Electrophysiologic effects of epinephrine in humans

The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.     

Effect of verapamil studied by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia.

Atrioventricular (AV) conduction, ventriculoatrial (VA) conduction, and the mechanism of tachycardia, were studied by programmed electrical stimulation before and after the administration of verapamil, in 10 patients with paroxysmal re-entrant supraventricular tachycardia. In 7 patients the tachycardia circuit was confined to the AV node. In 3 patients an accessory pathway conducting only in the ventriculoatrial direction was used during tachycardia. When administered intravenously during tachycardia, verapamil terminated the arrhythmia in 9 patients. Verapamil lengthened the effective and the functional refractory period of the AV node and the AV nodal transmission time in all patients in whom this could be studied. As a result of these changes, it was not possible to initiate tachycardia in 3 patients. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in 5 patients, and increased in 2 patients. In 6 of these 7 patients the tachycardia zone shifted to longer premature beat intervals. Verapamil resulted in slowing of the heart rate during tachycardia. Apart from slowing in heart rate during tachycardia and termination of tachycardia after intravenous verapamil, the 3 patients with an accessory pathway showed no beneficial effect of verapamil on the mechanism of initiation of tachycardia. Five patients were restudied after 2 to 3 weeks of oral administration of verapamil. Though less, effects were similar to those obtained after intravenous administration.     

Electrophysiological effects of lorcainide, a new antiarrhythmic drug. Observations in patients with and without pre-excitation.

The electrophysiological effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 23 patients with atrioventricular conduction disturbances (four patients), ventricular tachycardia (five patients), and accessory atrioventricular pathway (14 patients). Lorcainide did not affect the refractory period of the atrium, ventricle, atrioventricular node, or the AH interval. It lengthened the duration of the HV interval, the refractory period of the accessory pathway, and the width of the QRS complex. The drug terminated ventricular tachycardia in four of five patients. It is concluded that the drug may be of potential benefit in patients with ventricular tachycardia or accessory atrioventricular pathways (especially those with a short refractory period). Lorcainide is contraindicated in patients with bundle-branch block and prolonged HV interval.     

Electrophysiologic and antiarrhythmic actions of bepridil : Comparison with verapamil and ajmaline for atrioventricular reentrant tachycardia

Bepridil (2 mg/kg intravenously) was given to 20 patients with atrioventricular (AV) reentrant tachycardia and its effects were compared with those of verapamil (0.15 mg/kg intravenously) in 8 patients and ajmaline (0.75 mg/kg intravenously) in 12. After baseline electrophysiologic measurements, the drugs were given during sustained AV reentrant tachycardia (8 patients had dual AV nodal pathways and 12 had an accessory AV pathway). Verapamil terminated AV reentrant tachycardia in 7 patients and bepridil terminated it in 6. In 8 of the patients who received ajmaline, AV reentrant tachycardia was terminated and in 6 of this group bepridil did so. Bepridil was more successful in terminating AV reentrant tachycardia in those with dual AV nodal pathways than in those with an accessory AV pathway. Bepridil slowed sinus rate by 10% (p <0.0001), whereas verapamil did not change it significantly. Both verapamil and bepridil administration prolonged AV nodal conduction (39% and 44%, respectively), lengthened AV nodal effective refractory period (18% and 17% respectively) and increased the Wenckebach cycle length of the AV node (24% and 25%, respectively) to a significant degree (p <0.05). Bepridil also lengthened atrial and ventricular effective refractory periods (p <0.01) and QT interval (p <0.0001) in the group as a whole; in those receiving ajmaline and bepridil only atrial refractoriness was significantly altered (p <0.05). After treatment for 3 to 5 days with oral bepridil, 19 patients underwent repeat study. There was further slowing in sinus rate and prolongation in both atrial effective refractory period and QT interval; the AV Wenckebach cycle length had returned toward the control level, but was still significantly increased (p <0.01). In the 17 cases in whom reinducibility of AV reentry tachycardla was tested, 7 had no inducible arrhythmia, 6 had non-sustained AV reentrant tachycardia and 4 had sustained but slower tachycardia. Thus, bepridil has both AV nodal and myocardial electrophysiologic actions which suggest a useful role in the treatment and prophylaxis of supraventricular arrhythmias.     

Monophasic action potentials in a patient with multiform ventricular tachycardia without QT prolongation.

A 41 year old woman had multiform ventricular tachycardia without QT prolongation. Monophasic action potentials were recorded from the right ventricle during the attacks of multiform ventricular tachycardia and effective refractory periods were examined at the same sites. There was no abnormal hump to suggest early afterdepolarisation in the monophasic action potentials, but there was dispersion of the effective refractory period in the right ventricle (80 ms). Stimulation from the right ventricular apex, where the effective refractory period was shortest, reproducibly induced multiform ventricular tachycardia. Two weeks after admission, when her condition was stable, multiform ventricular tachycardia could not be induced and the dispersion of the effective refractory period in the right ventricle was 20 ms.     

Effect of amiodarone in the Wolff-Parkinson-White syndrome

The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients. All 15 patients had circus movement tachycardias; 7 also had atrial fibrillation. Programmed electrical stimulation was performed before and after 14 days of oral administration of amiodarone. The effective refractory period of the accessory pathway lengthened in an atrioventricular direction in all patients and in a ventriculoatrial direction in eight patients. The effective refractory period of the atrium and ventricle lengthened in 14 and 12 patients, respectively. After administration of amiodarone, circus movement tachycardia could no longer be initiated in five patients. The zone of tachycardia narrowed in four patients, did not change in two and increased in seven. The effect of amiodarone on initiation of circus movement tachycardia could be related to differences in effect of the drug and in the mechanism of tachycardia in individual patients. In all patients in whom tachycardias could still be initiated after treatment with amiodarone the heart rate during tachycardia was slower than before treatment. This slowing was caused by a decrease in conduction velocity of the circulatory wave in different parts of the tachycardia circuit. The effect of amiodarone in prolonging the refractory period of the accessory pathway makes this drug especially useful in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.     

Refractoriness as a determinant of tachycardia inducibility in the right ventricle

The use of more than one right ventricular site for programmed electrical stimulation has been reported to increase the number of patients in whom ventricular tachycardia can be provoked. To determine a possible reason for these observations, programmed ventricular tachycardia studies were evaluated in 316 patients (185 men and 131 women) with a mean age of 63 +/- 7 years who presented with ventricular tachycardia or cardiac arrest. The underlying cardiac disease was atherosclerosis (81%), cardiomyopathy (15%), valvular heart disease (3%), and miscellaneous conditions (1%). Programmed electrical stimulation studies employed a six-beat pacing train, at a cycle length of 500 msec with the introduction of one to three premature stimuli at twice diastolic threshold at the right ventricular apex. If ventricular tachycardia at the right ventricular apex could not be provoked in a patient, the study was repeated at the right ventricular outflow tract. A total of 36 patients were studied at the right ventricular outflow tract. Eleven (31%) were provoked into ventricular tachycardia, while 25 (69%) were not. No difference existed between the QRS, QT, and QTc intervals between those having ventricular tachycardia provoked at the outflow tract compared to those without inducible tachycardia at the right ventricular outflow tract. The effective refractory period was 280 +/- 5 msec at the right ventricular outflow tract in those patients not inducible, and 226 +/- 4 msec in those inducible (p less than 0.05). We defined the change in ventricular refractory period as the difference in the effective refractory period at the right ventricular outflow tract minus the effective refractory period at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.     

Therapy of ventricular tachycardia

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

婴幼儿无休止室性心动过速临床分析

目的:探讨婴幼儿无休止特发性室性心动过速的临床特点及诊治方法。方法:对2005年7月至2013年8月,在北京儿童医院住院确诊为婴幼儿无休止特发性室性心动过速的18例患儿的临床表现、实验室检查及治疗方法,进行回顾性分析。结果:婴幼儿无休止特发性室性心动过速男女比例2.6∶1,平均年龄13个月,就诊形式以烦躁哭闹为表现的6例,呕吐尿少的3例,发现心跳快的8例,伴有阿-斯发作(adams-stokes综合征)即心源性脑缺血综合征的4例,肺炎时发现心脏大的1例。心电图表现为持续的室性心动过速,速率160~300次/min,QRS时限为0.08~0.12s,V1以右束支阻滞形态的15例,来源于左心室,V1以左束支阻滞形态的3例,来源于右心室。心脏彩超4例正常,7例心脏左心室扩大,7例左心室中至重度扩大,心脏收缩功能减低,提示为心动过速心肌病,左心室型的盐酸维拉帕米缓释片应用12例,7例有效,5例无效,盐酸普罗帕酮片应用9例,3例有效,胺碘酮应用5例,1例有效。右心室型的应用酒石酸美托洛尔片3例,2例有效,胺碘酮应用1例,无效。洋地黄、三磷酸腺苷、利多卡因及艾斯洛尔无效,电击复律6例(20次),2例(4次)有效。4例行射频消融,室性心动过速消失,均无复发。结论:婴幼儿无休止特发性室性心动过速临床症状轻重不一,由于速率快,持续时间长易出现心动过速心肌病,并发心力衰竭、心源性休克及心脏猝死。药物治疗难度大,准确的分型有利于准确用药。射频消融为较好的根治方法。     

Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation

In 108 patients with reproducible initiation of ventricular tachycardia by programmed ventricular stimulation, the ventricular tachycardia was initiated only by left ventricular stimulation in 12 (11 percent). Programmed ventricular stimulation included single and double extrastimuli at three cycle lengths and bursts of rapid pacing to cycle lengths of 250 ms. Clinical, electrocardiographic, angiographic, hemodynamic and electrophysiologic data were available in 74 of 96 patients with ventricular tachycardia initiated by right ventricular stimulation (Group A) and in all 12 patients with ventricular tachycardia initiated only by left ventricular stimulation (Group B). There were no significant differences between Groups A and B in clinical characteristics, hemodynamics or presence and site of infarction or aneurysm. Comparison of electrophysiologic variables revealed no significant differences between Groups A and B in mean A-H interval (92 ± 22 versus 89 ± 15 ms, respectively), H-V interval (59 ± 15 versus 59 ± 15 ms) or right ventricular (241 ± 38 versus 260 ± 40 ms) or left ventricular (232 ± 28 versus 251 ± 42 ms) effective refractory period. Ventricular tachycardia with right bundle branch block and superior axis was more prevalent in Group B (92 percent versus 31 percent, p <0.001) but was observed in 32 patients in Group A.It is concluded that 11 percent of patients with clinically documented sustained ventricular tachycardia will require left ventricular programmed stimulation to reproducibly initiate the tachycardia. No clinical, anatomic, electrocardiographic or electrophysiologic features can predict whether left ventricular programmed stimulation will be required. Because initiation of ventricular tachycardia by programmed ventricular stimulation has important prognostic and therapeutic implications in such patients, stimulation should be performed from the left ventricle when the tachycardia is not initiated by stimulation from the right ventricle.     

Anti-arrhythmia and pro-arrhythmia effects of oral cibenzoline therapy in sustained ventricular tachycardia]

The efficacy and safety of the new class-I antiarrhythmic drug cibenzoline was assessed in 12 patients with spontaneous and inducible ventricular tachycardia. Programmed ventricular stimulation, 24-h ambulatory electrocardiogram (ECG), and continuous ECG monitoring were performed without antiarrhythmic drugs and after oral administration of 254 +/- 80 mg of the substance. Oral cibenzoline suppressed the induction of tachycardia in only one patient. Induction of tachycardia was more difficult in two patients, unchanged in four patients, and easier in two patients. Cycle length of induced tachycardia and QT-interval corrected for frequency were not changed significantly; effective refractory period of the right ventricle was prolonged. Twenty-four hours of ambulatory monitoring during cibenzoline treatment (n = 9) showed no significant increase in the frequency of ventricular premature complexes. However, spontaneous sustained ventricular tachycardia developed in three patients after initiation of cibenzoline treatment. In two patients, termination of induced ventricular tachycardia was significantly more difficult under cibenzoline; several DC-shocks were required to terminate the tachycardia. Thus, the use of oral cibenzoline in patients with sustained spontaneous and inducible ventricular tachycardias showed a low antiarrhythmic efficacy at programmed stimulation and a high incidence of spontaneous ventricular tachycardia.     

Sotalol in supraventricular tachycardia. Electrophysiologic measurements in Wolff-Parkinson-White syndrome and AV node re-entry tachycardia

The electrophysiologic effects of sotalol were studied in 11 patients with Wolff-Parkinson-White syndrome and 9 patients with AV nodal reentrant tachycardia. Electrophysiologic studies were performed before and after intravenous infusion of 80 mg sotalol over a period of 5 minutes. Sotalol prolonged the effective refractory period of the right atrium and the right ventricle. Both AV node and accessory pathway conduction were depressed by sotalol in antegrade and retrograde directions. Induction of reentrant tachycardia was prevented in 6 of 18 patients. The rate of reentrant tachycardia decreased from 182 +/- 29/min to 153 +/- 14/min (p less than 0.01) and the ventricular rate during atrial fibrillation from 148 +/- 14/min to 112 +/- 12/min (p less than 0.05). Sotalol exhibited a depressant effect on all parts of the reentrant circuit: atrium, ventricle, AV node, and accessory pathway. Thus, sotalol is effective in the therapy of patients with recurrent supraventricular tachycardias.     

Idiopathic recurrent sustained ventricular tachycardia in children and adolescents

The electrophysiologic characteristics of recurrent sustained ventricular tachycardia were studied in seven pediatrie patients. The mechanisms of the ventricular tachycardia were evaluated using programmed electrical stimulation. Ventricular tachycardia could be reproducibly initiated in two patients and terminated in one patient in the basal state. It could be initiated in one additional patient and terminated in two additional patients after administration of a type IB drug. In four patients, ventricular tachycardia could not be initiated or terminated by programmed electrical stimulation. The site of origin of the ventricular tachycardia determined by catheter endocardial mapping was the right ventricular outflow tract in four patients, the interventricular septum in two patients and the inferior left ventricle in one patient. The ventricular tachycardia more frequently had an automatic than a reentrant mechanism, and originated more often in the right than in the left ventricle; it was not frequently associated with structural heart disease in this group of patients.     

Electrophysiologic effects of penticainide in patients with supraventricular tachycardia

The electrophysiologic effects of the new class-I antiarrhythmic drug pentisomide were investigated after intravenous (5 mg/kg) application in nine patients with atrioventricular nodal reentrant tachycardia and six patients with atrioventricular tachycardia. Pentisomide did not change sinus cycle length, effective refractory period of the right ventricle (ERP-RV), the AV-node (ERP-AVN) and QT interval. Intranodal (AH-interval) and infranodal conduction time (HV-interval), effective refractory period of the right atrium (ERP-A), QRS duration, antegrade effective refractory period of the accessory pathway (ERP-Kent), ventricular cycle length during atrial fibrillation and tachycardia cycle length were significantly (P less than 0.05) increased. Intravenous pentisomide prevented induction of the tachycardia in 5/9 patients with atrioventricular nodal tachycardia and in 2/6 patients with atrioventricular tachycardia. The electrophysiologic properties of pentisomide indicate that it might be a useful drug in the treatment of supraventricular tachycardia.     

Surgery for ventricular tachycardia associated with right ventricular dysplasia: disarticulation of right ventricle in 9 of 10 cases.

Ten patients (nine men, one woman; mean age 39 years) with arrhythmogenic right ventricular dysplasia underwent surgery to control life-threatening drug refractory ventricular arrhythmias. All had ventricular tachycardia causing syncope and six had a history of cardiac arrest. In all a minimum of three antiarrhythmic drugs (mean five) had been ineffective. At operation, the right ventricle was grossly diseased in all patients. Ventricular tachycardias were induced and mapped intraoperatively in all patients. The surgical plan was to ablate the arrhythmogenic focus if it was less than 4 cm2; one patient was so managed. Of the remaining nine, four underwent partial (approximately 40% of the right ventricular free wall) and five underwent total right ventricular disarticulation. All survived the operation and are alive at a mean follow-up interval of 24 months (range 5 to 67). Two patients developed new sustained ventricular tachycardias. These were well tolerated and, unlike the original arrhythmias, were easily controlled by drug treatment. All patients who underwent right ventricular disarticulation manifested signs of right heart failure in the early postoperative period, but these lessened progressively with the development of systolic septal movement into the right ventricular cavity. All 10 patients are in New York Heart Association class I or II at last review. In selected patients with arrhythmogenic right ventricular dysplasia, surgery offers a curative treatment for ventricular tachycardia and should be considered for patients whose arrhythmias are life-threatening and refractory to drug treatment.     

Effect of digitalis in patients with paroxysmal atrioventricular nodal tachycardia.

Atrioventricular (A-V) conduction, ventriculo-atrial conduction and mechanism of tachycardia were studied by programmed electrical stimulation before and after the administration of ouabain in 15 patients suffering from paroxysmal supraventricular re-entrant tachycardia. In 13 patients the tachycardia circuit was confined to the A-V node. In two patients the stimulation study showed that an accessory pathway was used in a ventriculo-atrial direction during tachycardia. Ouabain lengthened the effective and functional refractory period of the A-V node and A-V nodal transmission time in all patients in whom this could be studied. Only six patients showed lengthening in ventriculo-atrial conduction time or refractory period of the ventriculo-atrial conduction system. In seven patients no tachycardia could be initiated after ouabain. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in five patients, showed no change in two patients, and increased in one patient. In these eight patients the tachycardia zone shifted to longer premature beat intervals. Ouabain resulted in slowing of cardiac rate during tachycardia. Both patients who used an accessory pathway during tachycardia showed no change in width of their tachycardia zone following ouabain administration. Seven patients were restudied two weeks after chronic oral administration of digoxin. The results were similar to those obtained following ouabain administration. This indicates that in patients suffering from paroxysmal A-V nodal tachycardia the effect of chronic oral digoxin administration can be predicted from the study of the effect of ouabain during programmed stimulation of the heart.     

Electrophysiologic and clinical factors influencing response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia

Clinical and electrophysiologic data from 51 consecutive patients with sustained monomorphic ventricular tachycardia inducible during programmed ventricular stimulation were evaluated to determine what variables predict the response to intravenous class IA antiarrhythmic agents. All patients received acute drug testing in the electrophysiologic laboratory with either intravenous procainamide or intravenous quinidine. Ventricular tachycardia suppression was achieved in 9 out of 51 patients (18%). The age, gender, left ventricular ejection fraction, baseline right ventricular effective refractory period, baseline HV interval, and baseline ventricular tachycardia cycle length were not predictive of ventricular tachycardia suppression with intravenous procainamide or quinidine during programmed ventricular stimulation. The degree of prolongation of the right ventricular effective refractory period after drug administration did not predict success or failure to suppress inducible ventricular tachycardia. The degree of prolongation of the HV interval was also not predictive. In addition, the degree of prolongation of the right ventricular effective refractory period or the HV interval did not predict the change in the ventricular tachycardia cycle length after drug administration in patients who remained inducible. These data indicate that the response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia cannot be predicted on the basis of various clinical and electrophysiologic parameters.     

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.     

Radiofrequency ablation of idiopathic left ventricular tachycardia in children

INTRODUCTION: Nowadays radiofrequency catheter ablation is an alternative to medical treatment in adult patients with idiopathic left ventricular tachycardia. AIM: To asses indications, results and long term follow-up of using this technique in children. : Radiofrequency catheter ablation was performed in five consecutive patients without structural heart disease, mean age 8.6+/-7.1 years (range, 1.3 to 17) and suffering from resistance to medical treatment left ventricular tachycardia (2.4+/-0.9 antiarrhythmic drugs per patient). Palpitations and syncope were the clinical manifestations in four patients while congestive heart failure in the other one. Six types of tachycardia were identified in the five-patient group. All of them responded to intravenous verapamil. There were 3 incessant tachycardias and the other three were paroxysmal ones. The ablation site was selected using activation mapping during tachycardia and pace-mapping. The Tachycardia cycle length was 275+/-123 ms and showed right bundle branch block with superior axis (left in 4 and right in 2 cases). The ablation target was located in the mid-septal region of the left ventricle in 3 cases, in the apical and inferior septal region in 2 other cases and in the anterior free wall in the other one. Local activation times preceded in 33+/-13 ms at QRS beginning and with a 12/12 agreement pattern in 5 cases and 9/12 in 1, in whom ablation was unsuccessful. At follow-up, the 4 patients with effective ablation have been tachycardia-free for 35.8+/-17 months. CONCLUSIONS: Radiofrequency catheter ablation is a useful method of treatment in children with idiopathic left ventricular tachycardia, including those under two years old.