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Biomedical subjects

E N Prystowsky

Publications and source records attributed to E N Prystowsky.

At least 91 records · Page 5Linked to original sources
PubMed1988

Prospective evaluation of a discriminant function for prediction of recurrent symptomatic ventricular tachycardia or ventricular fibrillation in coronary artery disease patients receiving amiodarone and having inducible ventricular tachycardia at electrophysiologic study.

Induction of ventricular tachycardia (VT) at electrophysiologic study in patients taking amiodarone poorly predicts recurrence of VT. Consequently, a discriminant function was developed (using parameters based on retrospective data) that appeared to identify high-risk patients. These parameters included ventricular effective refractory period, corrected QT interval, initiation of a repetitive ventricular response and the mode of VT induction. In the present study these parameters were prospectively evaluated in 60 patients with coronary artery disease and sustained VT or ventricular fibrillation (VF), in whom VT was still induced at electrophysiologic study during amiodarone therapy. Thirteen patients had recurrent events (sudden death in 8 and sustained VT in 5) and 47 patients had no symptomatic arrhythmia recurrence (follow-up for 16 +/- 2 months, mean +/- standard error of the mean). The ventricular effective refractory period, corrected QT interval and presence of a repetitive ventricular response did not discriminate between patients with and without symptomatic arrhythmia recurrence. However, an easier mode of VT induction during amiodarone therapy versus control was highly predictive of arrhythmia recurrence: 9 of 13 (69%) recurrences were in this group. In contrast, only 4 of 44 (9%) patients who had either the same or harder mode of VT induction had a recurrent event. Overall, 9 of 16 (56%) patients with an easier mode of VT induction had a recurrence, including 6 of the 8 patients with subsequent sudden cardiac death. It is concluded that electrophysiologic testing during amiodarone therapy is useful to identify high-risk patients.

Administration, Oral↗
PubMed1988

Antiarrhythmic therapy for asymptomatic ventricular arrhythmias.

The rationale for treatment of patients with nonsustained asymptomatic ventricular arrhythmias is the theoretical benefit of preventing more serious ventricular arrhythmias and sudden cardiac death. Because of the high costs involved and the serious side effects, such as proarrhythmia, associated with this therapy, the decision to treat this patient group for a potential protective effect must be weighed carefully. Risk factors identifying those patients most likely to have further complications include the presence of heart disease and left ventricular dysfunction, and the relative severity of these conditions. Those patients who fit into high-risk groups are the ones most likely to benefit, although this benefit is still unproved. If antiarrhythmic therapy is given, it is recommended that it be started in the hospital and that the efficacy of treatment be assessed by serial electrophysiologic-pharmacologic testing or noninvasive means. Empiric treatment, especially started out-of-hospital, is discouraged because it is least likely to benefit the patient and most likely to cause harm.

Anti-Arrhythmia Agents↗
PubMed1988

The effects of slow channel blockers and beta blockers on atrioventricular nodal conduction.

The PR interval on the electrocardiogram represents the time that it takes an impulse to travel through the atrium and atrioventricular (AV) conduction system to the ventricles. Normally, activation is slowest in the AV node, and variations in PR interval most commonly parallel changes in AV nodal activation time. The AV nodal conduction time and effective refractory period are rate dependent and, in adult humans, are usually prolonged with increasing atrial paced rates. In addition, alterations in autonomic tone effect AV nodal conduction as well as sinus rate. The effect is usually in the same direction but often to different degrees. In patients with normal AV nodal function, parasympathetic and sympathetic tone are balanced at rest, but in patients with abnormal AV conduction, the effect of the parasympathetic system is more marked. Drugs including the slow channel blockers and beta blockers, affect AV nodal function. Slow channel blockers inhibit the slow inward calcium current, which may prolong conduction and refractoriness in the AV node. However, whereas diltiazem and verapamil have been shown to prolong AV nodal conduction and refractoriness in humans, nifedipine, a potent vasodilator, cannot be used in doses large enough to affect the AV node. The increase in PR interval caused by verapamil is minimal, and at doses of less than 480 mg/d, AV block occurs infrequently. When AV block occurs, it is first degree block in most patients, and it is usually asymptomatic. The electrophysiologic effects of diltiazem are similar to those of verapamil. Beta blockers also have a negative dromotropic effect on the AV node. They prolong the AH interval and AV nodal refractory periods and may lengthen the PR interval. The prolonged PR interval rarely results in more than first degree AV block in patients receiving maintenance therapy. In selected patients, combination therapy with a slow channel blocker and a beta blocker rarely causes second-degree AV block.

Adrenergic beta-Antagonists↗
PubMed1988

Parasympathetic and sympathetic alterations of Mobitz type II heart block.

This study examined the effects of changes in parasympathetic and sympathetic tone on the cycle length at which Mobitz type II second degree atrioventricular (AV) block occurred. Four patients who had electrocardiographic evidence of type II AV block and confirmation of block in the His-Purkinje system during electrophysiologic study were evaluated. These patients received intravenous atropine (1.0 to 2.4 mg), propranolol (0.15 mg/kg body weight) or isoproterenol (1 and 2 micrograms/min) alone or in combination. In two of three patients receiving propranolol, the atrial pacing cycle length at which 1:1 His-Purkinje conduction occurred was prolonged relative to control (from 360 to 470 ms and 440 to 590 ms, respectively). In contrast, atropine in the presence of beta-adrenergic blockade shortened the cycle length at which 1:1 His-Purkinje conduction occurred in three of four patients receiving the drug (470 to 390, 630 to 570 and 590 to 560 ms, respectively). Isoproterenol also improved His-Purkinje conduction in the one patient receiving this drug. No agent affected the duration of the HV interval during spontaneous sinus rhythm or right atrial pacing. Thus, drugs that alter autonomic tone influence abnormal His-Purkinje conduction minimally during sinus rhythm but, importantly, may modulate the atrial pacing cycle length at which type II AV block occurs.

Aged↗
PubMed1988

Surgical division of Wolff-Parkinson-White pathways utilizing the closed-heart technique: a 2-year experience in 47 patients.

Kent bundle interruption for ventricular preexcitation has been successfully accomplished utilizing several different surgical techniques. The external closed-heart technique of Guiraudon combining surgical dissection and cryoablation has been used to interrupt 52 accessory pathways in 47 consecutive patients since May, 1985. The 35 male and 12 female patients ranged in age from 10 to 67 years (mean, 30 years). There were 25 left free wall, 13 right free wall, 13 posterior septal, and 1 anterior septal accessory pathways. Preoperative and intraoperative electrophysiological studies were performed in all patients to induce the arrhythmia and localize all accessory pathways. The operation consisted of dissection of the atrioventricular fat pad. Following this, the delta wave and retrograde accessory pathway conduction disappeared, thereby indicating successful pathway ablation. In 4 patients with right-sided accessory pathways, interruption of the pathway required cryoablation. Cryolesions (made with cryoprobe at -60 degrees C for two minutes) were created in the region of the accessory pathway insertion. All accessory pathways were successfully ablated without any deaths or heart block. Concomitant surgical procedures were performed in 4 patients. Two patients required a second operation the next day for an accessory pathway not found at the initial operation. Three patients had postpericardiotomy syndrome, and 4 had recurrent atrial fibrillation requiring therapy. The remaining patients have had no arrhythmia recurrence and have remained drug free after a follow-up of 1 month to 22 months (mean, 12.5 months). We conclude that the closed-heart technique of accessory pathway ablation is safe and reproducible, obviates the necessity for aortic cross-clamping and cardioplegic arrest, and allows instantaneous monitoring of conduction over the pathway.

Adolescent↗
PubMed1988

Procainamide infusion test: inability to identify patients with Wolff-Parkinson-White syndrome who are potentially at risk of sudden death.

Persistence of preexcitation in sinus rhythm with procainamide infusion has been reported to occur in patients with a short anterograde accessory pathway effective refractory period (AERPAP) and this test has been proposed as a reliable noninvasive method to identify patients with the Wolff-Parkinson-White syndrome who are at risk of sudden death. However, sudden death correlates best with a shortest preexcited RR interval during atrial fibrillation (SRRPE) of 260 msec or less. We infused 10 to 12 mg/kg procainamide to 56 patients to determine whether persistence or loss of preexcitation in sinus rhythm identified patients with SRRPEs of 260 or less or greater than 260 msec, respectively. Atrial fibrillation was induced in 53 patients. Of these, 32 patients had persistence of preexcitation with procainamide infusion and SRRPE in this group of patients was shorter than that in patients in whom preexcitation was lost (194 +/- 44 vs 235 +/- 55 msec, p less than .05). However, preexcitation persisted after procainamide infusion in only 31 of 46 (67%) patients with SRRPEs of 260 msec or less. Furthermore, 15 of 21 patients who lost preexcitation had SRRPEs of 260 msec or less and two of these patients had a history of ventricular fibrillation. The correlation between AERPAP and SRRPE was studied in a separate group of 79 patients with single accessory pathways. There was a significant (p less than .001) but poor (r = .58) correlation between these two variables. Thus, the procainamide test regarding accessory pathway refractoriness often cannot be extrapolated to SRRPE.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1988

Issues in the selection of an antiarrhythmic agent.

The approach to patients with cardiac arrhythmias involves four steps: diagnosis, determination of whether therapy is needed, choice of appropriate treatment, and evaluation of efficacy of therapy. Factors affecting the decision to treat a patient include the presence and type of symptoms associated with the tachyarrhythmia, as well as the frequency with which the arrhythmia occurs. Antiarrhythmic drugs are usually recommended as first-line therapy although nonpharmacologic approaches are preferable in certain specific situations. There are minimal data for most arrhythmias that aid the physician in the selection of a specific drug for a given patient, and many agents will often be equally effective. Most often drugs are selected that have the least potential to produce harmful side effects to the patient; thus, choice of therapy must be individualized. Newer agents are effective but their antiarrhythmic and side effect profiles will not be understood fully until they have been used widely in diverse patient populations. Regardless of which drug is prescribed, invasive or noninvasive methods should be employed to evaluate therapeutic efficacy.

Anti-Arrhythmia Agents↗
PubMed1987

Beta-blocker therapy for the Wolff-Parkinson-White syndrome.

Two types of arrhythmias are associated with the Wolff-Parkinson-White syndrome: those in which the accessory pathway is a required part of the reentrant circuit, e.g., orthodromic atrioventricular reciprocating tachycardia, and those that conduct over the accessory pathway but do not require its activation for maintenance of tachycardia, e.g., atrial flutter/fibrillation. Increased sympathetic tone shortens the refractoriness of atrial and ventricular tissue; however, conduction in the atrium and ventricle is not considered the limiting factor for maintenance of atrioventricular reciprocating tachycardia or conduction over the accessory pathway in atrial arrhythmias. Intravenous beta-adrenergic blockers given to patients in the resting state have a minimal to moderate effect in depressing atrioventricular nodal conduction, but have little or no effect on accessory pathway refractoriness or conduction in most patients. In patients presenting with atrioventricular reentry, intravenous administration of beta-adrenergic blocking drugs often is not effective to terminate tachycardia. However, long-term oral therapy with these agents may be beneficial, especially in patients in whom enhanced sympathetic tone is responsible for the initiation or maintenance of tachycardia.

Adrenergic beta-Antagonists↗
PubMed1987

Supernormal conduction in accessory atrioventricular connections.

Prospective electrophysiologic evaluation of 74 patients with ventricular preexcitation revealed 4 patients who had supernormal anterograde conduction over an accessory atrioventricular pathway. In each patient, anterograde conduction over the accessory pathway was present at relatively slow sinus rates, but the accessory pathway anterograde effective refractory period was substantially prolonged. During premature atrial stimulation, a "window" of supernormal conduction was identified at which closely coupled atrial extrastimuli conducted over the accessory pathway, whereas longer premature intervals resulted in accessory pathway block. Causes other than supernormal conduction to explain this phenomenon, for example, phase 4 block, were unlikely in each case. Although the mechanism of supernormal conduction in humans is unknown, the electrophysiologic findings in our patients are similar to those reported in patients with supernormal conduction in the His-Purkinje system.

Adult↗
PubMed1987

Electrophysiologic and antiarrhythmic effects of oral encainide in patients with atrioventricular nodal reentry or nodoventricular reentry.

Three patients with drug-resistant atrioventricular (AV) nodal reentrant tachycardia and two patients with reciprocating tachycardia associated with nodoventricular pathways received oral encainide after a control drug-free electrophysiologic study. In one patient with AV nodal reentry, encainide prolonged anterograde AV nodal conduction, produced complete ventriculoatrial (VA) block, and prevented tachycardia induction. Encainide had no effect on AV or VA conduction in the second patient with AV nodal reentry, and tachycardia with similar cycle length was still induced. The third patient was not studied while receiving encainide, but spontaneous AV nodal reentrant tachycardia occurring multiple times daily was abolished. In both patients with nodoventricular pathways, anterograde AV nodal and VA conduction were prolonged by encainide and tachycardia was no longer inducible. Two patients with AV nodal reentry were given long-term encainide therapy and have been free of recurrent arrhythmias for 16 and 30 months. One patient with a nodoventricular pathway has been without arrhythmia recurrence after 73 months of encainide therapy; the other patient required addition of propranolol to encainide because of recurrent tachycardia. We conclude that encainide can prolong anterograde AV nodal and VA conduction and prevent induced and spontaneous tachycardia in some patients with drug-resistant and highly symptomatic AV nodal or nodoventricular reentry.

Administration, Oral↗
PubMed1987

Pharmacokinetic and electrophysiologic interactions of amiodarone and procainamide.

The effects of amiodarone on the pharmacokinetic and electrophysiologic properties of procainamide were examined in eight patients treated for recurrent ventricular arrhythmias who received intravenous procainamide, 6 to 15 mg/kg, at control and after 1 to 2 weeks of oral amiodarone treatment. Compared with control, procainamide plasma clearance decreased from 0.43 +/- 0.12 L/kg-hr to 0.33 +/- 0.12 L/kg-hr (P less than 0.01), plasma elimination half-life increased from 3.77 +/- 0.64 hours to 5.21 +/- 0.42 hours (P less than 0.01), and volume of distribution was unchanged from 2.31 +/- 0.74 L/kg to 2.47 +/- 0.90 L/kg during amiodarone treatment. As single agents, intravenous procainamide and oral amiodarone produced equivalent increases in QRS duration, rate-corrected QT interval, right ventricular effective refractory period, and cycle length of induced ventricular tachycardia. After the addition of intravenous procainamide to amiodarone the QRS duration, rate-corrected QT interval, and, in six of eight patients, ventricular tachycardia cycle length were significantly increased compared with control or either drug alone, suggesting additive electrophysiologic effect. However, acceleration of induced ventricular tachycardia occurred in one patient with combined treatment, suggesting a potential for adverse electrophysiologic interactions. These findings indicate that amiodarone has pharmacokinetic and electrophysiologic interactions with procainamide and suggest that the intravenous dose of procainamide be reduced by 20% to 30% during concurrent drug administration.

Aged↗
PubMed1987

Wolff-Parkinson-White syndrome and sudden cardiac death.

Every year, individuals with no history of heart disease succumb to sudden cardiac death (SCD). Pathologic examination of the hearts usually reveals various forms of heart disease as hypertrophic cardiomyopathy or coronary artery disease. In other cases, however, there is no obvious structural heart disease, and it is possible that some of these individuals died because of a cardiac arrhythmia involving an accessory pathway. If this were the case, the most likely scenario would be onset of atrioventricular reciprocating tachycardia (AVRT), degeneration of the AVRT into atrial fibrillation with a rapid ventricular response over the accessory pathway, and subsequent death caused by the development of ventricular fibrillation. Although these events have been documented, albeit rarely, during intracardiac electrophysiologic studies, in reality very little is known about the natural history of asymptomatic and untreated patients with Wolff-Parkinson-White (WPW) syndrome. In fact, SCD in a previously asymptomatic patient with WPW syndrome is probably relatively rare. Whether asymptomatic WPW patients should undergo electrophysiologic or pharmacologic testing to determine their 'potential' to develop serious cardiac arrhythmias is controversial. The present paucity of data concerning the natural history of WPW syndrome in asymptomatic patients militates against successful identification of those patients who are at risk for sudden death. Long-term prospective studies are necessary to clarify which asymptomatic patients with WPW syndrome require treatment.

Death, Sudden↗