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Biomedical subjects

E N Prystowsky

Publications and source records attributed to E N Prystowsky.

At least 109 records · Page 6Linked to original sources
PubMed1986

Encainide for treatment of supraventricular tachycardias associated with the Wolff-Parkinson-White syndrome.

Thirty-three patients with supraventricular tachycardia associated with the Wolff-Parkinson-White syndrome were treated with encainide for 26 months (mean). Encainide at a mean dosage of 187 mg/day abolished or markedly decreased episodes of palpitations in 24 of 33 (73%), and no patient had syncope or required cardioversion while receiving the drug. Encainide was well tolerated and was discontinued in only 2 patients because of side effects (6%). Only 1 patient (3%) had a proarrhythmic effect while taking encainide (ventricular tachycardia). Fourteen of 16 patients (88%) with atrial fibrillation continue receiving encainide. Episodes of palpitations have been abolished or markedly decreased and no patient has had syncope or required cardioversion. All 14 of these patients had either anterograde block in the accessory pathway during atrial fibrillation or greater than or equal to 75 ms increase in the shortest R to R interval formed by 2 preexcited QRS complexes. Encainide prolonged refractory periods of the atrial (p = 0.064) and ventricular (p = 0.061) muscle. It prolonged the cycle length at which 1:1 conduction of the accessory pathway in both the anterograde and retrograde directions occurred (both, p less than 0.001). Induction of atrioventricular-reciprocating tachycardia (AVRT) was prevented in 36% of patients at repeat electrophysiologic study. The AVRT cycle length increased 112 ms (mean, p less than 0.001) in those patients in whom AVRT was still inducible. The loss of delta waves recorded with the 12-lead scalar electrocardiogram during encainide therapy was a significant predictor of anterograde accessory pathway block (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Subthreshold conditioning stimuli prolong human ventricular refractoriness.

This study tested whether a subthreshold stimulus (Sc) inserted before a premature stimulus prolonged the right ventricular effective refractory period in humans, and whether the degree of effective refractory period lengthening was influenced by heart rate, Sc current intensity or Sc pulse duration. Sc at current intensity 10 mA and pulse width 2 ms prolonged mean effective refractory period from 255 ms to 277 ms (p less than 0.001, n = 20). The increase in effective refractory period was similar in 6 patients studied at pacing cycle lengths 600 (259 to 289 ms) and 400 ms (236 to 258 ms). When Sc current intensities were varied at 2, 5 or 10 mA at a constant pulse duration of 100 ms the effective refractory period progressively prolonged by 6, 40 and 81 ms respectively (p less than 0.02, n = 6). The pulse duration of Sc at a constant current of 10 mA significantly influenced effective refractory period prolongation. With Sc pulse durations of 2, 10, and 100 ms the effective refractory period prolonged by 16, 33 and 66 ms respectively (p less than 0.01, n = 7). Thus, subthreshold impulses prolong the effective refractory period in human right ventricular myocardium. The prolongation of effective refractory period depended on Sc current intensity and pulse duration but was independent of heart rate at the cycle lengths tested. The use of subthreshold stimuli as antiarrhythmic therapy may be feasible in some patients.

Adult↗
PubMed1986

Survivors of cardiac arrest: prevention of recurrence by drug therapy as predicted by electrophysiologic testing or electrocardiographic monitoring.

Sixty-two patients (44 men and 18 women, aged 15 to 75 years) resuscitated from at least 1 cardiac arrest unrelated to acute myocardial infarction were studied. No patient was taking antiarrhythmic drugs at the time of the initial cardiac arrest. Thirty-five patients had coronary artery disease (CAD) and 27 did not. Before drug therapy, control electrophysiologic studies induced ventricular tachycardia (VT) in 43 of 58 patients (74%) (30 of 35 with CAD and 17 of 27 without CAD). At control continuous electrocardiographic monitoring for 48 hours or longer, only 19 of 62 patients (31%) had spontaneous VT, 5 of whom had no VT induced at control electrophysiologic study. Mean follow-up was 22 months. Fourteen of 41 patients, 8 of 25 with and 6 of 16 without CAD, had VT suppressed with drugs during serial electrophysiologic testing, and none had a recurrent arrhythmic event. VT was suppressed in 12 of 14 patients receiving conventional drugs. Of 27 patients with VT induced during all drug studies, 6 died from cardiac arrest and 4 had recurrent VT. Drug efficacy in 20 patients was guided by continuous electrocardiographic monitoring, and 4 of 9 patients in whom VT and ventricular pairs were suppressed by drug therapy, as documented by continuous electrocardiographic monitoring for 48 hours or longer, died of cardiac arrest. Overall, 26 patients were discharged receiving amiodarone therapy, and 5 died of cardiac arrest and 3 had recurrent sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Determination of the earliest site of ventricular activation in Wolff-Parkinson-White syndrome: application of digital continuous loop two-dimensional echocardiography.

Surgical and transcatheter ablation of accessory atrioventricular (AV) connections (Wolff-Parkinson-White syndrome) requires accurate localization of the accessory pathway. In a canine model of endocardial pacing, a continuous loop two-dimensional echocardiographic technique was developed for determining the earliest site of ventricular activation. This technique was then used to localize accessory AV connections in patients. Echocardiographic images were acquired on videotape and converted to a digital continuous loop format, from which the earliest site of systolic motion was determined. In six dogs, using six distinct endocardial sites, two blinded observers accurately identified the earliest site of ventricular activation in 31 (86%) of 36 and 32 (89%) of 36 locations. Determination of the earliest site of ventricular activation with the continuous loop digital technique was superior to standard analog analysis in overall accuracy (p less than 0.02) and in intraobserver variability (p less than 0.004). After validation of this technique, 21 patients with 22 accessory AV connections with anterograde conduction were studied. The earliest site of mechanical activity was determined during sinus (10 patients) or atrial paced (11 patients) rhythms by two blinded observers and compared with electrophysiologic mapping and surface electrocardiograms. Digitally processed echocardiograms correctly localized the earliest site of ventricular activation in 18 of 22 connections and predicted an adjacent location in the remaining 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Alteration of human right bundle branch refractoriness by changes in duration of the atrial drive train.

We studied the effect of drive train duration on human right bundle branch refractoriness. Seven patients with a QRS duration of 0.10 sec or less and no preexcitation had functional right bundle branch block induced reproducibly with premature atrial stimulation. Refractoriness of the right bundle branch was defined as the longest H1H2 interval resulting in right bundle branch block and was determined in each patient at a constant pacing cycle length but at five to seven different atrial drive train durations varying from four to 99 complexes. In all seven patients, right bundle branch refractoriness decreased with increasing drive train duration (mean 15 msec). One-third of this decrease (5.0 msec) occurred between drive train durations of four and eight complexes, and close to two-thirds (9.3 msec) occurred between drive train durations of eight and 64 complexes. Very little further decrease (0.7 msec) occurred between 64 and 99 complexes. We conclude that right bundle branch refractoriness shortens progressively as the preceding drive train duration increases. This phenomenon may in part explain the disappearance of functional right bundle branch block during supraventricular tachycardia after a variable number of complexes without a change in cycle length of tachycardia.

Adult↗
PubMed1986

The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways.

In this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The V1V1 interval during tachycardia minus the longest V1V2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p less than .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p less than .05 free wall vs posterior or anterior septal).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular Node↗
PubMed1986

The implantable transvenous cardioverter: long-term efficacy and reproducible induction of ventricular tachycardia.

We followed 11 patients for 5 to 27 months (mean 14.9) after implantation of a permanent transvenous low-energy synchronized cardioverter to evaluate both long-term reproducibility of ventricular tachycardia (VT) induction via noninvasive programmed electrical stimulation with the cardioverter and efficacy of cardioversion. Induction and termination of VT were attempted at implantation and approximately every 3 months thereafter. All patients had coronary artery disease and were receiving antiarrhythmic drug therapy (amiodarone in eight). VT cycle length, morphology, and mode of induction were reproducible on multiple occasions in nine patients; clinical VT was induced inconsistently in two patients. Multiple VT episodes in five patients had one morphology, whereas two morphologies occurred in six patients. Synchronization of the shock within the QRS complex and right ventricular effective refractory periods determined via the cardioverter remained constant over the follow-up period. VT was terminated on every occasion in nine patients and on eight of nine occasions in one patient. Tachycardia was accelerated on three of five occasions in one patient. Consistently effective cardioversion energy (0.2 to 2.0 J) increased modestly in four patients. We conclude that patients with inducible monomorphic VT usually have sustained VT with similar characteristics inducible over a period of time and cardioversion and sensing functions of the cardioverter remain relatively stable over time.

Aged↗
PubMed1986

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.

Diagnosis, Differential↗
PubMed1985

Postvagal tachycardia.

Twenty-one patients were studied to investigate whether cardiac acceleration above control values occurred after cessation of enhanced vagal tone (postvagal tachycardia), and to determine the effects of selective autonomic blockade on postvagal tachycardia. Patients had neither sinus arrhythmia nor sinus nodal dysfunction. Enhanced vagal tone was induced by neck suction using a lead neck collar connected to a vacuum source. For each patient intracollar negative pressures of 50 to 60 mm Hg were induced for 2 seconds on 10 occasions. For all patients, sinus cycle length increased from 821 +/- 99 to 1,067 +/- 241 ms (p less than 0.001) during neck suction and decreased to 760 +/- 96 ms after termination of neck suction, a value significantly (p less than 0.001) less than control. Five of 16 patients had no postvagal tachycardia. Maximal shortening of sinus cycle length occurred 3 to 8 complexes after cessation of neck suction. Neck suction was induced in 7 patients before and during propranolol administration, 0.15 mg/kg intravenously, and the degree of postvagal tachycardia was unchanged. Atropine, 0.03 mg/kg intravenously, prevented neck suction-induced sinus slowing and acceleration in 3 of 3 patients. We conclude that postvagal tachycardia occurs and is not mediated through beta-adrenergic activity, but is inhibited by muscarinic blockade.

Atropine↗
PubMed1985

Electrophysiologic and antiarrhythmic properties of bepridil.

Bepridil has been shown to block both slow- and fast-channel activity in the heart. Electrophysiologic studies in man demonstrate that oral and intravenous bepridil prolongs sinus cycle length, PR interval and QT interval, without apparently changing the QRS interval. In addition, the drug depresses atrioventricular (AV) nodal conduction, resulting in an increased AH interval. Refractoriness in the AV node, atrium and ventricle is increased. There is usually little or no change in the HV interval. The antiarrhythmic properties of bepridil have been noted in patients with supraventricular tachycardia, ventricular premature complexes (VPCs) and sustained ventricular tachycardia (VT). In 17 patients, intravenous bepridil was compared with either verapamil or ajmaline. AV nodal reentrant tachycardia was terminated in all patients with bepridil and verapamil. However, ajmaline was somewhat more effective than bepridil in patients with AV reentry (8 of 8 versus 5 of 8). In 12 of these 17 patients, oral bepridil (500 mg/day for 3 days) suppressed the induction of tachycardia or slowed its rate. In 3 studies of oral bepridil for VPCs, the drug was effective in 68%, 69% and 70% of patients. Another group of studies evaluated bepridil in a total of 30 patients with sustained VT. Intravenous bepridil terminated VT in 17 of 26 patients. The induction of VT by programmed ventricular stimulation was also prevented in 7 of 17 patients. Although torsade de pointes has been reported, its incidence appears to be low.

Ajmaline↗
PubMed1985

Inhibition of premature ventricular extrastimuli by subthreshold conditioning stimuli.

The purpose of this study was to determine whether trains of subthreshold high frequency conditioning stimuli (333 Hz, 1 ms duration, 2 ms interval) delivered to the canine ventricle inhibited the response to a premature stimulus (S2) more effectively than did a single subthreshold conditioning stimulus. It was found that trains of conditioning stimuli (mean 1.21 mA) inhibited the response to S2 152 ms beyond expiration of the ventricular effective refractory period, whereas a single conditioning stimulus inhibited S2 only 20 ms or less beyond the ventricular effective refractory period. In late diastole, trains of conditioning stimuli failed to inhibit S2 when the train of stimuli caused ventricular depolarization or the latter occurred in response to the next sinus impulse. Trains of conditioning stimuli did not induce ventricular arrhythmias. Lidocaine or autonomic blockade did not alter the response to trains of conditioning stimuli. Trains of conditioning stimuli or a single conditioning stimulus inhibited the response to S2 only when they were delivered at the same electrode site. By lengthening the ventricular effective refractory period, trains of conditioning stimuli could prevent or terminate tachycardias, but this possibility is constrained, at present, by the spatial limitations of the technique.

Animals↗
PubMed1985

Electrophysiologic effects and clinical efficacy of oral propafenone therapy in patients with ventricular tachycardia.

The effects of the antiarrhythmic agent propafenone were evaluated in 25 patients with recurrent symptomatic ventricular tachycardia. Oral propafenone was given to a maximal dose of 300 mg every 8 hours. Ten of the 25 patients developed side effects or had inadequate suppression of spontaneous ventricular arrhythmias during propafenone therapy. Electrophysiologic studies were performed before and during drug therapy on the 15 patients who had a satisfactory clinical response. Propafenone increased the PR interval from 168 +/- 46 to 188 +/- 25 ms (p less than 0.007), the HV interval from 47 +/- 10 to 65 +/- 13 ms (p less than 0.005), the shortest atrial pacing cycle length to maintain 1:1 atrioventricular (AV) nodal conduction from 385 +/- 44 to 436 +/- 42 ms (p less than 0.005), the ventricular effective refractory period from 231 +/- 17 to 255 +/- 19 ms (p less than 0.001) and the ventricular functional refractory period from 260 +/- 15 to 278 +/- 17 ms (p less than 0.002). Before propafenone therapy, all 15 patients had ventricular tachycardia induced by programmed ventricular stimulation. During propafenone treatment, 12 patients still had ventricular tachycardia induced, and the tachycardia cycle length significantly increased from 236 +/- 44 to 374 +/- 103 ms (p less than 0.001). Ten patients were considered to have satisfactory electrophysiologic response to propafenone on the basis of either the inability to initiate ventricular tachycardia or a marked increase in ventricular tachycardia cycle length associated with lack of symptoms during the induced tachycardia. These patients were discharged receiving propafenone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Amiodarone: risk factors for recurrence of symptomatic ventricular tachycardia identified at electrophysiologic study.

Ventricular tachycardia induced by programmed electrical stimulation during amiodarone therapy often does not preclude a good clinical response. The purpose of this study was to determine whether use of discriminant analysis could distinguish patients who remained asymptomatic from those who subsequently developed symptomatic ventricular tachycardia or cardiac arrest. Studies were performed in 37 patients with sustained ventricular tachycardia who still had ventricular tachycardia induced during programmed electrical stimulation during amiodarone therapy. The mean follow-up time was 14.1 +/- 1.3 months (+/- SEM). Twenty-three patients remained asymptomatic, whereas 14 patients had symptomatic recurrence of their ventricular tachycardia. In patients with recurrence of arrhythmia compared with asymptomatic patients, administration of amiodarone caused a longer ventricular effective refractory period (296 +/- 8 versus 271 +/- 7 ms, p less than 0.05) and a greater change in corrected QT [QTc] interval (90 +/- 18 versus 44 +/- 9 ms, p less than 0.02), but no difference in the decrease in premature ventricular complexes after treatment with amiodarone. During amiodarone therapy, nonbundle branch reentrant repetitive ventricular responses were induced by a single ventricular extrastimulus during sinus rhythm in 9 of 14 patients with recurrent arrhythmias compared with 2 of 21 asymptomatic patients (p = 0.001). Also, less aggressive pacing techniques were required to induce ventricular tachycardia in 9 of 14 symptomatic patients compared with 4 of 23 asymptomatic patients (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1985

Amiodarone treatment in patients with ventricular arrhythmias.

Amiodarone has been used in the therapy of supraventricular and ventricular tachycardia, and has often been categorised as a class III rather than a class I agent. However, in patients with ventricular arrhythmias, amiodarone 800mg daily for 14 days prolonged the right ventricular effective refractory period by a mean of 18.8 msec (p less than 0.05), and HV interval by a mean of 5.2 msec (p less than 0.05), these changes being similar to those noted with drugs such as quinidine, procainamide, disopyramide and encainide. The antiarrhythmic efficacy of amiodarone was evaluated in 196 patients with recurrent sustained ventricular tachycardia, recurrent ventricular fibrillation or recurrent nonsustained ventricular tachycardia. Coronary artery disease, dilated (congestive) cardiomyopathy, or other forms of heart disease were present in most patients. After 1 month of therapy, 177 patients continued to receive amiodarone and, during the remainder of the follow-up period, 139 patients had no recurrence of spontaneous ventricular tachycardia or ventricular fibrillation. Sudden cardiac death occurred in 15 patients after a mean treatment period of 10.4 months. Overall, amiodarone was an effective form of therapy in patients with ventricular tachycardia and ventricular fibrillation.

Adolescent↗