Pirmenol in termination of paroxysmal supraventricular tachycardia

An assessment was made of the effect of pirmenol in the termination of paroxysmal supraventricular tachycardia (SVT). Sinus rhythm was restored by intravenous administration in 11 of 17 patients during a spontaneous attack. Another 8 patients were studied electrophysiologically. Pirmenol terminated an induced SVT in 3 of 5 patients having an atrioventricular (AV) intranodal re-entry mechanism but in none of 3 patients having an atrioventricular bypass tract as one re-entrant limb. The overall success in restoring sinus rhythm was 14 of 25 patients (56%). The drug was hemodynamically well tolerated even in cases of continued SVT. Pirmenol increased the atrial effective refractory period and had no obvious effect on AH and HV intervals. The functional refractory period of the AV node was decreased, probably by an anticholinergic effect. The effective and functional refractory periods of retrograde atrioventricular conduction via the AV node and bypass tract were increased in some patients. The mechanism terminating the AV intranodal SVT was a block in the retrograde part of the dual AV nodal pathway, a typical antiarrhythmic Class I effect.     

Vagal techniques for termination of paroxysmal supraventricular tachycardia

Maneuvers that reflexly increase vagal tone were deployed to terminate the tachycardia in 68 consecutive patients with paroxysmal supraventricular tachycardia. The order and success rate of the protocol was as follows: 57 episodes were terminated with carotid sinus pressure alone or after pretreatment with edrophonium, 5 were terminated with the Valsalva maneuvers and 6 were terminated with phenylephrine. Potency testing showed that phenylephrine evoked the greatest increase in vagal tone. All cases demonstrated slowing of tachycardia ranging from 40 to 220 ms ± standard error of the mean (mean 79.0 ± 3.8 ms) followed by abrupt termination. Pauses after termination ranged from 900 to 3,300 ms (mean 1,683.8 ± 66.6) with 54 patients showing pauses of 2,000 ms or less. Termination was highly reproducible showing an overall success of 148 (92 percent) of 160 trials among 22 selected cases. The extent of increased vagal tone needed to terminate paroxysmal supraventricular tachycardia was raised by augmented sympathetic tone (infusion of isoproterenol) and decreased by reduced sympathetic tone (pretreatment with propranolol). Thus, paroxysmal supraventricular tachycardia can be rapidly, safely and consistently terminated by maneuvers that reflexly increase vagal tone.     

Pirmenol in the termination of paroxysmal supraventricular tachycardia

The effects of pirmenol in terminating paroxysmal supraventricular tachycardia were studied in 25 patients. Pirmenol was administered as 1 or 2 injections of 50 mg to 17 patients during a spontaneous attack, or as a 50-mg bolus followed by steady infusion of 2.5 mg/min in 8 patients during a tachycardia that was induced electrophysiologically. Termination was successful in 11 of 17 patients who had a spontaneous attack and in 3 of 8 patients who had induced tachycardia. Pirmenol was effective in 3 of 5 patients with atrioventricular nodal reentrant mechanism, but in none of 3 patients with a reentrant tachycardia with a retrogradely conducting atrioventricular bypass tract. Conversion to sinus rhythm was achieved in 14 of 25 patients (56%). No hemodynamic adverse effects occurred. Pirmenol increased the atrial effective refractory period, but had little effect on conduction in the atrioventricular node and His-Purkinje system. Reentry was abolished through a block in the retrograde part of the dual atrioventricular nodal pathway, which is typical of class I antiarrhythmic agents.     

Implantable automatic scanning pacemaker for termination of supraventricular tachycardia

Thirteen patients suffering from reentrant supraventricular tachycardia have undergone implantation of a scanning extrastimulus pacemaker. This pacemaker is fully implanted and automatic, and it requires no external control device to activate or control it. The pacemaker is activated when tachycardia occurs. After four cycles an extrastimulus is induced with a preset coupling time from a sensed intracardiac potential, and every four cycles thereafter a further extrastimulus occurs, but on each occasion there is a decrement in coupling cycle by 6 ms until 90 ms of the cardiac cycle has been scanned by extrastimuli. When necessary, two extrastimuli can be introduced with a fixed but preset coupling time between them. Every four beats two extrastimuli are induced but the coupling time between the spontaneous cardiac potential and the first stimulus is decreased by 6 ms until 90 ms of the cardiac cycle has been scanned. The coupling time between the two stimuli is fixed throughout the scan. When termination of tachycardia occurs the successful timing variables are retained in the pacemaker memory so that at the onset of the next episode of tachycardia these settings are used first. Pacemaker pulse width, sensitivity, tachycardia trigger rate, coupling intervals for both stimuli and the use of single or double extrastimuli are all programmable transcutaneously.Three patients required single, and seven patients double ventricular premature stimuli; three patients required double atrial premature stimuli for termination of tachycardia. Despite frequent attacks of tachycardia before implantation, only two patients had a sustained attack of tachycardia after pacemaker implantation.     

Automatic pacemaker termination of two different types of supraventricular tachycardia

A new antitachycardia pacemaker system was used in a 58 year old woman to terminate two different types of supraventricular tachycardia by a single automatic pacing mode. During the invasive electrophysiologic study before pacemaker implantation (in the absence of medication), sustained episodes of atrioventricular (AV) nodal reentrant tachycardia and two short-lasting episodes of nonsustained atrial tachycardia were induced. After implantation, sustained episodes of both AV nodal tachycardia and atrial tachycardia were initiated. Both arrhythmias could be terminated reproducibly by a single pacing mode.     

抗心动过速起搏模式终止室上速的疗效比较

】目的评估短阵超速抑制和递减刺激法在室上速终止治疗中的疗效。方法在右室心尖部，随机选用短阵超速抑制和递减刺激等方法，对４４例室上速患者进行抗心动过速起搏研究。结果首选递减刺激法与短阵超速抑制法终止室上速的有效率分别为９２％和６８．４％（Ｐ＜０．０５）。结论终止室上速的抗心动过速起搏模式可首选用递减刺激法     

Electrocardiographic observations on the termination of supraventricular tachycardia by verapamil.

The effect of intravenous verapamil on the termination of supraventricular tachycardia (SVT) was studied by continuous electrocardiographic monitoring of 27 episodes of SVT. Progressive increase of the cycle length heralded conversion in eight episodes while cycle-length alternation preceded cessation of the arrhythmia in 13 episodes. In five patients the arrhythmia was either stopped or closely followed by a ventricular premature beat (VPB), followed by further VPBs in three. Runs of bizarre ventricular tachycardia followed initial sinus-beats in two patients. Sinus standstill, lasting 30 seconds, was observed in one patient. The first post SVT beats had an aberrant QRS configuration with a normal P-R interval in four cases and an aberrant QRS complex with a short P-R interval, resembling Wolff-Parkinson-White complexes, in a further seven patients. The possible mechanisms causing this variability of pre- and post-conversion period are discussed. It is suggested that some aspects of verapamil action may be explained by a parasympaticomimetic effect on the myocardium.     

Assessment of left ventricular function by radionuclide angiography during induced supraventricular tachycardia

Electrocardiographically synchronized radionuclide angiography was performed before, during and after induced paroxysmal Supraventricular tachycardia in 13 patients. Data were acquired with a computer-interfaced Anger camera in a left anterior oblique projection. No data were acquired during tachycardia until tachycardia had been sustained for 1 minute. Patients ranged in age from 20 to 64 years (mean ± standard deviation 42 ± 14.5). Three patients had organic heart disease and 10 did not. Baseline and tachycardia heart rates (beats/min) were 59 to 99 (73 ± 11) versus 141 to 228 (157 ± 22). Baseline and tachycardia left ventricular measurements (mean ± standard error) were as follows: ejection fraction 64 ± 2 versus 62 ± 4 percent (not significant), ejection rate 3.0 ± 0.1 versus 4.3 ± 0.4 mean ventricular counts/s (p < 0.001), normalized end-diastolic counts 72.7 ± 7.8 versus 48.7 ± 6.7 × 10³ counts (p < 0.001), normalized stroke counts 37.1 ± 3.4 versus 23.3 ± 2.7 × 10³ counts (p < 0.001) and normalized count cardiac output 2,717.5 ± 273.0 versus 3,620.2 ± 403.7 × 10³ counts/min (p < 0.005). Although ejection fraction for the whole group did not change significantly, it decreased during tachycardia by 5 percentage points or more in five patients. These were the three patients with heart disease and the two normal patients with the fastest heart rate during tachycardia (228 and 214 beats/min, respectively).In summary, paroxysmal Supraventricular tachycardia was characterized by a marked decrease in left ventricular end-diastolic and stroke volumes but increased ejection rate and cardiac output without significant change in ejection fraction. Heart disease or rapid heart rate during tachycardia appeared to have a deleterious effect on ejection fraction.     

Reflex mechanisms responsible for early spontaneous termination of paroxysmal supraventricular tachycardia

The incidence and possible mechanism of early spontaneous termination of paroxysmal supraventricular tachycardia was studied in 20 consecutive patients. Episodes of induced tachycardia that terminated spontaneously within the 1st minute after initiation were included. Tachycardias ending spontaneously were associated with a reproducible course of hypotension at the onset followed by blood pressure recovery above control levels and termination. Spontaneous termination of tachycardias occurred within the A-V node 18 to 45 seconds (mean +/- standard error of the mean 27.9 +/- 5.3) after their onset. In the supine position (0 degrees) 9 (45 percent) of 20 patients showed spontaneous termination in 36 (16 percent) of 219 episodes of tachycardia. In the head-dependent position (-20 degrees) only 1 (8 percent) of 13 patients manifested spontaneous termination in 2 (4 percent) of 54 episodes. In the head up position (+60 degrees) only 1 (6 percent) of 18 patients exhibited termination in 2 (2 percent) of 102 episodes. After partial cholinergic blockade with intravenous hyoscine butylbromide, 20 mg, or atropine, 0.6 mg, none of five patients showed spontaneous termination in 25 episodes. After beta adrenergic blockade with 10 mg of propranolol intravenously, none of 16 patients showed spontaneous termination in 87 episodes of tachycardia. We conclude that the initial hypotension during tachycardia evokes a sympathetic response that increases blood pressure and this increase in turn causes a rise in vagal tone that breaks the tachycardia.     

External pacing for the termination of sustained supraventricular tachycardia in children

Cardiac pacing from either endocardial or transesophageal sites has proven useful in termination of sustained supraventricular tachycardia in children. In two patients we demonstrated the efficacy of external pacing in the termination of sustained supraventricular tachycardia. The ease and apparent safety of the technique make it an attractive addition to our current therapies for supraventricular tachycardia in children. The usefulness of external pacing in treating pediatric arrhythmias needs further evaluation.     

Recurrent supraventricular tachycardia induced by antitachycardia pacemaker

We report a case of sensing malfunction in which supraventricular tachycardia was repeatedly induced, then terminated appropriately, by an antitachycardia pacemaker.     

Diltiazem in paroxysmal supraventricular tachycardia: electrocardiographic findings at termination]

The effects of diltiazem hydrochloride (0.3 mg/kg i.v. over 2 min.) was studied by continuous electrocardiographic monitoring in 60 patients. Conversion to sinus rhythm was achieved in 55 patients (91%). Electrocardiographic findings were: undisturbed sinus rhythm in 20 patients; A-V junctional rhythm in 4 patients; complex ventricular arrhythmias (ventricular tachycardia or complex VPCs) in 19 patients. Patients with complex ventricular arrhythmias were matched against patients with normal sinus rhythm, with respect to the following parameters: age, sex, heart disease, tachycardia duration, tachycardia cycle length, sinus cycle length, pre- and post-infusion blood pressure. No differences between the two groups of patients were found. Ventricular arrhythmias occurring at the termination of supraventricular tachycardia are difficult to explain. Nevertheless, these arrhythmias are not associated with organic heart disease. They could be the expression of triggered activity.     

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.     

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.     

External cardiac programmed stimulation for noninvasive termination of sustained supraventricular and ventricular tachycardia

To examine the feasibility of using a noninvasive temporary pacemaker for termination of well-tolerated supraventricular (SVT) and ventricular tachycardia (VT), a standard external demand pacemaker was modified to allow stimulation with single or multiple extrastimuli and overdrive pacing. To evaluate the efficacy, safety and tolerance of external cardiac programmed stimulation, a standard arrhythmia termination protocol was used in 223 tachycardias in 22 patients. The technique of external cardiac programmed stimulation was used in 209 episodes of SVT in 13 patients. It terminated 95% of the episodes with success in 19 of 20 episodes of atrioventricular nodal reentrant tachycardia and 179 of 189 episodes of atrioventricular reciprocating tachycardia. Of 198 episodes of SVT terminated by the technique 168 (85%) were terminated by a single extrastimulus and 28 (14%) by double extrastimuli. Only 2 episodes of SVT required overdrive pacing for termination. External cardiac programmed stimulation did not result in atrial fibrillation or arrhythmia acceleration. Of 14 episodes of sustained monomorphic VT 5 were terminated by external cardiac programmed stimulation. One tachycardia was terminated by a single extrastimulus, 1 by double extrastimuli and 3 by overdrive pacing. Arrhythmia acceleration occurred once and was terminated by endocardial pacing. On 27 separate occasions patient evaluation of maximal discomfort included 4 ratings of mild, 10 of moderate, 11 of severe and 2 of intolerable discomfort. External cardiac programmed stimulation is effective and safe in patients with well-tolerated sustained supraventricular or ventricular arrhythmias.