Sex-specific triggers for right ventricular outflow tract tachycardia.

BACKGROUND: Right ventricular outflow tract tachycardia (RVOT-VT) is a common arrhythmia in young patients without heart disease. The arrhythmia is characterized by repetitive bursts and premature ventricular contractions with a left bundle branch block, inferior-axis QRS morphology, and symptoms of palpitations. Although more frequent in women, sex-specific triggers for symptomatic RVOT-VT have not been identified. METHODS AND RESULTS: We interviewed 34 women and 13 men referred for ablation of RVOT-VT to determine if predictable but sex-specific exacerbations in symptomatic RVOT-VT exist. After a general query asking if there was predictability to what triggered palpitations, we then specifically queried all patients about symptomatic RVOT-VT initiation with exercise, stress, caffeine, fatigue, and, in women only, periods of recognized hormonal flux. The times identified as states of hormonal flux included premenstrual, gestational, perimenopausal, and coincident with the administration of birth control pills. In response to the completed interview, the most common recorded trigger for RVOT-VT in women was recognized states of hormonal flux with 20 (59%) of 34 women responding positively and 14 (41%) of the 34 indicating that states of hormonal flux were the only recognizable triggers. Men were more likely than women to report that their RVOT-VT was predictably triggered by exercise, stress, or caffeine: 12 (92%) of 13 men versus 14 (41%) of 34 women (P <.01). CONCLUSIONS: Triggers for RVOT-VT initiation are sex specific. Women have RVOT-VT initiation with recognized states of hormonal flux. Men more commonly have RVOT-VT initiated by exercise or stress. These data have important implications related to patient education and counseling in the setting of RVOT-VT and may influence the timing of drug treatment and electrophysiologic evaluation in selected patients.

Electroanatomic magnetic mapping during ablation of isthmus-dependent atrial flutter.

INTRODUCTION: Although recent studies have demonstrated that the endpoint of isthmus conduction block is superior to that of termination and subsequent inability to induce atrial flutter (AFl), the optimal method for determining isthmus conduction block has not been determined. Electroanatomic magnetic mapping during coronary sinus (CS) pacing may provide a reliable endpoint for AFl ablation. METHODS AND RESULTS: Catheter mapping and ablation was performed in 42 patients with isthmus-dependent AFl. The patients were divided into two groups, based on procedural endpoint: Group I (28 patients) - isthmus conduction block was determined based on multipolar catheter recordings and electroanatomic mapping, and Group II (14 patients) - isthmus conduction block was determined by electroanatomic mapping during CS pacing alone. In Group I, ablation procedures were acutely successful in 25 of 28 patients (89 %). A 100 % concordance between the data presented by multipolar catheter recordings and electroanatomic mapping was noted in determining the presence or absence of isthmus conduction block. In Group II, ablation procedures were acutely successful in 13 of 14 patients, 13 (93 %). After a mean of 16.3+/-3.7 months follow up, there was 1 atrial flutter recurrence in the 38 patients (2.6 %) with demonstrated isthmus block at the end of the procedure. CONCLUSIONS: Electroanatomic magnetic mapping during CS pacing is comparable to the multipolar catheter mapping technique for assessing isthmus conduction block as an endpoint for AFl ablation procedures.

Concomitant device and drug therapy: current trends, potential benefits, and adverse interactions.

Antiarrhythmic drug therapy in patients with implantable cardioverter defibrillators (ICDs) has decreased over the last 10 years. This trend, primarily seen with class I agents, has occurred mainly in patients with a cardiac arrest. However, despite this overall decrease, antiarrhythmic drug therapy remains an important adjuvant to ICD therapy. In addition to primary prevention of ventricular tachycardia and supraventricular tachycardia, antiarrhythmic drug therapy may potentiate tachycardia rate slowing and make ventricular tachycardia more tolerated hemodynamically and possibly more amendable to pacing therapy. Some of the class III antiarrhythmic drugs may actually lower defibrillation threshold. Unfortunately, these drugs may have adverse interactions with ICDs. An increase in defibrillation threshold or rate-dependent increase in pacing threshold may interfere with the effectiveness of device therapy. Proarrhythmic effects of antiarrhythmic drugs may enhance the frequency of device use. The bradycardic effects of antiarrhythmic drug therapy may similarly enhance the requirements for persistent bradycardia pacing and lead to early battery depletion and other adverse consequences. An awareness of potential benefits and adverse effects of antiarrhythmic drug therapy along with careful electrophysiologic assessment are necessary for optimum combination drug and device therapy.