, from 291 ± 70 to 335 ± 85 ms and 323 ± 68 to 423 ± 109 ms, respectively, after verapamil administration.

In 2 cases in which verapamil had a terminating effect, 5 mg of verapamil restored sinus rhythm but 10 mg caused premature beats resembling VT complexes. In another 2, 5 mg of verapamil lengthened the minimal premature interval; 10 mg increased both minimal and maximal premature intervals and lengthened the VT cycle.

The chronic oral aukninistration of verapamil resulted in disappearance of VT attacks in 2 of 4 patients and a decrease in both their number and duration in 2 of 4 patients in whom both termination and prevention were seen in the electrophysiologic study. However, in 4 patients who had only termination, the VT episodes remained unchanged in 2 and even increased in the other 2.     

动态心电图中的室速：心电学与临床特点

１５例动态心电图上≥１０个室性心动的非持续性和持续性室速（ＮＳＶＴ和ＳＶＴ），共计１３９阵。大部分室速（ＶＴ）的联律间期或≤４００ｍｓ或≥６００ｍｓ；短联律间期（＜５００ｍｓ）的ＶＴ频率高，多形室速（ＰＶＴ）多见；ＰＶＴ较单形室速（ＭＶＴ）频率高，联律间期短；９６％的ＶＴ发生在日间清醒状态下；所有病例无ＱＴ间期延长；与猝死和晕厥有关的心电学特征包括ＶＴ的频率，发作阵数，持续时间和ＰＶＴ；极短联律间期的ＶＴ可能进展为室颤。     

Evaluation of bepridil efficacy by electrophysiologic testing in patients with recurrent ventricular tachycardia: Comparison of two regimens

Summary The purpose of the study was to evaluate this effect of different doses of intravenous and oral bepridil on the induction of ventricular tachycardia. Thirty-eight patients underwent electrophysiologic evaluation for recurrent ventricular tachycardia (VT). Sustained monomorphic VT was induced by programmed ventricular stimulation, using up to three extrastimuli in all patients. The effects of intravenous bepridil (2 mg/kg) were evaluated during the initial study. Intravenous bepridil prevented the induction of sustained VT in eight patients (21%). Electrophysiologic study was repeated after oral bepridil. In six patients the study was stopped because of adverse effects or VT recurrence. Thirty-two patients underwent repeat study 7 days later, taking oral bepridil, 500 mg/day (n=16) or 900/day (n=16). A dose of 500 mg/day of bepridil prevented the induction of sustained VT in only one patient. A dose of 900 mg/day of bepridil prevented the induction of sustained VT in eight patients. There were no significant clinical adverse effects, except in one patient receiving intravenous bepridil. The response to intravenous bepridil did not predict the response to oral bepridil. The response to intravenous or oral bepridil was not related to the plasma level of bepridil but was related to a higher left ventricular ejection fraction. Eight patients (21%) in whom VTs were noninducible on oral bepridil were discharged on 300 mg/day of bepridil if their initial loading dose was 500 mg/day or on 600 mg/day if their initial loading dose was 900 mg/day. They remained free of VT during a follow-up of at least 6 months. In conclusion, this study suggests that oral bepridil at the dose of 600 mg/day may be of value in patients with recurrent VT.     

Electrophysiologic and antiarrhythmic properties of bepridil

Bepridil has been shown to block both slow- and fast-channel activity in the heart. Electrophysiologic studies in man demonstrate that oral and intravenous bepridil prolongs sinus cycle length, PR interval and QT interval, without apparently changing the QRS interval. In addition, the drug depresses atrioventricular (AV) nodal conduction, resulting in an increased AH interval. Refractoriness in the AV node, atrium and ventricle is increased. There is usually little or no change in the HV interval. The antiarrhythmic properties of bepridil have been noted in patients with supraventricular tachycardia, ventricular premature complexes (VPCs) and sustained ventricular tachycardia (VT). In 17 patients, intravenous bepridil was compared with either verapamil or ajmaline. AV nodal reentrant tachycardia was terminated in all patients with bepridil and verapamil. However, ajmaline was somewhat more effective than bepridil in patients with AV reentry (8 of 8 versus 5 of 8). In 12 of these 17 patients, oral bepridil (500 mg/day for 3 days) suppressed the induction of tachycardia or slowed its rate. In 3 studies of oral bepridil for VPCs, the drug was effective in 68%, 69% and 70% of patients. Another group of studies evaluated bepridil in a total of 30 patients with sustained VT. Intravenous bepridil terminated VT in 17 of 26 patients. The induction of VT by programmed ventricular stimulation was also prevented in 7 of 17 patients. Although torsade de pointes has been reported, its incidence appears to be low.     

Sustained ventricular tachycardia responsive to verapamil in patients with hypertrophic cardiomyopathy. Clinical and electrophysiological assessment of drug efficacy

Recently, we examined 2 cases of hypertrophic cardiomyopathy (HCM) presenting with sustained ventricular tachycardia (VT). One case was a 62 year old male with midventricular hypertrophy and monomorphic sustained VT. After admission, the efficacies of procainamide, disopyramide, aprindin, flecainide, mexiletine and verapamil were evaluated by means of continuous electrocardiographic monitoring. Verapamil prevented the recurrence of sustained VT and markedly reduced the frequency and number of runs of nonsustained VT. In the electrophysiologic study, rapid VT was induced by double extrastimuli at the right ventricular apex. Intravenous verapamil at a dose of 10 mg prevented the induction of VT. The patient was discharged on verapamil and remains asymptomatic after 3 months of follow up. The other case was a 34 year old female who was a survivor of cardiac arrest. Monomorphic VT was observed on emergency admission and was converted to sinus rhythm by direct current cardioversion after resuscitation. In the electrophysiologic study, rapid VT was induced by double extrastimuli at the right ventricular outflow tract. Verapamil at a dose of 10 mg prevented the induction of VT. These 2 cases of HCM are rare in that they presented with sustained VT. It is also of interest that verapamil, which has been used conventionally in HCM, prevented VT.     

Analysis of the pattern of initiation of sustained ventricular arrhythmias in patients with implantable defibrillators

INTRODUCTION: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease. METHODS AND RESULTS: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating beat of all ventricular arrhythmias was 523 +/- 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty-two (85%) of the arrhythmia episodes were initiated by a late-coupled premature beat, 33 (13%) were initiated by an early-coupled premature beat, and 5 episodes (2%) were initiated with a short-long-short sequence. The pattern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias. CONCLUSION: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late-coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia.     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

Early interruption of antiarrhythmia treatment in the acute phase of infarction complicated by ventricular arrhythmia

18 patients with myocardial infarction complicated by severe ventricular arrhythmias (polymorphic VEBs or bigeminy = 5; VT = 11; VF = 2) were treated with antiarrhythmics which were stopped after 24 hours (intravenous infusion of mexiletine 0.5 mg/kg/hr after a loading dose). This treatment resulted in one failure (recurrent VF) and 17 successes, after increasing the dose in 3 cases of VT. After stopping treatment, 72% of patients had no further arrhythmia. 5 cases had recurrent VT within 72 hours, which was controlled by oral mexiletine in 4 cases. The ejection fraction was significantly decreased in the group with recurrent VT. Plasma assays were of little help. Stopping the antiarrhythmic treatment after 24 hours does not therefore present any particular risks and can be proposed even in cases with severe arrhythmias.