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Biomedical subjects

E N Prystowsky

Publications and source records attributed to E N Prystowsky.

At least 145 records · Page 8Linked to original sources
PubMed1984

Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome.

We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.

Adolescent↗
PubMed1983

Enhanced parasympathetic tone shortens atrial refractoriness in man.

The purpose of this study was to determine the effects of enhanced vagal tone on human right atrial refractoriness in 12 patients. A specially built neck collar connected to a vacuum source was placed around the patient's neck and enhanced vagal tone was produced during neck suction using intracollar negative pressures of 50 to 60 mm Hg. Refractory periods were determined with a catheter electrode positioned in the high right atrium near the sinus node. Induced neck suction increased the spontaneous sinus cycle length from 837 +/- 96 to 1.136 +/- 273 ms (p less than 0.001) and shortened the atrial effective refractory period from 241 +/- 24 to 230 +/- 20 ms (p less than 0.01) and the atrial functional refractory period from 272 +/- 32 to 262 +/- 29 ms (p less than 0.01). In 2 of 2 patients, collar-induced decreases in atrial refractoriness and increases in spontaneous cycle length were prevented after atropine (0.03 mg/kg) was given intravenously. It is concluded that enhanced vagal tone mediated through muscarinic receptors shortens atrial refractory periods in man.

Adolescent↗
PubMed1983

Cellular electrophysiologic abnormalities of diseased human ventricular myocardium.

Using standard microelectrode techniques, the cellular electrophysiologic features of ventricular myocardium resected from 8 patients with refractory arrhythmias were studied in vitro. Action potentials from damaged myocardium compared with normal myocardium had reduced resting membrane potential, amplitude, and maximal upstroke velocity. Tetrodotoxin, but not verapamil, suppressed 3 action potentials with resting potentials of -60 to -64 mV and Vmax less than 70 V/s. Verapamil, but not tetrodotoxin, suppressed 4 action potentials with resting potentials of -44 to -57 mV and Vmax less than 20 V/s. Unidirectional block, Wenckebach block, and summation occurred in damaged zones. Exit block from and frequency-dependent entrance block into an ectopic focus were noted. Subthreshold responses in the focal area induced by action potentials in the surrounding myocardium and by subthreshold current pulses injected through the recording microelectrode altered the spontaneous discharge rate of the focus, as previously described for modulated parasystole. Pulses early in the spontaneous cycle delayed the next expected discharge, and later pulses accelerated the subsequent discharge. Pulses injected at the singular point completely suppressed automaticity (annihilation). Tetrodotoxin and verapamil suppressed automaticity in some fibers. Single action potentials induced in quiescent fibers triggered and terminated sustained rhythmic activity. These data suggest that depressed fast responses, slow responses, and subthreshold potentials can generate and modulate ectopic activity in damaged human ventricle and that fast- and slow-channel blocking agents and single premature stimuli can terminate such activity.

Action Potentials↗
PubMed1983

Pathophysiology of arrhythmias: clinical electrophysiology.

We have endeavored to relate known electrophysiologic mechanisms of arrhythmia development to clinically occurring arrhythmias, realizing that definitive conclusions can only be surmised at present. Arrhythmias that may be due to disorders of impulse formation include slow atrial, junctional, and ventricular escape rhythms, certain types of atrial tachycardias (such as those produced by digitalis), accelerated junctional (nonparoxysmal junctional tachycardia) and idioventricular rhythms, and parasystole. Arrhythmias that may be due to disorders of impulse conduction include flutter and fibrillation, atrioventricular nodal reentrant tachycardia, reciprocating tachycardias associated with an accessory pathway, sinus nodal reentry, some atrial tachycardias, and many ventricular tachycardias. Understanding the mechanism of the tachycardia, in some instances, helps direct rational therapeutic approaches.

Animals↗
PubMed1983

Clinical efficacy of amiodarone in treatment of recurrent ventricular tachycardia and ventricular fibrillation.

The clinical antiarrhythmic efficacy of amiodarone treatment was examined in 196 patients with recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) resistant to other antiarrhythmic drugs. Patients had received a mean of 4.4 +/- 1.9 unsuccessful drug trials over a mean of 15.2 months prior to amiodarone treatment of recurrent VF in 57 patients; recurrent, sustained VT in 95 patients; and recurrent, nonsustained VT in 44 patients. Amiodarone dosage during the first 2 to 4 weeks of treatment was 800 to 1600 mg/day. During long-term follow-up, amiodarone dosage was reduced to 200 to 600 mg/day, based on the control of arrhythmia and patient tolerance. Electrophysiologic studies were performed prior to and after 2 or more weeks of amiodarone treatment. After a mean follow-up of 16.2 +/- 13.0 months, 126 (64%) of 196 patients continued successful treatment with amiodarone. At electrophysiologic study, amiodarone prevented VT induction in 13 patients, and although VT was induced in 101 patients, 80 patients continued treatment for 14.2 months without recurrence of spontaneous VT. Amiodarone treatment was discontinued because of recurrent VT in 22 patients, sudden cardiac death in 15 patients, adverse effects in 12 patients, and noncardiac death in 21 patients. In nine patients, recurrent VT/VF appeared related to amiodarone-induced exacerbation of arrhythmia. Pulmonary toxicity occurred in seven patients, and 19 patients developed blue skin discoloration. Other adverse effects were usually dosage related. In summary, amiodarone was a highly effective antiarrhythmic drug, but at the dosages employed, the risk of significant adverse effects warrants careful surveillance during treatment.

Adolescent↗
PubMed1983

Relationships between amiodarone dosage, drug concentrations, and adverse side effects.

The relationships between size of loading dose and drug concentration, size of maintenance dose and drug concentration, and pulmonary and cutaneous adverse side effects and drug dosage were examined in patients given amiodarone. Amiodarone and metabolite concentrations in plasma and red cell samples were measured by specific high-pressure liquid chromatography. During drug loading, a daily dose schedule of 1600 mg/day produced significantly higher drug concentrations than did a loading dose schedule of 800 mg/day. During maintenance therapy, amiodarone dosage correlated with drug concentrations but with a wide interpatient variability for any given dosage level. The ratio of desethylamiodarone to amiodarone remained relatively constant over different dosage or drug concentration ranges, but increased with duration of treatment, suggesting a time-dependent metabolic function that may be analogous to the time-dependent attainment of maximal antiarrhythmic effect. The occurrence of pulmonary toxicity from amiodarone was not related to duration of treatment or cumulative dose of drug, buy may relate to the magnitude of the maintenance dose of amiodarone. Blue skin discoloration occurred in 19 (36%) of 53 patients receiving amiodarone for longer than 17 months, and may relate to the cumulative dose.

Amiodarone↗
PubMed1983

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia.

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.

Adult↗
PubMed1983

Syncope and ventricular tachycardia in patients with ventricular preexcitation.

Four patients with ventricular preexcitation whose syncope initially was attributed to an arrhythmia utilizing the accessory pathway are presented. At electrophysiologic study, the electrophysiologic characteristics of the accessory pathways were considered unlikely to support a tachycardia of a rate sufficient to result in syncope. Programmed stimulation of the right ventricle, however, reproducibly induced ventricular tachycardia to which the syncope was subsequently attributed in 3 patients. The importance of identifying ventricular tachycardia as the cause of syncope in these patients is emphasized.

Adult↗
PubMed1983

Intracardiac recording by catheter electrode of accessory pathway depolarization.

At electrophysiologic study in a patient with the Wolff-Parkinson-White syndrome, intracardiac catheter recordings demonstrated a deflection that occurred 30 ms before ventricular activation. The rapid deflection was present during ventricular preexcitation but not during normal atrioventricular conduction. All QRS complexes were preexcited to varying degrees during atrial fibrillation, yet the deflection consistently preceded ventricular activation by 30 ms. This deflection most likely represents the rare recording of a Kent bundle depolarization with an intracardiac electrode catheter.

Adult↗
PubMed1983

Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.

The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) less than or equal to 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) less than or equal to 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (delta AH) less than or equal to 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and delta AH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR less than or equal to 60 msec, 36 (23%) shortest PCL 1:1 less than or equal to 300 msec, 76 (48%) delta AH less than or equal to 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither delta AH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and delta AH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.

Adolescent↗
PubMed1983

Drug therapy of cardiac arrhythmias.

The authors provide an overview of the general features of pharmacokinetics and report the pharmacodynamic and pharmacokinetic interactions of selected antiarrhythmic drugs. Their clinical experience in the use of investigational antiarrhythmic drugs is also presented.

Amiodarone↗
PubMed1983

Clinical electrophysiology of ventricular tachycardia.

Programmed ventricular stimulation, electrophysiologic effects of various antiarrhythmic drugs, and the results of serial electrophysiologic testing in patients with ventricular arrhythmias are discussed. The use of discriminant analysis to predict the efficacy of antiarrhythmic drugs is also briefly analyzed.

Anti-Arrhythmia Agents↗