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S H Hohnloser - One of the best experts on this subject based on the ideXlab platform.
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prospective comparison of flecainide versus Quinidine for the treatment of paroxysmal atrial fibrillation flutter
American Journal of Cardiology, 1996Co-Authors: Gerald V Naccarelli, Paul Dorian, S H Hohnloser, Philippe CoumelAbstract:Abstract In order to compare the efficacy and long-term tolerability of flecainide acetate versus Quinidine, 239 patients with paroxysmal atrial fibrillation were prospectively treated with flecainide (n = 122) or Quinidine (n = 117) in an open-label, randomized trial. All patients were followed for 1 year after initiation of therapy unless their antiarrhythmic drug was discontinued due to an inadequate therapeutic response or intolerable side effects. Although both drugs were equally effective in adequately controlling recurrences of atrial fibrillation (difference, p = 0.282; not significant), fewer flecainide patients had to have their therapy discontinued due to adverse experiences (p = 0.012). Based on both endpoints (efficacy and tolerability), an estimated 70.5% of flecainide versus 55.4% of Quinidine patients would remain effectively treated at the end of 1 year on therapy (p ≤ 0.007). The findings of this prospective study suggest that in the treatment of paroxysmal atrial fibrillation (1) flecainide and Quinidine are equally effective in the acceptable suppression of symptomatic paroxysmal atrial fibrillation; (2) flecainide is better tolerated than Quinidine and is less likely to be discontinued due to adverse effects; and (3) given the overall endpoint of efficacy and tolerability, more patients are likely to continue long-term therapy with flecainide than with Quinidine.
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efficacy and proarrhythmic hazards of pharmacologic cardioversion of atrial fibrillation prospective comparison of sotalol versus Quinidine
Journal of the American College of Cardiology, 1995Co-Authors: S H Hohnloser, Andreas Van De Loo, Frank BaedekerAbstract:Objectives. This study compared the efficacy and safety of sotalol and Quinidine for conversion and prevention of recurrent atrial fibrillation. Background. Atrial fibrillation is the most common arrhythmia. Pharmacologic therapy has been advocated for both immediate restoration of sinus rhythm and prevention of recurrent atrial fibrillation. Quinidine is the therapeutic mainstay for both purposes, but its safety has recently been questioned. Although sotalol has been used successfully to maintain sinus rhythm after direct current cardioversion, its efficacy in pharmacologically reverting atrial fibrillation has not been examined. Methods. Fifty consecutive patients with persistent atrial fibrillation were randomized to receive Quinidine or sotalol for up to 7 days to restore sinus rhythm. Patients were followed up for 6 months. Results. Quinidine was more effective than sotalol in terminating atrial fibrillation (60% vs. 20%, p = 0.009). When nonresponders to drug therapy underwent subsequent direct current cardioversion, total conversion rates in the Quinidine and sotalol groups were comparable (88% vs. 68%, p = 0.17), as was the efficacy of the two drugs in preventing recurrent atrial fibrillation. Side effects necessitating drug discontinuation were more often observed with Quinidine. No patient receiving sotalol but four patients receiving Quinidine had drug-associated arrhythmia (torsade de pointes in three patients, sustained ventricular tachycardia in one patient). Precordial QT dispersion determined on the surface electrocardiogram (ECG) increased with Quinidine (mean ± SD 34 ± 9 vs. 44 ± 16 ms, p = 0.02), indicating enhanced inhomogeneity in ventricular repolarization. There was no change in QT dispersion in patients receiving sotalol (36 ± 18 vs. 40 ± 17 ms, p = 0.44). Conclusions. Quinidine is more effective than sotalol in terminating atrial fibrillation but is associated with more side effects. The proarrhythmic risk may be related to Quinidine's propensity to increase disparity in ventricular repolarization. This risk warrants careful ECG monitoring during the 1st 4 to 7 days of therapy. Because most proarrhythmic effects occurred shortly after restoration of sinus rhythm, observation should continue ≥2 to 3 days after sinus rhythm is reestablished.
J Tonet - One of the best experts on this subject based on the ideXlab platform.
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long term efficacy of low doses of Quinidine on malignant arrhythmias in brugada syndrome with an implantable cardioverter defibrillator a case series and literature review
Heart Rhythm, 2012Co-Authors: Manlio F Marquez, Aime Bonny, Eduardo Hernandezcastillo, Antonio De Sisti, Jorge Gomezflores, Santiago Nava, Francoise Hiddenlucet, P Iturralde, Manuel Cardenas, J TonetAbstract:BACKGROUND To prevent the recurrence of ventricular arrhythmias (VA) in Brugada syndrome (BrS), only Quinidine has been consistently reported to have a beneficial effect. Recommended doses are≥1 g/d. The efficacy of lower doses of Quinidine has been suggested on the basis of a few isolated experiences. OBJECTIVES To describe the efficacy and safety of doses≤600 mg/d of Quinidine after cardioverter-defibrillator implantation in BrS at 2 referral centers and to compare those results with a comprehensive review of the literature. METHODS In a retrospective analysis of medical records from the 2 centers, 6 men with BrS who received≤600 mg/d of Quinidine sulfate or hydroQuinidine after cardioverter-defibrillator implantation were identified. Quinidine was initiated after arrhythmic syncope or appropriate shocks, including arrhythmic storm in 4. A literature search was performed to find previous cases with symptomatic BrS reported as having received≤600 mg/d of Quinidine. RESULTS Quinidine prevented recurrence of VA in all patients from our series without side effects during a median follow-up of 4 years (from 2 to 8 years). In the literature review, 14 additional adults were found. With the exception of 3, Quinidine effectively suppressed arrhythmic events in all of them. Four subjects who discontinued the medication experienced VA recurrence, successfully treated by restarting Quinidine. CONCLUSIONS Low doses of Quinidine were well tolerated and effective to prevent the recurrence of VA, including arrhythmic storm, in subjects with BrS with an implantable cardioverter-defibrillator. Effectiveness of Quinidine or hydroQuinidine in doses≤600 mg/d is 85%.
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long term efficacy of low doses of Quinidine on malignant arrhythmias in brugada syndrome with an implantable cardioverter defibrillator a case series and literature review
Heart Rhythm, 2012Co-Authors: Manlio F Marquez, Aime Bonny, Eduardo Hernandezcastillo, Antonio De Sisti, Jorge Gomezflores, Santiago Nava, Francoise Hiddenlucet, P Iturralde, Manuel Cardenas, J TonetAbstract:BACKGROUND To prevent the recurrence of ventricular arrhythmias (VA) in Brugada syndrome (BrS), only Quinidine has been consistently reported to have a beneficial effect. Recommended doses are≥1 g/d. The efficacy of lower doses of Quinidine has been suggested on the basis of a few isolated experiences. OBJECTIVES To describe the efficacy and safety of doses≤600 mg/d of Quinidine after cardioverter-defibrillator implantation in BrS at 2 referral centers and to compare those results with a comprehensive review of the literature. METHODS In a retrospective analysis of medical records from the 2 centers, 6 men with BrS who received≤600 mg/d of Quinidine sulfate or hydroQuinidine after cardioverter-defibrillator implantation were identified. Quinidine was initiated after arrhythmic syncope or appropriate shocks, including arrhythmic storm in 4. A literature search was performed to find previous cases with symptomatic BrS reported as having received≤600 mg/d of Quinidine. RESULTS Quinidine prevented recurrence of VA in all patients from our series without side effects during a median follow-up of 4 years (from 2 to 8 years). In the literature review, 14 additional adults were found. With the exception of 3, Quinidine effectively suppressed arrhythmic events in all of them. Four subjects who discontinued the medication experienced VA recurrence, successfully treated by restarting Quinidine. CONCLUSIONS Low doses of Quinidine were well tolerated and effective to prevent the recurrence of VA, including arrhythmic storm, in subjects with BrS with an implantable cardioverter-defibrillator. Effectiveness of Quinidine or hydroQuinidine in doses≤600 mg/d is 85%.
Michael R Rosen - One of the best experts on this subject based on the ideXlab platform.
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effects of Quinidine on repolarization in canine epicardium midmyocardium and endocardium
Circulation, 1997Co-Authors: Eugene A Sosunov, Evgeny P Anyukhovsky, Michael R RosenAbstract:Background The antiarrhythmic action of Quinidine is associated with a slowing of conduction and prolongation of repolarization. The latter effect has no consistent correlation with Quinidine actions on action potential duration (APD) in isolated tissue experiments. To enhance our understanding of the mechanisms of Quinidine action, we studied its effect on APD in canine epicardial, midmyocardial, and endocardial tissues. Methods and Results Standard microelectrode techniques were used to study the effects of Quinidine 2.5 to 20 μmol/L on APD in ventricular epicardial, endocardial, and transmural (M-cell) slabs at cycle lengths (CLs) from 300 to 4000 ms. Qualitatively different time courses of actions and concentration- and rate-dependent effects were seen in M cells compared with the others. In endocardium and epicardium, Quinidine induced monotonic and concentration-dependent APD prolongation at all CLs. In contrast, the effects of Quinidine in M cells varied from prolongation to shortening, depending o...
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effects of Quinidine on repolarization in canine epicardium midmyocardium and endocardium i in vitro study
Circulation, 1997Co-Authors: Eugene A Sosunov, Evgeny P Anyukhovsky, Michael R RosenAbstract:Background The antiarrhythmic action of Quinidine is associated with a slowing of conduction and prolongation of repolarization. The latter effect has no consistent correlation with Quinidine actions on action potential duration (APD) in isolated tissue experiments. To enhance our understanding of the mechanisms of Quinidine action, we studied its effect on APD in canine epicardial, midmyocardial, and endocardial tissues. Methods and Results Standard microelectrode techniques were used to study the effects of Quinidine 2.5 to 20 μmol/L on APD in ventricular epicardial, endocardial, and transmural (M-cell) slabs at cycle lengths (CLs) from 300 to 4000 ms. Qualitatively different time courses of actions and concentration- and rate-dependent effects were seen in M cells compared with the others. In endocardium and epicardium, Quinidine induced monotonic and concentration-dependent APD prolongation at all CLs. In contrast, the effects of Quinidine in M cells varied from prolongation to shortening, depending on duration of superfusion, concentration, and CL. Experiments with E4031 and TTX suggested that in M cells, Quinidine-induced APD lengthening was attributable to block of delayed rectifier potassium current and APD shortening was due to inhibition of TTX-sensitive steady-state sodium current. Conclusions In vitro, there is a significant difference of Quinidine effects in M cells versus epicardial and endocardial cells that appears to reflect differences in the contributions of specific ion channels to the APD at the three sites. The differences may influence the actions of Quinidine on repolarization of the heart in situ and determine both the proarrhythmic and antiarrhythmic actions of the drug.
Frank Baedeker - One of the best experts on this subject based on the ideXlab platform.
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efficacy and proarrhythmic hazards of pharmacologic cardioversion of atrial fibrillation prospective comparison of sotalol versus Quinidine
Journal of the American College of Cardiology, 1995Co-Authors: S H Hohnloser, Andreas Van De Loo, Frank BaedekerAbstract:Objectives. This study compared the efficacy and safety of sotalol and Quinidine for conversion and prevention of recurrent atrial fibrillation. Background. Atrial fibrillation is the most common arrhythmia. Pharmacologic therapy has been advocated for both immediate restoration of sinus rhythm and prevention of recurrent atrial fibrillation. Quinidine is the therapeutic mainstay for both purposes, but its safety has recently been questioned. Although sotalol has been used successfully to maintain sinus rhythm after direct current cardioversion, its efficacy in pharmacologically reverting atrial fibrillation has not been examined. Methods. Fifty consecutive patients with persistent atrial fibrillation were randomized to receive Quinidine or sotalol for up to 7 days to restore sinus rhythm. Patients were followed up for 6 months. Results. Quinidine was more effective than sotalol in terminating atrial fibrillation (60% vs. 20%, p = 0.009). When nonresponders to drug therapy underwent subsequent direct current cardioversion, total conversion rates in the Quinidine and sotalol groups were comparable (88% vs. 68%, p = 0.17), as was the efficacy of the two drugs in preventing recurrent atrial fibrillation. Side effects necessitating drug discontinuation were more often observed with Quinidine. No patient receiving sotalol but four patients receiving Quinidine had drug-associated arrhythmia (torsade de pointes in three patients, sustained ventricular tachycardia in one patient). Precordial QT dispersion determined on the surface electrocardiogram (ECG) increased with Quinidine (mean ± SD 34 ± 9 vs. 44 ± 16 ms, p = 0.02), indicating enhanced inhomogeneity in ventricular repolarization. There was no change in QT dispersion in patients receiving sotalol (36 ± 18 vs. 40 ± 17 ms, p = 0.44). Conclusions. Quinidine is more effective than sotalol in terminating atrial fibrillation but is associated with more side effects. The proarrhythmic risk may be related to Quinidine's propensity to increase disparity in ventricular repolarization. This risk warrants careful ECG monitoring during the 1st 4 to 7 days of therapy. Because most proarrhythmic effects occurred shortly after restoration of sinus rhythm, observation should continue ≥2 to 3 days after sinus rhythm is reestablished.
Jerry L Bauman - One of the best experts on this subject based on the ideXlab platform.
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comparison of sotalol versus Quinidine for maintenance of normal sinus rhythm in patients with chronic atrial fibrillation
American Journal of Cardiology, 1999Co-Authors: Mary Ross Southworth, Dawn G Zarembski, Marlos A G Viana, Jerry L BaumanAbstract:Many clinicians choose sotalol for the prevention of recurrences of atrial fibrillation (AF) as an alternative to Quinidine, which has been associated with an increase in long-term mortality. Using meta-analytic techniques, we compared the effects on maintenance of sinus rhythm and mortality of combined groups of patients with chronic AF treated with sotalol, Quinidine, or a control drug. Rates of conversion at 6 months and mortality were combined for each group after performing sensitivity analysis to test for homogeneity. Bayesian estimates and corresponding 95% credibility intervals were constructed to compare the probabilities of achieving sinus rhythm and mortality among groups. A literature search revealed 4 sotalol studies, 6 Quinidine studies, and 5 control studies that met inclusion criteria established a priori. The point estimates for maintaining normal sinus rhythm (at 6 months) and corresponding credibility intervals for the 3 groups were sotalol 50% (range 42% to 58%), Quinidine 53% (range 48% to 59%), and control 32% (range 26% to 39%). When combining and comparing mortality effects, the following studies met the same inclusion criteria: 4 sotalol studies, 9 Quinidine studies, and 7 control studies. The point estimates and corresponding credibility intervals for mortality in the 3 groups were sotalol 2.2% (range 0.6% to 4.8%), Quinidine 3.0% (range 1.7% to 4.7%), and control 1.1% (range 0.3% to 2.4%). Sotalol and Quinidine are comparable in their ability to maintain sinus rhythm at 6 months (about 50%) and both agents are superior to control. There is a trend for both agents to increase mortality with long-term therapy. These data do not support choosing sotalol over Quinidine as a safer alternative for preventing recurrences of chronic AF.
