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At least 469 records · Page 26Linked to original sources

PubMed1985

The yield of programmed ventricular stimulation in mitral valve prolapse patients with ventricular arrhythmias.

A high-risk subset of patients with mitral valve prolapse (MVP) and a predisposition to sudden cardiac death (SCD) has been proposed. We analyzed the results of programmed ventricular stimulation (PVS) in 20 patients with MVP and ventricular arrhythmias (ventricular premature depolarization in 6, ventricular couplets in 2, nonsustained ventricular tachycardia [VT] in 7, ventricular fibrillation [VF] in 5) and in 12 "normal" control subjects. With the use of an identical stimulation protocol from the right ventricular apex (twice diastolic threshold, three extrastimuli), 9 of 20 MVP patients and 1 of 12 normal subjects had inducible ventricular arrhythmias (p less than 0.05). When more aggressive attempts at ventricular stimulation were used, an additional five MVP patients had positive responses to PVS while no normal subjects did. In the MVP group, the following arrhythmias were induced: nonsustained polymorphic VT in 10, VF in three, and ventricular flutter in one. In all but two patients, triple ventricular extrastimuli were required to elicit this response. Two of the 10 MVP patients undergoing electropharmacologic testing had a successful antiarrhythmic regimen identified, while 13 patients were discharged on empiric antiarrhythmic therapy. At a follow-up of 19.8 +/- 13.1 months, all 19 MVP patients who could be contacted were alive. Five patients had symptomatic recurrences at follow-up including two SCD survivors (VT in one and VF in one). In conclusion, it was found that the majority of MVP patients with ventricular arrhythmias have inducible ventricular tachyarrhythmias during PVS and are more susceptible to this than patients without structural heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Propafenone therapy for ventricular tachycardia in the setting of congestive heart failure.

The combined occurrence of impaired left ventricular function and ventricular tachyarrhythmias portend a high annual mortality. Although antiarrhythmic drugs can reduce ventricular arrhythmias, the prognosis may be unchanged. We administered propafenone to 12 patients with ventricular tachyarrhythmias and left ventricular ejection fractions less than 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in five of six patients. In eight patients studied before and during therapy, there was no significant change in left ventricular ejection fraction determined by nuclear ventriculography. Propafenone was discontinued in three patients due to side effects. All patients remain alive and without recurrence of clinically significant arrhythmia over a mean follow-up period of 14 months. Propafenone is an effective drug for the management of ventricular tachyarrhythmias, and may be used in patients with impaired left ventricular function.

Administration, Oral↗

PubMed1985

Aggravation of electrically provoked ventricular tachycardia during treatment with propafenone.

Propafenone is a new class Ic antiarrhythmic agent currently being investigated in the United States. It is generally well tolerated. We administered propafenone to 16 patients with ventricular tachycardia (VT) that had been refractory to conventional antiarrhythmic drug therapy. Three of these 16 patients developed electrically provoked incessant VT during treatment with propafenone without other evidence of toxicity. These arrhythmias subsided after lidocaine was administered. Propafenone therapy was discontinued in each case. Incessant VT did not develop in any of these patients in the absence of antiarrhythmic drugs or on antiarrhythmic drugs other than propafenone. Alternative effective treatment was identified for each patient. Although VT was initially provoked by pacing in each of these patients, these observations suggest that propafenone, like some other class Ic drugs, may favor the development of incessant VT in occasional patients. This appears most likely to occur in patients with ventricular dysfunction and prior sustained VT or ventricular fibrillation.

Aged↗

PubMed1985

Comparison of propafenone and disopyramide for treatment of chronic ventricular arrhythmias: placebo-controlled, double-blind, randomized crossover study.

In a double blind, placebo-controlled study, the efficacy of propafenone, a new antiarrhythmic drug was compared to that of disopyramide. Sixteen patients with frequent and complex premature ventricular contractions (PVCs) were studied by serial 24-hour ambulatory monitoring, while they were receiving propafenone, 300 mg, and disopyramide, 200 mg, both every 8 hours. A reduction in the mean frequency of PVCs per hour, in comparison to the placebo period, from 574 +/- 535 to 100 +/- 130, was observed after propafenone (p less than 0.005) and from 629 +/- 455 to 231 +/- 280 after disopyramide (p less than 0.008). A greater than 70% reduction in PVCs in comparison to placebo was observed in 11 of 14 after propafenone and 9 of 15 after disopyramide (NS). A greater than or equal to 90% reduction in PVCs was observed in 9 of 16 with propafenone and in 4 of 15 with disopyramide (p less than 0.05). The suppression of complex PVCs (repetitive, polymorphic, or more than 5/min with bigeminism) was observed in 11 of 14 after propafenone and in 9 of 14 after disopyramide. The abolition of nonsustained ventricular tachycardia was observed in 6 of 6 and 3 of 5, respectively, after propafenone and disopyramide (p less than 0.05). A lower incidence of side effects, 4 of 16 vs 8 of 16, was observed during propafenone than during disopyramide treatment. We conclude that propafenone, in a dose of 900 mg daily, is more effective than disopyramide, in a dose of 600 mg daily, in the treatment of frequent and complex PVCs and nonsustained ventricular tachycardias. Propafenone also showed a lower incidence of side effects.

Adult↗

PubMed1983

Clinical efficacy and electrophysiology of oral propafenone for ventricular tachycardia.

Sixteen patients with ventricular tachycardia (VT) or nonfatal cardiac arrest were treated with propafenone (P), 900 mg/day. Electrophysiologic studies were performed before and during therapy with P. All patients had inducible sustained VT at the baseline study. During P therapy, VT was not inducible in 1 patient, was unsustained in 1 and was harder to induce in 2 patients. P increased the cycle length of VT from 307 +/- 67 to 382 +/- 107 ms. Five patients began outpatient therapy with P, including 2 in whom VT was slowed to less than 125 beats/min. Two are arrhythmia-free during follow-up of 2 and 8 months. P significantly increased intraatrial conduction time (from 44 +/- 12 to 72 +/- 22 ms), AH interval (from 115 +/- 36 to 152 +/- 45 ms), HV interval (from 55 +/- 18 to 92 +/- 42 ms), QRS duration (from 140 +/- 36 to 180 +/- 48 ms) and QT interval (from 402 +/- 30 to 459 +/- 60 ms). P increased atrial (from 247 +/- 36 to 288 +/- 38 ms) and ventricular (from 249 +/- 20 to 277 +/- 32 ms) effective refractory periods, Sinus cycle length did not change, but the corrected sinus node recovery time increased (from 162 +/- 85 to 821 +/- 1,607 ms). P aggravated arrhythmias in 4 patients. The plasma P concentration, measured either at the time of electrophysiologic studies of when therapy was discontinued, was 753 +/- 428 ng/ml. P suppressed ventricular ectopic beats in 33% and increased them in 1 patient. P has antiarrhythmic activity against VT similar to that of other antiarrhythmic drugs and has potential for serious adverse effects in some patients.

Administration, Oral↗

PubMed1984

Electrophysiologic effects of propafenone on canine ischemic cardiac cells.

The electrophysiologic effects of propafenone were studied by conventional microelectrode techniques in ischemic myocardial and Purkinje fibers from 1-day-old myocardial infarction in the dog. Propafenone reduced the amplitude and rate of rise of normal myocardial and Purkinje action potentials and had little effect on the resting potential. In the control state, both ischemic myocardial and Purkinje fibers had reduced resting potential, action potential amplitude and upstroke velocity. These fibers were more susceptible to the depressant effects of propafenone than normal fibers. Ischemic myocardial fibers were particularly sensitive to the actions of propafenone that resulted in marked depression of action potential characteristics, with little effect on resting potential. These changes resulted in cycle length-dependent conduction disorders in ischemic epicardial preparations. However, in ischemic endocardial preparations in which triggered activity could be initiated, propafenone reversibly suppressed the triggered activity. Termination of the triggered activity was preceded by slowing of the rate, which was attributed to a decrease in the rate of rise of the delayed afterdepolarizations. This activity terminated when the delayed afterdepolarization failed to attain threshold potential. This study suggests that propafenone has a membrane-anesthetic effect, with the abnormal fast channel in ischemic cells being more sensitive; propafenone depresses delayed afterdepolarizations in ischemic Purkinje fibers; and the actions of propafenone could result in an antiarrhythmic effect in vivo on both reentrant ventricular rhythms in ischemic myocardium and triggered rhythms in ischemic Purkinje fibers.

Action Potentials↗

PubMed1984

A controlled trial of propafenone for treatment of frequent and repetitive ventricular premature complexes.

The effectiveness of oral propafenone was evaluated for the treatment of ventricular premature complexes (VPCs) in 12 patients, using a single-blind, dose-ranging trial followed by a double-blind comparison with placebo, and then an open-label, long-term protocol. During dose ranging, 8 of 12 patients achieved greater than or equal to 80% suppression of total VPCs (mean 83%) (p less than 0.01 vs single-blind placebo). Paired VPCs were suppressed greater than or equal to 90% and ventricular tachycardia was eliminated in 11 of the 12 patients (p less than 0.01). The effectiveness of propafenone for treatment of VPCs was confirmed during the double-blind trial (p less than 0.05 vs double-blind placebo) and during treatment for 6 months (p less than 0.05 vs initial single-blind placebo). Propafenone prolonged the PR interval by 16% (p less than 0.01 vs single-blind placebo) and the QRS interval by 18% (p less than 0.001). Left ventricular systolic performance decreased as assessed by 2-dimensional echocardiography (p less than 0.01 vs single-blind placebo). Propafenone increased serum digoxin levels in 5 of 5 patients (mean increase of 83%). Side effects included exacerbation of congestive heart failure (1 patient) and conduction abnormalities (2 patients). Thus, propafenone is effective for treatment of total and repetitive VPCs. Although generally well tolerated, the drug reduces left ventricular systolic function and atrioventricular conduction and increases serum digoxin levels.

Adult↗

PubMed1984

New directions in antiarrhythmic drug therapy.

Cardiac arrhythmia causing sudden cardiac death is a serious worldwide public health problem. Antiarrhythmic agents have been available for therapy, but the conventional agents cause a high degree of intolerable side effects. The recent development of many new experimental antiarrhythmic agents has increased our capacity to effectively treat cardiac arrhythmias. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise testing and 24-hour ambulatory Holter monitoring, it can reasonably be decided which patient needs therapy and if therapy is going to be effective. Both aspects of the sudden death equation, ectopy frequency (triggering mechanism) and the ability to propagate sustained ventricular tachycardia (substrate), may be examined. Careful follow-up is needed to determine continued drug efficacy and the presence of side effects that may compromise patient compliance with therapy. If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate. A comprehensive approach to arrhythmia management may begin to reduce the high incidence of sudden death due to fatal arrhythmias.

Adrenergic beta-Antagonists↗

PubMed1985

Efficacy of propafenone compared with quinidine in chronic ventricular arrhythmias.

A double-blind, randomized study was designed to evaluate the efficacy of oral propafenone and oral quinidine in suppressing premature ventricular complexes (PVCs). Twenty-five men were studied for 3 weeks. Twelve were randomized to the quinidine group and 13 to the propafenone group. Small doses of the drugs were administered for 1 week (200 mg of quinidine every 6 hours or 300 mg of propafenone every 12 hours) and large doses were administered for another week (400 mg of quinidine every 6 hours or 300 mg of propafenone every 8 hours). Strict criteria were used to define responders to antiarrhythmic therapy. For more than 85% reduction in total PVCs per hour: During the low-dose week, 36% in the quinidine group and 50% in the propafenone group were responders (difference not significant [NS]), while during the high-dose week 33% and 64% were responders (NS). For more than 95% reduction of ventricular couplets per hour: During the low-dose week, 45% in each group were responders, while during the high-dose week, 56% and 60% were responders (NS). For 100% abolition of ventricular tachycardia (VT) beats per 24 hours: During the low-dose week, 60% in the quinidine group and 56% in the propafenone group were responders (NS); during the high-dose week 80% and 67% were responders (NS). There was no significant difference in the 2 groups in incidence of side effects. This study shows comparable efficacy and tolerance of propafenone and quinidine for the control of ventricular arrhythmias in ambulatory patients with diverse forms of heart diseases.

Adult↗

PubMed1985

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia.

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1958