Double-blind study of intravenous propafenone for paroxysmal supraventricular reentrant tachycardia

Propafenone was administered during electrophysiologic testing to determine its efficacy and safety for terminating and preventing reinduction of paroxysmal supraventricular reentrant tachycardia. Four men and 10 women (mean age 50 years, range 28 to 69) were studied. Five patients had Wolff-Parkinson-White syndrome with orthodromic atrioventricular (AV) reentrant tachycardia, three had a concealed accessory pathway with AV reentrant tachycardia and six had tachycardia due to reentry within the AV node. In the five patients with Wolff-Parkinson-White syndrome, propafenone terminated reentrant tachycardia in three (the tachycardia was reinducible in one) and had no effect in two. In the three patients with a concealed accessory pathway, propafenone terminated reentrant tachycardia in all three and prevented reinduction of the tachycardia in two. In the six patients with tachycardia due to reentry within the AV node, propafenone terminated and prevented reinduction of reentrant tachycardia. Propafenone had no effect on blood pressure, heart rate, PA interval, AV node refractoriness or rate of reentrant tachycardia. Propafenone significantly (p less than 0.05) prolonged the AH, HV, QRS and ventriculoatrial intervals and decreased the AV node Wenckebach rate. Of the nine patients receiving long-term oral propafenone therapy, eight had a reduction of at least 90% in reentrant tachycardia during a mean follow-up period of 14.5 months (range 11 to 22); all eight patients had had noninducible reentrant tachycardia after intravenous propafenone. One patient had increased frequency of reentrant tachycardia; this patient had had inducible reentrant tachycardia after intravenous propafenone. In conclusion, intravenously administered propafenone terminated reentrant tachycardia in 85% of patients and prevented reinduction in 71%, with no adverse hemodynamic effects.     

Electrophysiologic effects of intravenous propafenone

The electrophysiological effects of intravenous propafenone were studied with programmed electrical stimulation in 31 patients. Among them 29 cases with SVT (including WPW syndrome in 11, paroxysmal AF or Af in 3) and the other two cases were studied for other reasons. The results showed that: (1) Propafenone has significant effects on each part of the special conduction tissues of the heart as well as the accessory pathway. (2) It is an effective drug for treating AVNRT and the tachycardias associated with WPW syndrome. (3) There were no effects on sinus node function in all except one patient whose SNRT was prolonged to 2020 ms. (4) Neither blood pressure dropping nor other side effects were found during the studies.     

Electrophysiologic effects and clinical efficacy of propafenone in pediatric patients with paroxysmal supraventricular reentrant tachycardia

Twenty patients (pts) with recurrent paroxysmal supraventricular tachycardia (PSVT), 12 female and 8 male, aged 9.8 +/- 4.7 years, underwent an electrophysiologic study (EPS) in order to assess the effects of propafenone (Pf) administered intravenously (1.5 mg/Kg in 3'). Thirteen pts (Group I) had an accessory pathway (AP) which was concealed in 5 and overt in 8 and in 12 of them an orthodromic atrioventricular reentrant tachycardia (ORT) was induced. In 5 of 7 pts (Group II) without AP an idio-nodal reentrant tachycardia (AVNRT) was induced. After Pf the sinus cycle length decreased significantly from 668 +/- 165 to 612 +/- 109 msec and PA, AH, HV intervals and QRS duration increased significantly from 35 +/- 11, 71 +/- 18, 34 +/- 6 and 73 +/- 12 to 43 +/- 11, 87 +/- 15, 39 +/- 9 and 85 +/- 10 msec respectively. The atrial and ventricular effective refractory period (ERP) increased from 216 +/- 18 and 211 +/- 19 to 227 +/- 21 and 217 +/- 21 msec respectively. The anterograde and retrograde nodal ERP and anterograde and retrograde Wenckebach point increased from 240 +/- 48, 227 +/- 28, 278 +/- 37 and 287 +/- 38 to 270 +/- 58, 330 +/- 32, 340 +/- 59 and 408 +/- 37 msec respectively. Pf terminated the tachycardia (T) in all 12 pts of Group I after prolongation of the cycle length which increased from 299 +/- 46 to 383 +/- 69 msec.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects and efficacy of intravenous propafenone in terminating atrioventricular reentrant tachycardia in children

In pediatric patients with atrioventricular reentrant tachycardia, intravenous propafenone exhibits its electrophysiologic effects in a dose-dependent manner by slowing or blocking retrograde conduction at the accessory connection. The high drug efficacy (81%) in terminating tachycardia is not dependent on patient age or retrograde conduction properties of the accessory connection.     

Electrophysiologic effects and mechanisms of termination of supraventricular tachycardia by intravenous amiodarone

Electrophysiologic studies were performed in nine patients with reentrant paroxysmal supraventricular tachycardia (PSVT) during a control period and following 5 mg/kg body weight of intravenous amiodarone (Cordarone, Labaz) administered as a slow continuous infusion over 15 to 20 minutes. All nine patients had induction of sustained PSVT during control studies. In seven of nine patients (group 1) the tachycardia was due to atrioventricular (AV) nodal reentry, and in two of nine patients (group 2) a concealed retrograde bypass tract was incorporated in the reentrant process. In group 1, following amiodarone, all seven patients lost the ability to sustain PSVT with either absence of atrial echoes (one patient) or induction of ≤3 echo beats (six patients) with termination of PSVT in the antegrade pathway (three patients) or retrograde pathway (two patients) or both (one patient). In group 2, following amiodarone, both patients lost the ability to sustain PSVT with absence of atrial echoes (one patient) on induction of a single echo beat (one patient) with block in the retrograde pathway (i.e., the concealed retrograde bypass tract). Amiodarone significantly increased (1) atrial cycle length for AV nodal Wenckebach block, (2) antegrade functional refractory period of the AV node, (3) antegrade effective refractory period of the AV node, (4) ventricular paced cycle length for ventricular atrial block, and (5) the retrograde functional refractory period of the ventricular-atrial conducting system. Thus intravenous-amiodarone inhibited induction of sustained reentrant PSVT by inducing block in the antegrade or retrograde or both limbs of the reentrant circuit and was shown to have significant depressant effects on both antegrade and retrograde AV nodal conduction and refractory periods.     

Paroxysmal supraventricular tachycardia: experience with propafenone

The authors studied the efficacy of intravenous (IV) (1.5-2 mg/kg) and oral propafenone (450 to 900 mg/day) in 16 patients with paroxysmal, sustained, recurrent supraventricular tachycardia (SVT). In 5 patients IV propafenone was not given, because of intolerant SVT. Nine patients had Wolff-Parkinson-White syndrome. IV propafenone immediately stopped and prevented reinduction of SVT in 9/11 patients. Oral propafenone prevented SVT induction in 3 of 5 patients. In the 9 patients responsive to IV propafenone, oral propafenone was effective: in particular, in 6 patients SVT tachycardia was not induced by serial transesophageal pacings, and in the remaining 3 patients the arrhythmia was still induced but was slower and of brief duration (3-5 seconds). In 11/12 patients responsive to oral propafenone the minimum effective dosage in preventing the induction of the arrhythmia was 600 mg/day. In only 1 patient was the dose of 450 mg/day equally effective. Propafenone administration was not associated with major side effects. In conclusion, propafenone is very effective in the control of paroxysmal supraventricular tachycardia; intravenous propafenone can predict the efficacy of oral therapy.     

Electrophysiologic and haemodynamic correlates in supraventricular tachycardia

In 16 subjects with paroxysmal supraventricular tachycardia(SVT) we sought a relationship between haemodynamic changesassociated with artificially induced arrhythmias and the electrophysiologicalproperties of the related atrioventricular (A V) nodal reentrycircuit. In 10 patients (group 1) induced SVT was typical (longAH) and caused a significant fall in cardie output (–720ml min^-1) and arterial systolic pressure (–18 mmHg). Insix subjects (group 2), induced SVT was atypical (long HA )and did not significantly alter the output of the heart andsystolic pressure, despite the elicitation of similar tachycardia.The opposite AV nodal reciprocation pattern which resulted ina substantial increase in AH/HH in group 1 and in a slight riseof the same variable in group 2, may explain these haemodynamicdifferences. In fact, atrial and ventricular systoles occurredsimultaneously and impeded the ventricular filling in the formergroup, while a regular subsequence of contraction was maintainedin the latter group. In group 2, systolic arterial pressureand cardiac output fell to the same level as in group 1 whenright atrial pacing, at a similar rate of SVT, determined anincrease of AH/HH similar to that observed during typical tachycardia.Thus,the haemodynamic response to SVT differs significantly betweenthe two types of reciprocating tachycardia, particularly asregards cardiac output and blood pressure, and is mainly influencedby the temporal relationship between atrial and ventricularsystole, independent of the rate of contraction. The differentconduction velocities of the reciprocating circuit limbs andtheir interrelation seem to be major determinants of the haemodynamicpattern of SVT.     

Electrophysiologic effects of intravenous propafenone in Wolff-Parkinson-White syndrome

The electrophysiologic effects of intravenous propafenone were studied in 15 consecutive patients with accessory pathways. Thirteen patients had sustained orthodromic supraventricular tachycardia induced during baseline study, and two patients needed isoproterenol to render it sustained. In all except one patient, propafenone, 2 mg/kg given intravenously over a 10-minute period, was successful in converting the arrhythmia to sinus rhythm. Atrial fibrillation was inducible in 10 patients before propafenone, but was no longer inducible in seven of these patients after the drug. The HV interval (23 +/- 20 to 41 +/- 25 msec) and the anterograde (310 +/- 96 to 509 +/- 145 msec) and retrograde (256 +/- 30 to 334 +/- 105 msec) effective refractory periods of the bypass tract were all significantly prolonged after the drug. The pacing cycle length that produced conduction block over the bypass tract anterogradely (319 +/- 126 to 446 +/- 150 msec) and retrogradely (272 +/- 25 to 360 +/- 97 msec) was also increased. During orthodromic tachycardia, propafenone increased conduction time in both the anterograde and retrograde limbs of the tachycardia. Tachycardia terminated in the retrograde limb in 64% of the patients. We conclude that propafenone is very effective in terminating orthodromic tachycardia when given intravenously and that it should be considered in patients initially seen with atrial fibrillation and short refractory periods.     

艾司洛尔和普罗帕酮治疗阵发性室上性心动过速的临床疗效

目的观察艾司洛尔和普罗帕酮治疗阵发室上性心动过速（PSVT）的临床疗效,分析比较两种药物的差异。方法纳入PSVT患者120例,随机分为艾司洛尔组（n=60）和普罗帕酮（n=60）。两组在积极治疗原发病及纠正电解质紊乱、低氧血症,调整盐酸平衡的基础上,艾司洛尔组通过输液泵注射艾司洛尔,初始按负荷量0.5mg/kg,每次增加0.05mg/kg,直至显效,最大剂量≤0.25mg/kg。普罗帕酮组采用注射用水20mL＋普罗帕酮70mg缓慢注射（10min～15min）。结果两组治疗有效率无统计学差异（85.0%vs.83.3%,P〉0.05）,且减慢心率和降低血压的疗效接近（P〉0.05）。结论艾司洛尔注射液治疗PSVT与普罗帕酮同等有效。     

盐酸关附甲素终止阵发性室上性心动过速的开放研究-与普罗帕酮进行随机对比

目的研究盐酸关附甲素终止阵发性室上性心动过速（PSVT）的疗效、作用机制及不良事件。方法随机开放对照多中心试验。入选标准为18-70岁，体重45-80kg的自发或经食管起搏心房诱发的PSVT患者，持续15min以上，心室率〉120次／min患者。排除标准为病态窦房结综合征、房室阻滞或室内阻滞，停服影响心脏电生理的药物不足5个半衰期等。采用3：1随机静脉注射观察药盐酸关附甲素或对照药普罗帕酮。盐酸关附甲素按4mg／kg的剂量，普罗帕酮按1mg／kg的剂量于5min静脉注射完毕。转复为窦性心律则终止注射，若第一剂治疗无效补充注射第二剂。部分患者用食管导联心电监测。结果入选盐酸关附甲素组137例，普罗帕酮组46例。用药前两组间患者人口统计学资料及基线特征相似。盐酸关附甲素组与普罗帕酮组转复率分别为68．6％（94／137）和93．5％（43／46），P=0．0009。在房室反复型室上性心动过速，盐酸关附甲素转复率为67．9％，而房室结折返型为75．0％。食管导联监测发现两种类型室上性心动过速，转复中止部位均包括交界区前传和旁路逆传以及慢径前传和快径逆传。用药两组总体不良事件发生率相近，盐酸关附甲素组为12例（8．8％），严重程度均为轻度，无严重不良事件。结论本研究所采用的盐酸关附甲素的剂量可以有效转复阵发性室上性心动过速，在目前所使用的剂量下与普罗帕酮相比疗效稍差，无严重不良反应。     

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)     

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.     

Electrophysiologic effect of sotalol in supraventricular tachycardias

The electrophysiological effects of sotalol, a beta-blocking drug with class III antiarrhythmic properties were assessed in 20 patients (mean age 33 +/- 14.3 years) with supraventricular tachycardias. Sixteen patients had Wolff-Parkinson-White syndrome (overt n = 9, concealed n = 7), three patients AV-nodal reentrant tachycardias and another patient atrial tachycardias. Sotalol was administered intravenously (n = 16) in a dose of 1.5 mg/kg over 15 min. The effects of 320 to 480 mg/day oral sotalol were assessed in 7 patients. By intravenous and oral application of sotalol a significant increase in the AH interval, the refractory periods of the atrium and ventricle as well as a decrease of the antegrade and retrograde conduction capacity of the AV node or the accessory pathway were observed. The mean R-R interval during induced atrial fibrillation increased significantly in patients with Wolff-Parkinson-White syndrome from 224 +/- 52 ms to 277 +/- 59 ms (p less than 0.05). In 10 patients, sotalol was administered during supraventricular reentrant tachycardia. The cycle length of supraventricular tachycardia increased from 276 +/- 90 ms to 358 +/- 25 ms (p less than 0.01). The tachycardia terminated in 7 patients: in 5 patients block was observed in the AV node, while in another 2 patients tachycardia terminated retrogradely. After intravenous application supraventricular arrhythmias were no longer inducible in 5 of 12 patients. In a further 4 patients only non-sustained supraventricular tachycardias (4-20 QRS complexes) were inducible. In 2 patients the supraventricular tachycardia terminated distal to the His bundle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects of calcium channel blockers on supraventricular tachycardia in children

Calcium channel blockers (diltiazem or verapamil) were administered in 17 pediatric patients with supraventricular tachycardia to evaluate their drug effects on electrophysiologic properties and the tachycardia zone. Using electrophysiologic technique, 10 patients were diagnosed as having orthodromic reciprocating tachycardia (ORT), including three patients with concealed atrioventricular bypass tracts. Four patients were diagnosed as having atrioventricular nodal re-entrant tachycardia (AVNRT) of the slow-fast type and three patients were diagnosed as having intra-atrial re-entrant tachycardia (IART). Diltiazem was given to 10 patients; verapamil, to eight patients at doses of 0.15-0.2 mg/kg intravenously. Electrophysiologic properties and the tachycardia zone were then evaluated before and after the administration of calcium channel blockers. Diltiazem and verapamil produced no significant changes in the sinus node and atrial functions including basic sinus cycle length, sinoatrial conduction time, maximum sinus node recovery time and the effective atrial refractory period. Although sinus cycle length was shortened after verapamil in half the cases, it was due to increased sympathetic tone secondary to hypotension rather than to direct action of verapamil. Calcium channel blockers, however, prolonged the PR interval and significantly increased the effective refractory period of the atrioventricular node. Properties of the atrioventricular bypass tracts were not affected by calcium channel blockers. Diltiazem and verapamil were markedly effective in ORT and AVNRT. Their re-entrant circuits, including the atrioventricular node and the tachycardia zones, were shortened or resolved. However, IART showed no significant change in the tachycardia zone after the administration of calcium channel blockers, because the re-entrant circuit was not present within the atrioventricular node.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effect of a new Ca(2+)-antagonist, TA-3090 on supraventricular tachycardia and conduction system]

We investigated the effect of a new Ca-antagonist, TA-3090 on supraventricular tachycardia (SVT) and conduction system, comparing it with the effect of Diltiazem Hydrochloride, in 11 patients who had paroxysmal SVT attacks. Seven of the 11 patients presented atrioventricular reentrant tachycardia (AVRT) via retrograde concealed conduction through an accessory pathway, and the others presented AV nodal reentrant tachycardia (AVNRT). After SVT was induced by means of programmed electrical stimulation at high right atrium, TA-3090 (0.1 mg/kg body weight) or Diltiazem (0.2 mg/kg) was administered intravenously for 3 minutes. TA-3090 terminated nine of 11 SVTs, while Diltiazem terminated four of 4 SVTs. On termination of SVT, both drugs interrupted A-H conduction during AVRT and the slow pathway during AVNRT. After TA injection, five of 11 SVTs could not be induced by programmed electrical stimulation, while two of 4 SVTs could not be induced after Diltiazem. In AVRT, three patients in which TA-3090 prevented SVT induction had a longer AV node effective refractory period than that of the others in which TA-3090 could not prevent SVT (330 +/- 46 vs 210 +/- 24 msec, p less than 0.01). However, SVT was induced more easily than before in three of the 11 patients treated with TA-3090 administration, and in one of the 4 patients treated with Diltiazem administration.(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.