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.

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.