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Antiarrhythmic Drug Therapy (antiarrhythmic + drug_therapy)
Selected AbstractsTotal Atrioventricular Nodal Ablation Increases Atrial Fibrillation Burden in Patients with Paroxysmal Atrial Fibrillation Despite Continuation of Antiarrhythmic Drug TherapyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2003RIK WILLEMS M.D. Introduction: Total atrioventricular nodal (TAVN) ablation and pacing is an accepted and safe treatment for patients with drug-refractory paroxysmal atrial fibrillation (AF). Many patients develop permanent AF within the first 6 months after TAVN ablation. This usually is ascribed to the cessation of antiarrhythmic drug therapy. We hypothesized that TAVN ablation itself creates an atrial substrate prone to AF. Methods and Results: Patients participating in the Atrial Pacing Periablation for Paroxysmal Atrial Fibrillation (PA3) study who remained on stable antiarrhythmic drug therapy throughout follow-up were included in this analysis. AF burden and the development of persistent AF in the preablation period were compared to two consecutive postablation periods. Echocardiographic changes also were evaluated. Twenty-two patients remained on stable drug therapy (9 men and 13 women, age 59 ± 3 years). One patient developed persistent AF preablation compared to 10 postablation (P < 0.05). AF burden preablation was 3.0 ± 1.2 hours/day and increased to 10.4 ± 2.2 hours/day and 11.8 ± 2.3 hours/day in the two postablation follow-up periods (P < 0.05). In patients with fractional shortening (FS) >30% prior to ablation, FS decreased significantly from 39.4%± 1.3% to 36.4%± 1.7% (P < 0.05). In contrast, in patients with a FS ,30% prior to ablation, FS increased from 27%± 0.8% to 33.6 ± 1.7% (P < 0.05). Conclusion: TAVN ablation increases AF burden and facilitates the development of persistent AF in patients with paroxysmal AF despite the continuation of antiarrhythmic drugs. Loss of AV and/or interventricular synchrony may lead to altered cardiac hemodynamics resulting in atrial stretch and increasing AF burden. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1296-1301, December 2003) [source] Ionic Basis of Pharmacological Therapy in Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2007MANLIO F. MÁRQUEZ M.D. An implantable cardioverter-defibrillator is considered the only effective therapy to terminate ventricular arrhythmias in symptomatic patients with Brugada syndrome. However, it does not prevent future arrhythmic episodes. Only antiarrhythmic drug therapy can prevent them. There have been several reports of a beneficial effect of oral quinidine in both asymptomatic and symptomatic patients. Other possible beneficial oral agents could be Ito blockers. Intravenous isoproterenol has been reported to be especially useful in abolishing arrhythmic storms in emergency situations. Also, isolated case reports on the usefulness of cilostazol, sotalol, and mexiletine have been described. The present article reviews the mechanisms by which these drugs may act and their possible role in the pharmacotherapy of this disease. [source] Total Atrioventricular Nodal Ablation Increases Atrial Fibrillation Burden in Patients with Paroxysmal Atrial Fibrillation Despite Continuation of Antiarrhythmic Drug TherapyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2003RIK WILLEMS M.D. Introduction: Total atrioventricular nodal (TAVN) ablation and pacing is an accepted and safe treatment for patients with drug-refractory paroxysmal atrial fibrillation (AF). Many patients develop permanent AF within the first 6 months after TAVN ablation. This usually is ascribed to the cessation of antiarrhythmic drug therapy. We hypothesized that TAVN ablation itself creates an atrial substrate prone to AF. Methods and Results: Patients participating in the Atrial Pacing Periablation for Paroxysmal Atrial Fibrillation (PA3) study who remained on stable antiarrhythmic drug therapy throughout follow-up were included in this analysis. AF burden and the development of persistent AF in the preablation period were compared to two consecutive postablation periods. Echocardiographic changes also were evaluated. Twenty-two patients remained on stable drug therapy (9 men and 13 women, age 59 ± 3 years). One patient developed persistent AF preablation compared to 10 postablation (P < 0.05). AF burden preablation was 3.0 ± 1.2 hours/day and increased to 10.4 ± 2.2 hours/day and 11.8 ± 2.3 hours/day in the two postablation follow-up periods (P < 0.05). In patients with fractional shortening (FS) >30% prior to ablation, FS decreased significantly from 39.4%± 1.3% to 36.4%± 1.7% (P < 0.05). In contrast, in patients with a FS ,30% prior to ablation, FS increased from 27%± 0.8% to 33.6 ± 1.7% (P < 0.05). Conclusion: TAVN ablation increases AF burden and facilitates the development of persistent AF in patients with paroxysmal AF despite the continuation of antiarrhythmic drugs. Loss of AV and/or interventricular synchrony may lead to altered cardiac hemodynamics resulting in atrial stretch and increasing AF burden. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1296-1301, December 2003) [source] Mini-Maze Suffices as Adjunct to Mitral Valve Surgery in Patients with Preoperative Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2000ANTON E. TUINENBURG M.D. Mini-Maze and Mitral Valve Surgery. Introduction: After mitral valve (MV) surgery, preoperative atrial fibrillation (AF) often recurs while cardioversion therapy generally fails. Additional Cox maze surgery improves postoperative arrhythmia outcome, but the extensive nature of such an approach limits general appliance. We investigated the clinical outcome of a simplified, less extensive Cox maze procedure ("mini-maze") as adjunct to MV surgery. Methods and Results: Thirteen patients with MV disease and preoperative AF were treated with combined surgery (group 1). Nine control patients without previous AF underwent isolated MV surgery (group 2). We retrospectively compared the results to findings in 23 patients with preoperative AF who had undergone isolated MV surgery (group 3). In group 1, mini-maze took an additional 46 minutes of perfusion time. One 75-year-old patient died of postoperative multiple organ failure. Seven patients showed spontaneously converting (within 2 months) postoperative AF. After 1 year, 82% were in sinus rhythm (SR). No sinus node dysfunction was observed. In group 2, all patients were in SR after 1 year. In group 3, only 53% were in SR after 1 year, despite serial cardioversion and antiarrhythmic drug therapy. Exercise tolerance and heart rate were comparable for groups 1 and 2. Left atrial function was present in all but one patient in group 1 and in all patients in group 2 (after MV reconstruction). Conclusion: Adding a relatively simple mini-maze to MV surgery improves arrhythmia outcome in patients with preoperative AF without introducing sinus node dysfunction or persistent absence of left atrial function. The results of this type of combined surgery are encouraging and deserve further attention. [source] Prevention of sudden cardiac deathCLINICAL CARDIOLOGY, Issue S1 2005Eric N. Prystowsky M.D. Abstract It is often unclear why some patients suffer sudden cardiac death (SCD), or even what risk factors correlate best with the syndrome. This review describes current thinking on the prevention of SCD. Most studies have focused on the prevention of potentially fatal ventricular arrhythmias in patients post myocardial infarction (MI). While pharmacotherapy has a role in the prevention of SCD in patients post MI, the interpretation of drug trials can be problematic. This is because not all patients participating in such trials received optimized medical therapy by today's standards. As a result, trial outcomes for new therapies may not reflect their true efficacy when they are added to a background of best medical care. The two principal prophylactic modalities for SCD studied to date are antiarrhythmic drug therapy and use of an implantable cardioverter defibrillator (ICD). At the present time, antiarrhythmic drugs, such as the class III agent amiodarone, seem to display relatively limited efficacy for the primary prevention of sudden death in most patients post MI. Most clinical trials have found that ICD therapy has a significant mortality benefit in patients at high risk for ventricular arrhythmias. This has been demonstrated in primary prevention trials, and in secondary prevention trials such as Antiarrhythmics Versus Implantable Defibrillators (AVID), which studied patients who survived a near-fatal ventricular arrhythmia. Based on an analysis of secondary prevention trials, the single patient characteristic that best predicted an advantage of ICD therapy over antiarrhythmic drug therapy was a left ventricular (LV) ejection fraction , 35%. Cardiac resynchronization therapy has been established as having a mortality benefit in patients with dyssynchronous LV contraction associated with dilated cardiomyopathy. [source] | ||||||||||