Mechanism of action and the effectiveness of ethacizin in patients with paroxysmal atrioventricular nodal reciprocal tachycardia

An electrophysiologic study of ethacizin's mechanisms of action was carried out in patients with paroxysmal atrioventricular nodal tachycardia. Tachycardia was controlled by 0.5 mg/kg ethacizin in all patients. No patients demonstrated induced tachycardia in the presence of the drug, and 55% developed a complete retrograde atrioventricular block. The assessment of the preventive effect of oral ethacizin administration showed that paroxysms of tachycardia could not be provoked by esophageal electrostimulation of the heart in 87% of the patients. In the same patients, stable antiarrhythmic effect was maintained by long-term treatment with this drug. The suppression of retrograde stimulus conduction along the quick path of the atrioventricular node is assumed to be the principal electrophysiological mechanism of ethacizin action. Ethacizin can be used to control or prevent paroxysms of atrioventricular nodal tachycardia.     

Effectiveness and pharmacodynamics of tobanum in patients with paroxysmal reciprocal atrioventricular tachycardia]

The antiarrhythmic effects and pharmacodynamics of tobanum were evaluated in 28 patients wist paroxysms of reciprocal atrioventricular tachycardia, by using transesophageal cardiac pacing. The agent given in a single dose of 10 mg produced antiarrhythmic effects in 70% patients with paroxysms of atrioventricular nodal tachycardia and in 40% with atrioventricular tachycardia in the presence of the Wolff--Parkinson-White syndrome. After administration of the drug, its antiarrhythmic effect occurred on an average 1.5 h and retained for 27 h.     

Preventive efficacy of propafenone, its effect on functional state of the heart during long-term treatment of patients with paroxysmal atrioventricular arrhythmias

Efficacy and tolerability of propafenone were studied in the process of long-term treatment of patients with various forms of paroxysmal atrioventricular arrhythmias. It was established that propafenone appears to be highly effective remedy for prophylaxis of paroxysms of atrioventricular reciprocal nodal tachycardia and atrioventricular tachycardia in Wolf-Parkinson-White syndrome. The preparation did not exert negative influence on functional state of the heart. Side reactions requiring withdrawal of propafenone were observed in 12.7% of cases.     

三磷酸腺苷诊断房室结双径路的价值

目的评价三磷酸腺苷(ATP)试验诊断房室结双径路的价值.方法对经心内电生理研究证实的慢快型房室结折返性心动过速21例(研究组)和同期无房室结双径路征象、且不能诱发房室结折返性心动过速的14例(对照组),在心房起搏下给予递增的ATP剂量.结果研究组中17例具有房室结双径路电生理征象(包括1例心内电生理研究时无房室结双径路征象),其中1例诱发房室结回波,3例诱发房室结折返性心动过速;对照组则均不显示房室结双径路征象、房室结回波或房室结折返性心动过速.ATP试验诊断房室结双径路的敏感性为80%,特异性为93%.结论三磷酸腺苷试验诊断房室结双径路有较高的价值.     

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.     

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia.

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.     

P-synchronized ventricular stimulation in supraventricular tachycardia

The author used P-synchronized stimulation of the ventricles to prevent tachycardia paroxysms in patients with frequent drug-resistant paroxysms of supraventricular tachycardia (SVT). Electrophysiologic examinations revealed additional conductive pathways functioning during tachycardia in the retrograde direction in 12 patients whereas in 6 cases tachycardia was accounted for by the mechanism of the re-entry of the excitation wave inside the atrioventricular node. The detected mechanisms of SVT development made it possible to use a method of its prevention by ventricular electrostimulation in the P-synchronized mode. Stimulation parameters were determined by a specially devised technique during electrophysiological examination. Following this stimulation, tachycardia attacks were completely prevented and attempts to provoke them by various types of stimulation were unsuccessful.     

Radiofrequency ablation in a patient with atrioventricular reentrant tachycardia and atrioventricular nodal reentrant tachycardia with 2:1 atrioventricular block.

The authors report the case of 15-year-old girl with a history of palpitations and shortness of breath during exercise. The electrocardiogram showed ventricular preexcitation suggesting a Wolff-Parkinson-White syndrome with a posteroseptal accessory pathway. During the electrophysiological study a left posterospetal accessory pathway was identified and an orthodromic atrioventricular reentry tachycardia was reproducibly induced (cycle length 400 ms). After disappearance of the ventricular pre-excitation with radiofrequency ablation, a dual physiology of atrioventricular node condution was documented and a slow-fast atrioventricular nodal reentrant tachycardia was repeatedly induced. Upon induction, this tachycardia presented a proximal atrioventricular block with 2:1 condution converted to 1:1 condution with overdrive pacing from the proximal coronary sinus (cycle length 270 ms). Radiofrequency ablation of the slow pathway was performed with success. We discuss the need to suspect and seek different arrhythmogenic substracts of tachycardia in a single patient, the electrophysiologic conditions that could explain the inducibility of different arrhythmias in this case, and the controversy regarding ablation of more than one reentry circuit in a single procedure.     

Use of Doppler echocardiography for studying hemodynamics in paroxysmal supraventricular tachycardia

Eighteen patients in whom sustained supraventricular tachycardia paroxysms were induced by programmed transesophageal pacing were examined. Doppler echocardiography was used to study left ventricular systolic and diastolic function, as well as cardiac output and pulmonary systolic pressure during sinus rhythm and paroxysms. A profound decrease in the cardiac index during paroxysms was found in 2 patients, one of them had higher pulmonary pressure. The cardiac index increased on an average from 4.4 +/- 0.9 l/min.m-2 during sinus rhythm to 4.8 +/- 1.4 l/min.m-2 during paroxysms. The diastolic function of the left ventricle was ascertained to be one of he factors that determine cardiac index in supraventricular tachycardia paroxysms.     

Reproducibility of reciprocal atrioventricular tachycardia during intracardiac and transesophageal electric stimulation

A feasibility to provoke reciprocal atrioventricular tachycardias was examined in 23 patients with atrioventricular nodal tachycardia and 17 with orthodromal tachycardia in the presence of the Wolff-Parkinson-White syndrome with endocardiac and transesophageal diagnostic pacing. Atrioventricular nodal tachycardia could be induced in all 23 (100%) patients both by endocardiac and transesophageal pacing. Orthodromal tachycardia was provoked only in 9 (53%) of 17 patients by transesophageal pacing. It was generally noted that tachycardia induction required more "aggressive" regimens of transesophageal pacing than endocardiac one. Endocardiac diagnostic pacing is now a more informative technique, but transesophageal pacing requires further development.     

Antidromic atrioventricular reentrant tachycardia mimicking ventricular tachycardia in the setting of previous myocardial infarction

The differentiation between ventricular tachycardia and broad-complex supraventricular tachycardia can be extremely difficult, particularly in emergency situations. We report a case of hemodynamically compromising broad-complex tachycardia in a 63-year-old man. The patient had previously sustained an anteroseptal myocardial infarction and had subsequently undergone coronary artery bypass surgery because of triple-vessel coronary artery disease. Intravenous treatment with ajmalin terminated the tachycardia and revealed preexcited QRS complexes compatible with the presence of a left-sided atrioventricular accessory pathway. An antidromic atrioventricular reentrant tachycardia (identical to the clinical tachycardia) was induced during an electrophysiologic study. In conclusion, there are several causes of broad-complex tachycardia, even in patients with previous myocardial infarction, and, where doubt exists, electrophysiologic studies should be performed.     

First experiences with the effect of low-energy electric impulse on the atrioventricular junction in various types of paroxysmal supraventricular tachycardia

Efficient treatment of paroxysmal supraventricular reciprocal tachycardias (nodal and orthodromal) was studied in 29 patients by applying low-energy discharges (mean 2.3 +/- 0.1 kV) to the area of the atrioventricular junction. Late results of the treatment were assessed 7-22 months later. Cessation of tachycardia paroxysms was observed in 10 patients, their lower frequency (by more than 50%) was seen in 14 cases. The value of discharge energy, their numbers, relations between potential amplitudes produced by atria and His' bundle, feasibility of paroxysm induction, presence or absence of bundle-branch block were not prognostic criteria for efficiency of this mode of therapy in the present investigation. In the authors' opinion, the method is promising in the treatment of atrioventricular nodal and orthodromal paroxysmal tachycardias.     

房室结内折返性心动过速慢径路消融中房室传导阻滞的预防

目的 探讨房室结内折返性心动过速(AVNRT)慢径路消融中房室传导阻滞的预防措施。方法 72例AVNRT患者从小功率(5W)开始放电，逐步增加放电功率，根据放电时的反应，及时改换安全的放电部位；放电过程中不苛求房室交接区心律从有到无的规律；慢径路改良，不苟求慢径路消失，以不诱发心动过速为宗旨。结果 72例慢径路消融均成功，无一例发生房室传导阻滞的并发症，无一例远期复发。结论 从小功率开始放电，慢径路改良等措施，可有效预防房室传导阻滞，且对远期复发无影响。     

Comparison of adenosine effects on atrioventricular node reentry and atrioventricular reciprocating tachycardias

Background: Adenosine is an established first line therapy for the treatment of narrow complex tachycardias. The two most common etiologies of paroxysmal supraventricular tachycardia (SVT) are atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT). Hypothesis: We postulated that adenosine might have different effects on the termination of AVNRT vs. AVRT, and that these differences might assist in the noninvasive differentiation between these diagnoses. Methods: Fifty-nine patients referred for the diagnosis and treatment of SVT were included in the study. All patients had SVT induced during electrophysiology testing, and each patient received adenosine during SVT. The adenosine dose, time to tachycardia termination, and site of tachycardia termination were recorded. Seventeen patients required isoproterenol administration to initiate SVT. This subset of patients was compared with those not requiring isoproterenol. Results: There was no statistically significant difference in the adenosine dose or time to tachycardia termination when comparing patients with AVNRT with those with AVRT. All patients with AVNRT had termination of tachycardia in the antegrade direction with final activation in the atria. Patients requiring isoproterenol for tachycardia initiation experienced tachycardia termination significantly faster than those not requiring isoproterenol, although there was no difference in the dose of adenosine required for termination. Conclusion: These data demonstrate that patients with dual AV node physiology and AVNRT do not have altered sensitivity to adenosine compared with patients with AVRT and normal AV nodes. Further investigation will be required to determine the clinical utility of the significantly shorter time to tachycardia termination for patients receiving isoproterenol.     

伴连续性房室结功能曲线的房室结折返性心动过速的电生理分析

目的：探讨无房室结双径路特性的房室结折返性心动过速(AVNRT)的电生理特点。方法：所有心动过速患射频消融前常规行心内电生理检查。结果：845例射频病人中325例为AVNRT，其中有21例患房室结功能曲线呈连续性，其电生理特征：希氏束图上心房回波(A)先出现，A波落在室波升支或其前，希氏柬不应期内刺激心室，不能提前夺获心房，射频消融后心房刺激时AHmax明显缩短。结论：伴连续性房室结功能曲线的AVNRT患心房刺激不表现房室结双径路的电生理特性，其消融终点初步定为：心房心室S1S1、S1S2刺激不诱发AVNRT；无AHvH传导曲线跳跃；房室结前传不应期明显缩短。     

房室结双径路合并房室旁路的折返性心动过速及射频消融治疗

目的本研究旨在探讨房室结双径路（ＤＡＶＮＰ）合并房室旁路（ＡＰ）的电生理特征和射频消融要求。方法对２１８例阵发性室上性心动过速（ＰＳＶＴ）进行电生理检查，观察ＰＳＶＴ的前传和逆传途径，然后对ＡＰ或房室结慢径（ＳＰ）进行消融治疗。结果２１８例ＰＳＶＴ中检出ＤＡＶＮＰ＋ＡＰ１０例，检出率为４．６％。其中ＳＰ前传、ＡＰ逆传（ＳＰ－ＡＰ折返）４例，快径（ＦＰ）前传、ＡＰ逆传（ＦＰ－ＡＰ折返）１例，ＳＰ－ＡＰ折返并ＦＰ－ＡＰ折返或ＳＰ／ＦＰ交替前传折返４例，ＳＰ前传、ＦＰ逆传（ＡＰ旁观）１例。１０例患者均作ＡＰ消融，诱发房室结折返性心动过速（ＡＶＮＲＴ）的３例加作ＳＰ消融，术后随访均无复发。结论ＤＡＶＮＰ合并ＡＰ者ＡＰ均作为逆传途径，阻断ＡＰ是消融关键；ＡＰ旁观者也应作ＡＰ消融；仅有ＡＨ跳跃延长者不必接受房室结改良；ＡＰ消融者应作ＤＡＶＮＰ电生理检查。     

射频消融治疗具有快频率依赖性室房逆传特性的旁道

目的报道具有快频率依赖性室房逆传特性的房室旁道电生理检查及射频消融结果。方法4例患者,均有阵发性心悸史,且发作时心电图均显示为窄QRS波心动过速,按常规方法接受心脏电生理检查及射频消融治疗。结果4例均证实存在旁道的快频率依赖性室房逆传,且均诱发了房室折返性心动过速,室房逆传最早激动部位均为左房。于快频率心室刺激下标测消融靶点,消融均获成功。结论旁道的快频率依赖性传导为一种少见电生理现象,可伴发房室折返性心动过速。     

'Dual atrioventricular nodal pathways" in patients with Wolff-Parkinson-White syndrome.

'Dual atrioventricular nodal pathways" were found in five patients who also had the Wolff-Parkinson-White syndrome. All five patients had a re-entrant tachycardia that used the atrioventricular node for conduction in the anterograde direction and an accessory atrioventricular pathway for conduction in the retrograde direction. One of the patients also had a re-entrant tachycardia that originated within the atrium or the atrioventricular node. Dual atrioventricular nodal pathways were identified in three of the five patients during their first electrophysiological study because the effective refractory period of the accessory atrioventricular pathway in the anterograde direction was longer than the effective refractory period of the fast atrioventricular nodal pathway. In the other two patients the dual atrioventricular nodal pathways were found only after operative division of an accessory atrioventricular pathway. Re-entrant tachycardia that uses an accessory pathway may be cured by operative division of the accessory pathway. Tachycardia resulting from re-entry within the atrioventricular node cannot be cured by an operation unless the normal conduction system is divided and a permanent pacemaker implanted. These five patients indicate the importance of determining the aetiology of tachycardia by studying the tachycardia itself and not only the type of atrioventricular conduction present.     

Conduction abnormalities detected by electrophysiologic testing following repair of ostium primum atrioventricular septal defect

Since 1983 we have performed electrophysiologic studies in 6 patients who had previously undergone repair of an ostium primum atrioventricular septal defect. Information obtained during electrophysiologic studies was crucial in guiding appropriate pacemaker therapy in these patients. As judged from the resting electrocardiogram, sinus or junctional bradycardia was present in 3/6, atrial flutter / fibrillation in 2/6, and paced rhythm in 2 patients who had had ventricular pacemakers implanted for complete atrioventricular block. During maximal exercise testing 4 patients had reduced heart rates; 2 had sudden drops in heart rate at 1 min postexercise; 1 patient had exercise induced ventricular bigeminy; and 1 patient with atrial flutter and 2: 1-4: 1 block at rest developed 1: 1 conduction during Stage II with an effective ventricular rate of 220/min. During electrophysiologic studies, the maximum corrected sinus node recovery time was abnormal in five of the six, ranging from 410 to 5630 msec. There was no spontaneous atrial rhythm in the other patient. Complete atrioventricular block was present in 2 patients while the atrioventricular Wenckebach phenomenon occurred abnormally at atrial pacing cycle lengths greater than 450 msec in 2 others. Supraventricular tachycardia or atrial flutter/fibrillation, was either spontaneous or induced in 2/6 patients, while ventricular tachycardia was induced in 1/3 patients who underwent programmed ventricular stimulation. Electrophysiologic studies were important in unmasking severe sinus node disease in 3 patients and atrioventricular node disease in 2. We therefore recommend that electrophysiologic studies be strongly considered as part of the evaluation of conduction abnormalities following repair of ostium primum atrioventricular septal defect.     

Electrophysiological action of bepridil on atrioventricular accessory pathways

The electrophysiologic properties of bepridil, a calcium channel blocker with additional effects on fast response tissues, were investigated in 10 patients with atrioventricular accessory pathways. Seven patients had Wolff-Parkinson-White syndrome, and three had concealed atrioventricular pre-excitation. A dose of 4 mg/kg was administered intravenously over five minutes. Bepridil increased the AH interval and the functional refractory period of the atrioventricular node. The effective refractory periods of the right atrium and right ventricle were also increased. Bepridil prolonged refractoriness in the accessory pathway both in the anterograde and retrograde direction. After bepridil administration it was impossible to induce reciprocating tachycardia electrically in two patients because of conduction block in the normal pathway. On the other hand, the zone of tachycardia was often increased after bepridil. Nevertheless, the heart rate during tachycardia was slowed by depression of conduction in both the normal and accessory pathways. The findings of this study provide a basis for the antiarrhythmic action of bepridil in patients with atrioventricular accessory pathways.