Mg Of Propafenone Research Articles

Comparison of efficacy of pharmacological cardioversion with antazoline and propafenone versus electrical cardioversion in atrial fibrillation during cryoablation.

Antazoline with propafenone may be an alternative to electrical cardioversion (ECV) in restoring sinus rhythm in patients with atrial fibrillation (AF), including during balloon cryoablation. To compare the efficacy of antazoline with propafenone and ECV in restoring and maintaining sinus rhythm at discharge in patients with AF during cryoablation with special regard to type of AF. The study retrospectively analyzed 196 patients who underwent elective cryoablation. Eighty-nine patients who developed AF in the perioperative period were selected as the study group (32 women and 57 men). The study group was divided into two groups - 46 (51.7%) patients were given pharmacological cardioversion with 70 mg of propafenone and 100 or 200 mg of antazoline, whereas the other 43 (48.3%) patients underwent ECV. There were no statistically significant differences between the groups regarding: left atrial area, left atrium diameter, right atrial area and right atrium diameter. In the overall population, ECV was more effective than antazoline with propafenone therapy (31 [72.1%] vs. 20 [43.5%]; p = 0.01). A similar relationship was demonstrated in patients with persistent AF (13 [59.1%] vs. 3 [12.5%]; p = 0.002). There was no significant difference in the group of patients with paroxysmal AF (18 (85.6%) vs. 17 (77.3%); p = 0.7). In AF during the cryoablation procedure ECV appears to be more effective in restoring and maintaining sinus rhythm at discharge than antazoline with propafenone in the general AF patient population, especially in patients with persistent AF.

The successful pregnancy in patient with Wolff-Parkinson-White syndrome type B

Background: An aberrant accessory route is a hallmark of the rare heart rhythm condition called Wolff-Parkinson-White (WPW) syndrome. The onset of tachyarrhythmias, which can result in hemodynamic instability and even maternal mortality, is considered to be triggered by a variety of physiological changes that occur during pregnancy. Therefore, it is anticipated that effective management options for pregnant women who have WPW syndrome will be able to regulate tachyarrhythmias and give healthy pregnancies for both the mother and the fetus. Case Report: A 32-year-old pregnant woman with 34 weeks of gestational age arrived complaining of palpitations and breathing difficulties. The results of the ECG test revealed left branch bundle block (LBBB), a Wolff-Parkinson-White (WPW) type B pattern, and sinus tachycardia. Both an NST assessment and an echocardiographic evaluation revealed no fetal distress or structural abnormalities of the heart. The patient was treated with 300 mg of Propafenone, which was administered on a regular basis whenever the patient experienced palpitations. Due to a history of prior caesarean deliveries, the pregnancy had progressed to 40 weeks of gestation and caesarean birth under spinal anaesthesia was performed in this point. The infant was born healthy, full-term, and free from birth problems. Conclusion: One of the causes of tachyarrhythmias in WPW syndrome is pregnancy. Arrhythmias that could develop in women with WPW syndrome can be controlled with good pregnancy planning and management.

Safety of Pill-in-the-Pocket Class 1C Antiarrhythmic Drugs for Atrial Fibrillation.

Guidelines recommend that initial trial of a "pill-in-the-pocket" (PIP) Class 1C antiarrhythmic drug (AAD) for cardioversion of atrial fibrillation (AF) be performed in a monitored setting because of the potential for adverse reactions. This study sought to characterize real-world, contemporary use of the PIP approach, including the setting of initiation and incidence of adverse events. This retrospective cohort study included all patients at the Hospital of the University of Pennsylvania treated with a PIP approach for AF between 2007 and2020. A total of 273 patients (age 56 ± 13 years; 182 [67%] male; CHA2DS2VASc score 1.1 ± 1.2) took a first dose of PIP AAD. Flecainide was used in 151 (55%) and propafenone in 122 (45%). The first dose of PIP AAD was taken in a monitored setting in 167 (62%). Significant adverse events occurred in 7 patients (3%), 2 of whom had taken the doseinamonitored setting. Significant adverse events included unexplained syncope (1 of 7), symptomatic bradycardia/hypotension(4 of 7), and 1:1 atrial flutter (2 of 7). All occurred in patients taking 300mg of flecainide (n=4) or 600mg of propafenone (n=3). Electrical cardioversion was performed in 29 (11%) patients because of failure of the AAD to terminate AF. One patient required intravenous fluids and vasopressors for 2 hours because of persistent hypotension andbradycardia. Two patients required permanent pacemakers for bradycardia. The remaining patients required no intervention. Our data support the current recommendation to initiate PIP AAD in a monitored setting because ofrare significant adverse reactions that can require urgent intervention.

A CASE OF CORTICOSTEROID-ASSOCIATED SUPRAVENTRICULAR TACHYCARDIA STORM

A CASE OF CORTICOSTEROID-ASSOCIATED SUPRAVENTRICULAR TACHYCARDIA STORM

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

A previously healthy 73-year-old woman presented to hospital with acute atrial fibrillation. After intravenous procainamide failed to restore sinus rhythm, she was treated with 300 mg of oral propafenone and discharged with a prescription for propafenone and propranolol. Six hours later she took 150 mg of propafenone as prescribed. Within 1 hour she became dyspneic and collapsed. On arrival in hospital she was unconscious, with a wide complex tachycardia and no obtainable blood pressure. After defibrillation and lidocaine, she converted to a wide complex sinus rhythm, but remained profoundly hypotensive despite intravenous epinephrine and dopamine. Hypertonic sodium bicarbonate (HCO3) was administered and, shortly thereafter, her blood pressure increased, her QRS duration normalized and her clinical status improved dramatically. In this case of severe refractory propafenone-related cardiac toxicity, intravenous HCO3 led to a profound clinical improvement. Emergency physicians should be familiar with the syndrome of sodium-channel blocker poisoning and recognize the potentially important role of bicarbonate in its treatment.

Kinetics of Buccal Absorption of Propafenone Single Oral Loading Dose in Healthy Humans

Buccal absorption has an advantage when compared with other administration routes because of its rapid onset of action. We examined the pharmacokinetics of buccal-absorbed propafenone in healthy humans. 1. After a single oral administration of 150 mg of propafenone, the average peak concentration of propafenone was 27.9±2.5 ng/ml, and that of 5-hydroxypropafenone was 61.7±6.6 ng/ml ( n=5). The times to reach peak serum concentrations of propafenone and 5-hydroxypropafenone were 1.8±0.1 hr and 1.5±0.2 hr, respectively. 2. After a buccal absorption of 150 mg of propafenone, the time to reach peak serum concentration of propafenone was 16.9±2.3 min ( n=8). The average peak concentration of propafenone was 30.4±1.4 ng/ml ( n=8), and the concentrations of 5-hydroxypropafenone were below the detection limit in all subjects. The rapid upstroke of serum concentrations of propafenone by buccal administration may cause rapid onset of pharmacological conversion.

The Role of Genetically Determined Polymorphic Drug Metabolism in the Beta-Blockade Produced by Propafenone

Propranolol and the sodium-channel-blocking antiarrhythmic agent propafenone share structural features. Although propafenone's beta-blocking actions are readily demonstrable in vitro, clinically significant beta-blockade occurs inconsistently in vivo. In this study, we tested the hypothesis that genetically determined variations in the biotransformation of propafenone to its 5-hydroxy metabolite account for variations in the drug's beta-blocking action. We assessed beta-blockade by measuring the reduction in tachycardia produced by boluses of isoproterenol and treadmill exercise in 14 normal subjects during treatment with placebo and with 150, 225, and 300 mg of propafenone every eight hours for five days each. Nine subjects (with the extensive-metabolizer phenotype) metabolized most of the propafenone to 5-hydroxy propafenone, and five (with the poor-metabolizer phenotype) did not produce this metabolite. At the lower dosages, beta-blockade was present in both groups but was significantly greater in the subjects with poor metabolism, in whom deficient 5-hydroxylation was associated with higher plasma propafenone levels. At the highest dose, a similar degree of beta-blockade was observed in the two groups. Propafenone also had a higher affinity for beta 2 receptors in vitro than either of its major metabolites. We conclude that the degree of beta-blockade during propafenone therapy reflects genetically determined variations in the metabolism of the parent drug, which is necessary for beta-blockade, and that this action of propafenone is considerably enhanced in patients with deficient 5-hydroxylation of propafenone.

Interaction between digoxin and propafenone.

The pharmacokinetic and pharmacodynamic interactions between digoxin and propafenone were investigated in 10 hospitalized patients with heart disease and cardiac arrhythmias. During steady state (0.25 mg/day) the glycoside was combined with 600 mg of propafenone daily for 1 week. The mean +/- SD serum digoxin concentration (SDC) was 0.97 +/- 0.29 ng/ml before and 1.54 +/- 0.65 ng/ml (p less than 0.003) during propafenone administration. Propafenone induced a mean decrease in 31.1 and 31.7% in total and renal digoxin clearances, respectively. The increase in SDCs was accompanied by a decrease in heart rate (HR) and shortening of QTC (QT interval corrected for HR). In patients receiving digoxin and propafenone simultaneously, the SDCs should be monitored and the digoxin dose reduced if there is evidence of toxicity.

Plasma and Saliva Propafenone Concentrations at Steady State

Twenty-four healthy male subjects were administered 300mg of propafenone every 8h for 6 d in each of two phases that were separated by 2 d. Plasma samples were collected during the approach to steady state for each phase, and plasma and saliva samples were collected frequently at steady state. Both plasma and saliva propafenone were assayed by a specific HPLC method. Two estimates of elimination half-life (l1/2), mean steady-state concentration (CPSS¯), time to maximal concentration (tmax), and maximal concentration (CPmax), were estimated for each subject. Also mean steady-state saliva concentrations (CSSS¯), time to maximal saliva concentration (tSmax), and maximal saliva concentrations (CSmax) were estimated. A large inter subject variance in both t1/2 and CPSS¯ were observed in the 24 subjects, with the t1/2 values ranging from 2.1 to 27.2h and the CPSS¯ values from 0.3 to 3.03 μg/mL. Each subject was quite consistent for the two phases, suggesting a relatively low intrasubject variance for propafenone kinetics. A histogram shows most subjects to have t1/2 values between 2 and 10 h, with diminishing numbers of subjects at greater t1/2 values rather than a bimodal distribution. Saliva concentrations ranged from 12 to 72% of the corresponding plasma concentrations, being 24.7 ± 11.1% of the simultaneously collected plasma sample overall (mean ± SD). A significant (p<0.001) positive correlation exists between CPSS¯ and CSSS¯.

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 (Ms). 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.

Propafenone: Noninvasive evaluation of efficacy

Propafenone, a new antiarrhythmic drug, was administered to 60 patients with a history of refractory ventricular tachyarrhythmias, including ventricular fibrillation in 16 and ventricular tachycardia (VT) in 44. A noninvasive protocol was followed utilizing ambulatory monitoring and exercise testing for evaluation of drug effect. The protocol involved acute drug testing with 450 mg of propafenone followed by maintenance therapy with 150 to 300 mg t.i.d. for 4 days. The protocol was completed by 57 patients; in 3 patients side effects developed that necessitated discontinuation of the drug before evaluation. When evaluated by monitoring, 34 patients (60%) responded to the drug, with total elimination of runs of VT, a greater than 90% reduction in couplets and a greater than 50% decrease in the frequency of ventricular premature beats. Based on exercise testing, 36 patients (63%) were deemed responders. When both exercise and monitoring were considered, 30 of 57 patients (53%) responded to propafenone. The acute drug test predicted the response to maintenance therapy in 84% of patients. Propafenone did not change left ventricular function in patients with normal ejection fractions (greater than 50%). However, in those with an ejection fraction less than 50%, propafenone significantly reduced this value (34% vs 29%, p less than 0.01). Side effects occurred in 20 patients (33%) and included nausea, congestive heart failure, aggravation of arrhythmia and conduction abnormalities. Eleven patients have continued on propafenone for an average of 16 months with continued efficacy and freedom from side effects.