Electrophysiologic effects and clinical efficacy of flecainide in children with recurrent paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous flecainide were evaluated in 16 patients aged 9 +/- 4 years: 15 with recurrent paroxysmal supraventricular tachycardia (SVT) and 1 with overt accessory pathway and history of syncope. Eleven patients had an accessory pathway; it was concealed in 2, overt in 9 and in 10 of these patients an orthodromic atrioventricular reentrant tachycardia was induced. Five patients without accessory pathway had an atrioventricular nodal reentrant tachycardia. After intravenous flecainide (1.5 mg/kg) the effective refractory period of the atrium and ventricle increased significantly; the anterograde and retrograde effective refractory periods of the atrioventricular node did not. Flecainide blocked retrograde conduction in the accessory pathway in 4 patients (effective refractory period 245 +/- 41 ms) and anterograde conduction in 8 of 9 patients (effective refractory period 284 +/- 57 ms). The mean cycle length of orthodromic reciprocating tachycardia and atrioventricular nodal reentrant tachycardia increased significantly. After flecainide tachycardia was noninducible in 6 patients with orthodromic reciprocating tachycardia and in 1 with atrioventricular nodal reentrant tachycardia. It was inducible but nonsustained (less than or equal to 30 seconds) in 1 patient with orthodromic reciprocating tachycardia and in 3 with atrioventricular nodal reentrant tachycardia. Fifteen patients continued oral flecainide treatment for 19 +/- 11 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical electrophysiologic effects of lorcainide in patients and its effect on the conduction of accessory pathway in Wolff-Parkinson-White syndrome

The electrophysiologic effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 20 patients with and without Wolff-Parkinson-White (WPW) syndromes. Lorcainide shortened the sinus cycle length from 721.0 +/- 125.9 to 649.5 +/- 100.1 ms (P less than 0.001), but did not influence sinus node function and AV node conduction and refractoriness, slightly increased atrial effective period (ERP) (P less than 0.02) and did not change ventricular ERP (P less than 0.2), obviously lengthened atrial conduction time, H, H-V interval and the width of V wave. Lorcainide caused complete antegrade block of the accessory pathway (AP) in six of 9 WPW patients and resulted in exclusive conduction over the AV nodal. His conduction in two patients with atrial flutter. It also prolonged the retrograde conduction time and refractoriness of AP, and prevented initiation of orthodromic atrioventricular tachycardia (O-AVRT) in six of 12 patients by blocking of the retrograde conduction of the AP, increased the cycle length of tachycardia from 321.7 +/- 43.6 to 361.7 +/- 54.9 ms (P less than 0.005) by marked prolongation of retrograde AP conduction time in 6 patients in whom O-AVRT could still be induced. It is concluded that intravenous lorcainide does not affect sinus node and AV node function, slightly influences atrial and ventricular refractoriness, obviously suppresses atrial, His bundle and intraventricular conduction, and is an effective antiarrhythmic drug for patients with WPW by blocking both the antegrade and retrograde conduction of the AP.     

Cibenzoline: electrophysiologic effects of a new class I anti-arrhythmia agents in supraventricular tachycardia

Cibenzoline, an imidazoline derivate, is a new class 1 antiarrhythmic agent. The electrophysiologic effects and antiarrhythmic properties of cibenzoline (100 mg i.v.) were evaluated in 22 patients with paroxysmal supraventricular tachycardia: 12x Wolff-Parkinson-White Syndrome, 9x AV nodal reentrant tachycardia, 1x atrial tachycardia. Cibenzoline shortened the sinus cycle length from 742 +/- 103 ms to 661 +/- 87 ms (p less than 0.001) and the sinus node recovery time from 1026 +/- 106 ms to 926 +/- 135 ms (p less than 0.001). The substance lengthened the AH interval from 93 +/- 19 ms to 112 +/- 24 ms (p less than 0.001) and the HV interval from 42 +/- 12 ms to 61 +/- 14 ms (p less than 0.001). The effective refractory periods of the atrium and right ventricle did not change significantly, but the effective refractory period of the AV node in antegrade (269 +/- 42 ms vs 278 +/- 46 ms; p less than 0.05) and retrograde direction (281 +/- 57 ms vs 413 +/- 124 ms; p less than 0.001) increased markedly. Cibenzoline prolonged the effective refractory period of the accessory pathway in retrograde direction from 263 +/- 41 ms to 428 +/- 101 ms (p less than 0.001). The effective refractory period of the antegrade accessory pathway did not change. During atrial stimulation inducibility of the reentrant tachycardia was suppressed in 14 of 22 patients and the inducibility of atrial fibrillation in 7 of 12 patients. The RR interval of the reentrant tachycardia was prolonged from 353 +/- 57 ms to 420 +/- 57 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects of flecainide acetate on sinus node function, anomalous atrioventricular connections, and pacemaker thresholds

The acute electrophysiologic effects of i.v. flecainide acetate (2 mg/kg body weight) were assessed in 71 patients undergoing electrophysiologic study. Ten patients underwent investigation for sinus node dysfunction. Sinus cycle length shortened slightly, from 980 +/- 292 to 931 +/- 276 ms (p less than 0.01). Uncorrected or corrected sinus node recovery times or sinoatrial conduction time (according to the methods of Strauss and Narula) did not change in 6 patients with normal sinus node function and in 3 of 4 patients with abnormal sinus node function at rest. In the remaining patient maximal sinus node recovery time increased from a value at rest of 5,185 ms to 23,460 ms after flecainide. In the same patient sinoatrial conduction times at rest increased from 159 ms (Strauss method) and 143 ms (Narula method) to 1,398 and 1,455 ms, respectively, after flecainide. Thirty-three patients underwent electrophysiologic evaluation of anomalous atrioventricular (AV) pathways and reentrant tachycardias. Flecainide significantly prolonged accessory AV pathway anterograde and retrograde refractoriness. Anterograde accessory pathway block occurred in 33% of patients and retrograde accessory pathway block in 44%. Flecainide was successful in the acute termination of 86% of orthodromic atrioventricular reentrant tachycardias. In 15 patients with dual AV nodal pathways, only retrograde "fast" AH pathway refractoriness was significantly increased by flecainide, which was successful in the acute termination of 88% of intra-AV nodal reentrant tachycardias. In 28 patients who underwent endocardial pacing threshold assessment before and after i.v. flecainide, the acute threshold rose by a maximum of 117%, whereas the chronic threshold rose by a maximum of 83%.(ABSTRACT TRUNCATED AT 250 WORDS)     

AV nodal reentrant tachycardia using three different AV nodal pathways

In a patient with frequent paroxysmal supraventricular tachycardia, an electrophysiologic study was performed. Although by programmed atrial stimulation only double AV nodal pathways could be documented, three distinct forms of AV nodal reentrant tachycardia could be induced. By programmed atrial stimulation a typical AV nodal reentrant tachycardia was initiated, by programmed ventricular stimulation, an AV nodal reentrant tachycardia was induced with an antegrade conduction time of 215 ms and a retrograde conduction time of 160 ms. Furthermore, a third form of tachycardia was induced with alternating cycle length due to two different antegrade conduction times, whereas retrograde conduction time was almost identical, irrespective of the antegrade conduction time. The patient received betaxolol (20 mg day-1); during a second electrophysiologic study, the tachycardia could not be induced, and it did not occur spontaneously during a follow-up period of 14 months.     

Curative surgery for atrioventricular junctional ("AV nodal") reentrant tachycardia

A new surgical approach was studied prospectively in 10 consecutive patients with atrioventricular (AV) junctional reentrant tachycardia. The aim was to abolish tachycardia yet preserve normal AV conduction. On the basis of electrophysiologic study before operation, patients were classified as type A (ventriculoatrial [VA] intervals during tachycardia less than or equal to 40 ms) (seven patients) or type B (VA intervals greater than 40 ms) (three patients). Dual AV junctional pathways were demonstrable with single extrastimulus testing in seven patients before operation. Endocardial mapping during tachycardia at surgery revealed earliest atrial activation anteromedial to the AV node in type A patients and posterior to the node in the type B patients. The perinodal atrium in the region of earliest atrial activation during tachycardia was carefully disconnected from the AV node. After operation, AV junctional reentrant tachycardia was not inducible at comprehensive electrophysiologic study in any patient, and no clinical recurrences have occurred during a follow-up period of 2 to 14 months (mean 8 +/- 4). Normal AV conduction was preserved in all cases. Anterograde slow AV junctional pathway conduction was abolished in five of seven cases. Retrograde His to atrium conduction time was prolonged in type A patients but the capacity for retrograde VA conduction remained excellent. Retrograde His to atrium conduction was interrupted or severely compromised in the type B patients. These data show that there are at least two types of AV junctional reentry. Perinodal atrium appears to be part of the reentrant circuit in human AV junctional reentry. Although the most consistent effect of surgery was on the retrograde limb of the circuit, anterograde slow pathway conduction was also modified. AV junctional reentry is surgically curable with a high success rate.     

Mechanisms and management of paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia (PSVT) is defined as a regular rapid heart beat, which initiates and terminates suddenly. PSVT may have a variety of electrophysiologic mechanisms, including atrial tachycardia, atrioventricular (AV) nodal reentry, and tachycardia involving an accessory AV connection. Atrial tachycardia may be reentrant or may be caused by abnormal automaticity or triggered activity. AV nodal reentry, in which the reentrant circuit is confined to the AV node or the region around the AV node, is the most common type of PSVT in adults. Orthodromic supraventricular tachycardia is the most frequently found tachycardia in patients with accessory AV connections. During orthodromic supraventricular tachycardia, antegrade conduction occurs via the AV node, and retrograde conduction occurs via an accessory AV connection. Other types of PSVT, including junctional tachycardia, are less common. A definitive diagnosis of the PSVT mechanism usually requires electrophysiologic testing, but clinical and electrocardiographic clues may be present. Understanding the mechanism of PSVT can alter therapy because the response to antiarrhythmic drugs may be somewhat different depending on the PSVT type. In addition, the risks and efficacy of catheter ablation for curing PSVT may differ depending on the PSVT type. A better understanding of PSVT mechanisms, which has developed over the past 20 years, has led to dramatic improvements in therapy.     

Comparison of pre- and postoperative conduction patterns in patients surgically cured of atrioventricular node reentrant tachycardia

Patients with atrioventricular (AV) node reentrant tachycardia characteristically have short and constant retrograde His-atrium conduction times (H2A2 intervals) during the introduction of ventricular extrastimuli. It has therefore been suggested that the tachycardia circuit involves retrograde conduction up an accessory pathway located in perinodal tissue. If the mechanism of surgical cure of AV node reentrant tachycardia is interruption of this accessory pathway, postoperative changes in retrograde conduction would be expected. Thirteen patients with drug-refractory AV node reentrant tachycardia underwent surgery. Preoperatively, H2A2 intervals were short and constant. During AV node reentrant tachycardia, earliest atrial activation was seen near the His bundle and was 0 to 25 ms before ventricular activation in all patients except one. Surgery consisted of dissection of right atrial septal and anterior inputs to the AV node and central fibrous body. Postoperatively, the H2A2 interval remained short and constant compared with preoperative values although it was slightly prolonged (74 +/- 18 versus 61 +/- 21 ms, p less than 0.005). Twelve of the 13 patients are free of tachycardia after 28 +/- 13 months and no patient has had evidence of AV node block. Thus, surgical cure of AV node reentrant tachycardia is highly successful; however, there is no reason to postulate an accessory pathway or use of perinodal tissue as part of the tachycardia circuit and the mechanism of surgical success remains obscure.     

Clinical, electrophysiologic and antiarrhythmic efficacy of moricizine HCl

The electrophysiologic effects and antiarrhythmic efficacy of moricizine HCl (1.5 to 2.0 mg/kg intravenously, and 600 to 800 mg orally/24 hours) were studied using electrophysiologic testing, ambulatory electrocardiographic monitoring, exercise stress testing and transesophageal stimulation of the left atrium. Moricizine HCl had no significant effects on the sinus node in patients with normal nodal function and did not depress sinoatrial conduction time even in patients with serious node dysfunction. Moricizine HCl significantly lengthened the following intervals: PA (32 +/- 5 to 40 +/- 5 ms), AH (82 +/- 13 to 92 +/- 12 ms), HV (45 +/- 12 to 50 +/- 12 ms), paced cycle length 1:1 atrioventricular node conduction (340 +/- 14 to 352 +/- 14 ms) and paced cycle length 1:1 ventriculoatrial conduction (300 +/- 14 to 400 +/- 13 ms). The refractory periods of atrium, atrioventricular node and ventricular myocardium did not change significantly, and there was no alteration of the QRS or QT intervals. The drug abolished anterograde and retrograde conduction over the accessory pathway and increased the refractory period of accessory pathway in all patients. Intravenous moricizine HCl terminated and prevented tachycardia in 72% and 68% of the patients, respectively. Oral moricizine HCl (600 to 800 mg/24 hours) prevented tachycardia in 40% of patients with a preexcitation syndrome. Intravenous moricizine HCl terminated atrioventricular nodal reentrant paroxysmal tachycardia in 66% of patients, whereas 40% responded to the oral drug. Moricizine HCl 600 to 800 mg/24 hours suppressed ventricular premature beats in 60% of patients. A similar drug, Ethacizine, had the same electrophysiologic effects as moricizine HCl but was more potent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of combined propranolol and verapamil for evaluation of surgical ablation of accessory atrioventricular connections in patients without structural heart disease

Successful surgical ablation of atrioventricular (AV) accessory connections may be confirmed during postoperative electrophysiologic testing by the absence of accessory connection conduction in both the anterograde and retrograde directions. Whereas the former may be readily apparent by examination of the surface electrocardiogram during sinus rhythm or atrial pacing, assessment of the latter may be complicated by the frequent presence of enhanced retrograde AV nodal conduction in the postoperative period. Consequently, availability of interventions that selectively affect AV nodal conduction and refractoriness without concomitant effects on accessory connections may be helpful for assessing the success of the surgical procedure. In this study the effects of combined propranolol and verapamil administration on electrophysiologic properties of the AV node and the accessory AV connection were assessed both pre- and postoperatively in 17 patients (12 men and 5 women, mean age 33 years) undergoing surgical ablation of accessory connections. Preoperatively, electrophysiologic characteristics of all but 1 of the accessory AV connections were unaffected by propranolol and verapamil administration. Postoperatively, on the other hand, propranolol and verapamil significantly prolonged both the retrograde AV node effective refractory period (baseline: 272 +/- 34 ms vs after drugs: 384 +/- 70 ms [p less than 0.0001]) and the shortest cycle length maintaining 1:1 ventriculoatrial conduction (baseline: 357 +/- 99 ms vs after drugs: 485 +/- 64 ms [p less than 0.0001]). Late postoperative electrophysiologic evaluation (7 +/- 3 weeks) revealed no evidence of residual accessory AV connection conduction, and all patients remain asymptomatic at 21 +/- 10 months follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Depressant effect on the retrograde atrioventricular nodal conduction of beta-adrenergic blockade by propranolol in humans

Propranolol is known to have a depressant effect on anterograde atrioventricular (AV) nodal conduction in normal subjects and in those with AV nodal reentrant tachycardia. Using His bundle recording and programmed ventricular stimulation, the effect of propranolol-induced beta-adrenergic blockade (1 mg/kg intravenously) on retrograde AV nodal conduction was studied in 17 patients without (group I) and nine with (group II) AV nodal reentrant tachycardia. During baseline studies the ventricular pacing cycle length that induced ventriculoatrial block was 338 +/- 60 ms (range 260 to 450 ms) in group I and 305 +/- 39 ms (range 260 to 375 ms) in group II patients (not significant). After injection of propranolol, the ventricular pacing cycle length that induced ventriculoatrial block in group I patients was 416 +/- 97 ms (range 300 to 550 ms) (P less than 0.001, compared to baseline state) in 15 patients, and complete block occurred in two patients. In group II patients ventriculoatrial block occurred at a ventricular pacing cycle length of 375 +/- 97 ms (range 260 to 510 ms) (P less than 0.02 compared to baseline value) in eight patients, and complete block occurred in one patient. Retrograde AV nodal conduction expressed as the H2A2 interval was 75 +/- 33 ms (range 35 to 150 ms) in group I and 49 +/- 16 ms (range 20 to 80 ms) in group II patients (P less than 0.05). Following the administration of propranolol, the H2A2 interval was prolonged in group I patients by 10 to 45 ms in 11 patients, no retrograde AV nodal conduction was observed in three patients, and there was no effect in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

从慢径消融发生的交界区心律试探房室结双径的本质

７６例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受房室结慢径消融术。６５例慢径阻断、９例双径存在但ＡＶＮＲＴ不能诱发、２例快径阻断。慢径阻断后，除快径的前传有效不应期（ＥＲＰ）缩短（２８７．０±７９．０ｍｓｖｓ３４４．０±８７．０ｍｓ，Ｐ＜０．０１）外，房室传导的文氏点、２１阻滞点、室房传导的１１点、快径逆传ＥＲＰ、前传和逆传功能不应期均无明显改变。共放电８４１次，其中无交界区心律的３１７次放电，无一次消融成功。６５例慢径阻断者，交界区心律减少或消失。以上结果提示快径和慢径可能是两条各具电生理特性的传导纤维。     

Epicardial mapping in patients with "nodoventricular" accessory pathways

Some patients with electrophysiologic features suggesting nodoventricular fibers have been shown to have right parietal atrioventricular (AV) accessory pathways with decremental conduction properties intraoperatively. The experience with 11 patients (7 women and 4 men, mean age +/- standard deviation 25 +/- 5 years) who had electrophysiologic features consistent with a nodoventricular pathway and who underwent operative correction was reviewed. At electrophysiologic study, all patients had absent or minimal preexcitation in sinus rhythm. During atrial pacing and extrastimulus testing, maximal preexcitation with left bundle branch block morphology developed and the AH and AV intervals progressively prolonged. Preexcited tachycardia was initiated in all patients (AV reentrant tachycardia in 10 patients and AV node reentrant tachycardia in 1 patient). At operation all patients had a right parietal accessory pathway demonstrated. Intraoperative mapping demonstrated the earliest site of ventricular activation during anterograde preexcitation to be at the midanterior right ventricle, consistent with insertion of these pathways into the right bundle branch system, in 7 patients. The ventricular insertion was at the AV groove in 4 patients, in keeping with the typical Wolff-Parkinson-White syndrome. Retrograde conduction over the pathway was not demonstrated in any patient. Two patients had evidence of a second accessory AV pathway in the left paraseptal region. Operative AV node ablation was electively performed in 2 patients without affecting preexcitation in either case. In 1 of these patients, accessory pathway conduction was temporarily abolished by ice mapping in the right anterolateral AV groove.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reappraisal of electrical cure of atrioventricular nodal reentrant tachycardia--lessons from a modified catheter ablation technique.

A modified catheter ablation technique was studied prospectively in 29 patients with atrioventricular (AV) nodal reentrant tachycardia. A His bundle electrode catheter was used for mapping and ablation. Cathodic electroshocks (100-250 J) were delivered from the distal two electrodes (connected in common) of the His bundle catheter to the site selected for ablation. The optimal ablation site recorded the earliest retrograde atrial depolarization, simultaneous or earlier than the QRS complex, with absence of a His bundle deflection during AV nodal reentrant tachycardia. One additional electrical shock was delivered if complete abolition of retrograde VA conduction persisted for more than 30 min and AV nodal reentrant tachycardia was not inducible during isoproterenol and/or atropine administration. With a cumulative energy of 323 +/- 27 J and a mean of 2.3 +/- 0.5 shocks interruption or impairment of retrograde nodal conduction was achieved. Antegrade conduction, although modified, was preserved in 27 patients, with persistence of complete AV block in 2 patients. Two of the 27 patients still need antiarrhythmic agents to control tachycardia, the other 25 patients were free of tachycardia within a mean follow-up period of 13 +/- 2 months (range 7 to 20 months). Twenty-three patients received late follow-up electrophysiological studies (3-6 months after the ablation procedures), and the AV nodal function curves were classified into 4 types. The majority of the patients (15/23) had loss of retrograde conduction. Among the 8 patients with prolongation of retrograde conduction, 4 patients still had antegrade dual AV nodal property but all without inducible tachycardia. In conclusion, preferential interruption or impairment of retrograde conduction was the major, but not the sole, mechanism of electrical cure of AV nodal reentrant tachycardia.     

Effects of standing on the induction of paroxysmal supraventricular tachycardia

To evaluate the effects of standing on induction of paroxysmal supraventricular tachycardia, electrophysiologic studies were performed in both the supine and standing positions in 22 patients with atrioventricular (AV) reciprocating tachycardia and in 11 with AV node reentrant tachycardia. AV reciprocating tachycardia was induced in 9 of the 22 patients with AV reciprocating tachycardia when they were in the supine position and in 17 when standing. The effective refractory period of the AV node markedly shortened, from 275 +/- 72 to 203 +/- 30 ms (n = 16, p less than 0.005) after standing. The effective refractory period of the accessory pathway shortened slightly, from 293 +/- 75 to 278 +/- 77 ms (n = 8, p less than 0.005), after standing. AV node reentrant tachycardia was induced in 3 of the 11 patients with AV node reentrant tachycardia when they were in the supine position and in 6 when standing. The effective refractory periods of the slow pathway and fast pathway shortened markedly, from 293 +/- 72 to 216 +/- 40 ms (n = 6, p less than 0.025) and from 416 +/- 85 to 277 +/- 50 ms (n = 10, p less than 0.005), respectively, after standing. Plasma norepinephrine levels increased during standing both in patients with AV reciprocating and in those with AV node reentrant tachycardia (n = 11, p less than 0.005, n = 8, p less than 0.005, respectively). In conclusion, standing, which is associated with increased sympathetic tone, changed the electrophysiologic properties of the reentrant circuits, facilitating induction of AV reciprocating tachycardia and AV node reentrant tachycardia.     

从慢慢型和慢快型房室结折返性心动过速电生理特性的差异分析折返环的不同

目的从慢慢型房室结折返性心动过速（AVNRT）和慢快型AVNRT的电生理特性的差异分析两型AVNRT间折返环的不同.方法在500例AVNRT患者中的59例慢慢型和60例慢快型之间,比较部分电生理特性的异同;同时在部分慢慢型和慢快型患者中应用2种方法（1）比较起搏时和心动过速时的HA间期的长度;（2）比较心动过速时心室刺激重整心动过速的不同.比较下传共径（LCP）的异同.结果慢慢型的前传慢径和逆传慢径有明显不同的传导时间;慢慢型的逆传慢径与慢快型的逆传快径有明显不同的传导时间和递减特性;和慢快型相比,2种方法均显示慢慢型有较长的LCP.结论 （1）慢慢型AVNRT中前传慢径和逆传慢径的传导时间明显不同;慢慢型较慢快型有较长的下传共径;（2）研究结果支持慢慢型AVNRT可能应用房室结的右侧后延伸和左侧后延伸分别形成心动过速的前传和逆传支而形成折返.     

Supraventricular tachycardia in patients without overt preexcitation

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.     

Electrophysiologic effects of diprafenone in supraventricular and ventricular tachycardia

The electrophysiologic effects of diprafenone were evaluated in 31 patients (9 X AV nodal reentrant tachycardia, 9 X Wolff-Parkinson-White syndrome, 4 X paroxysmal atrial fibrillation, 10 X recurrent ventricular tachycardia). Electrophysiologic studies were performed before and after intravenous infusion of 1.5 mg/kg body weight diprafenone in a period of 10 minutes. Diprafenone prolonged the mean RR interval during sinus rhythm from 690 +/- 109 ms to 789 +/- 93 ms and the maximal sinus node recovery time from 1081 +/- 216 ms to 1300 +/- 398 ms (p less than 0.001). The effective refractory period of the right atrium increased from 195 +/- 22 ms to 210 +/- 28 ms (p less than 0.01) and of the right ventricle from 220 +/- 20 ms to 235 +/- 20 ms (p less than 0.001). Diprafenone produced a prolongation of the antegrade effective refractory period of the AV node from 260 +/- 35 ms to 294 +/- 39 ms (p less than 0.01) and of the retrograde effective refractory period from 265 +/- 76 ms to 400 +/- 130 ms (p less than 0.001). The effective refractory periods of the Kent bundle increased: antegrade from 299 +/- 45 ms to 413 +/- 133 ms, retrograde from 252 +/- 33 ms to 286 +/- 169 ms (p less than 0.05). Suppression of inducibility was observed in 12 of 17 patients with supraventricular reentrant tachycardia, in 5 of 8 patients with atrial fibrillation and in 7 of 10 patients with recurrent ventricular tachycardia. The rate of supraventricular tachycardias decreased under the influence of the substance.(ABSTRACT TRUNCATED AT 250 WORDS)