Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome.

Sellers, T. Duncan; Campbell, R. W. F.; Bashore, Thomas M.; Gallagher, John J.

doi:10.1161/01.cir.55.1.15

Cited by 118 publications

(14 citation statements)

References 23 publications

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“…Programmed electrical stimulation was performed with rectangular stimuli of 1.8 to 2.0 msec and currents of twice late-diastolic threshold. The pacing protocol included: (1) incremental high right atrial and coronary sinus pacing, beginning at a cycle length just shorter than the spontaneous sinus cycle length and shortening the pacing cycle length by 10 to 20 msec decrements until AV block occurred or until limited by symptoms of the patient; (2) determinations of atrial and ventricular refractory period after every eighth sinus complex, or atrial or ventricular paced complex, a premature complex was introduced beginning in late diastole, and the premature coupling interval was shortened by 10 to 20 msec decrements until the effective refractory period of the chamber being tested was reached; (3) incremental right ventricular pacing, beginning at a cycle length just shorter than the spontaneous sinus cycle length and shortening the pacing cycle length by 10 to 20 msec decrements until ventriculoatrial block occurred or until limited by symptoms of the patient; (4) induction of AV reentrant tachycardia by programmed atrial or ventricular stimulation with one or two extrastimuli or bursts of atrial or ventricular pacing; (5) initiation of atrial fibrillation with bursts of atrial pacing at cycle lengths less than or equal to 250 msec.…”

Section: Methodsmentioning

confidence: 99%

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

Prystowsky¹,

Klein²,

Rinkenberger³

et al. 1984

Circulation

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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 was 328 ± 66 msec in patients in whom antegrade conduction block occurred, and it was 247 + 21 msec (p < .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 < .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 43.8 to 238.3 ± 87.9 msec (p < .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. Circulation 69, No. 2, 278-287, 1984. SUPRAVENTRICULAR TACHYCARDIA frequently occurs in patients who have accessory atrioventricular (AV) pathways. Reentrant tachycardia most commonly conducts antegradely over the normal AV pathway and retrogradely over the accessory pathway.

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Section: Methodsmentioning

confidence: 99%

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

Prystowsky¹,

Klein²,

Rinkenberger³

et al. 1984

Circulation

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show abstract

“…Thus, these agents should be used only when electrophysiologic studies have demonstrated their safety. Vaughn Williams Class IA antiarrhythmics are effective because of blockade in the accessory pathway [11].…”

Section: Antitachycardia Pacing For Supraventricular Tachycardiamentioning

confidence: 99%

Advances in the Management of Tachyarrhythmias

Herre

1987

J Intensive Care Med

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Recent developments of both diagnostic and therapeu tic techniques in the management of tachyarrhythmias have broadened the options available to physicians car ing for patients with tachyarrhythmias. Newer diag nostic methods allow more precise identification of the arrhythmia and better understanding of its mechanism. Long-term epidemiologic studies have identified groups of patients who do and do not require antiarrhythmic therapy. Antitachycardia pacemakers and automatic im plantable defibrillators allow effective treatment for pa tients for whom drugs were ineffective or in whom in tolerable side effects developed. Finally, several new antiarrhythmic agents have become available recently. Proper use of these new techniques and drugs requires greater understanding of the pathophysiology of cardiac arrhythmias.

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“…The actions of antiarrhythmic drugs on the accessory bypass tract in preexcitation have been defined at electrophysiology study and are summarized in Table 3. [54][55][56][57][58][59][60][61][62][63][64][65] In treatment of reciprocating tachycardia, drugs that influence either limb of the reentrant circuit may be effective. Drugs that have their sole action in slowing conduction and increasing refractoriness of the AV 62; for example, digoxin,…”

Section: Preexcitation Syndromesmentioning

confidence: 99%

Cardiac Electrophysiologic Testing: Its Role in the Selection of Antiarrhythmic Drug Regimens for Supraventricular and Ventricular Arrhythmias

et al. 1985

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Cardiac electrophysiology studies use intracardiac recording and programmed stimulation to define the mechanisms and most appropriate therapy for supraventricular and ventricular arrhythmias. Using these techniques, the majority of clinical tachycardias can be reproducibly initiated and terminated in the electrophysiology laboratory, thereby allowing the most appropriate therapy to be selected. With this approach, antiarrhythmic agents can be tested in a systematic, serialized fashion for efficacy, safety and patient tolerance. With both supraventricular and ventricular tachycardias, suppression of arrhythmia induction predicts freedom from recurrence, whereas inducibility carries a poor prognosis in clinical follow-up. Electrophysiology studies provide a safe and effective approach to the treatment of selected patients with cardiac arrhythmias.

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Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome.

Cited by 118 publications

References 23 publications

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

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

Advances in the Management of Tachyarrhythmias

Cardiac Electrophysiologic Testing: Its Role in the Selection of Antiarrhythmic Drug Regimens for Supraventricular and Ventricular Arrhythmias

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