Background-Successful antitachycardia pacing (ATP) terminates ventricular tachycardia (VT) up to 250 bpm without the need for painful shocks in implantable cardioverter-defibrillator (ICD) patients. Fast VT (FVT) Ͼ200 bpm is often treated by shock because of safety concerns, however. This prospective, randomized, multicenter trial compares the safety and utility of empirical ATP with shocks for FVT in a broad ICD population. Methods and Results-We randomized 634 ICD patients to 2 arms-standardized empirical ATP (nϭ313) or shock (nϭ321)-for initial therapy of spontaneous FVT. ICDs were programmed to detect FVT when 18 of 24 intervals were 188 to 250 bpm and 0 of the last 8 intervals were Ͼ250 bpm. Initial FVT therapy was ATP (8 pulses, 88% of FVT cycle length) or shock at 10 J above the defibrillation threshold. Syncope and arrhythmic symptoms were collected through patient diaries and interviews. In 11Ϯ3 months of follow-up, 431 episodes of FVT occurred in 98 patients, representing 32% of ventricular tachyarrhythmias and 76% of those that would be detected as ventricular fibrillation and shocked with traditional ICD programming. ATP was effective in 229 of 284 episodes in the ATP arm (81%, 72% adjusted). Acceleration, episode duration, syncope, and sudden death were similar between arms. Quality of life, measured with the SF-36, improved in patients with FVT in both arms but more so in the ATP arm. Conclusions-Compared with shocks, empirical ATP for FVT is highly effective, is equally safe, and improves quality of life. ATP may be the preferred FVT therapy in most ICD patients.

Background-The occurrence of atrial fibrillation after ablation of type I atrial flutter remains an important clinical problem. To gain further insight into the pathogenesis and significance of postablation atrial fibrillation, we examined the time to onset, determinants, and clinical course of atrial fibrillation after ablation of type I flutter in a large patient cohort. Methods and Results-Of 110 consecutive patients with ablation of type I atrial flutter, atrial fibrillation was documented in 28 (25%) during a mean follow-up of 20.1Ϯ9.2 months (cumulative probability of 12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17 clinical and procedural variables, only a history of spontaneous atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8, Pϭ0.001) and left ventricular ejection fraction Ͻ50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5, Pϭ0.001) were significant and independent predictors of subsequent atrial fibrillation. The presence of both these characteristics identified a high-risk group with a 74% occurrence of atrial fibrillation. Patients with only 1 of these characteristics were at intermediate risk (20%), and those with neither characteristic were at lowest risk (10%). The determinants and clinical course of atrial fibrillation did not differ between an early (Յ1 month) compared with a later onset. Atrial fibrillation was persistent and recurrent, requiring long-term therapy in 18 patients, including 12 of 19 (63%) with prior atrial fibrillation and left ventricular dysfunction. Conclusions-Atrial fibrillation after type I flutter ablation is primarily determined by the presence of a preexisting structural and electrophysiological substrate. These data should be considered in planning postablation management. The persistent risk of atrial fibrillation in this population also suggests a potentially important role for atrial fibrillation as a trigger rather than a consequence of type I atrial flutter. (Circulation. 1998;98:315-322.)

Intracellular recordings were made from eustachian ridge of cat right atrium to determine mechanisms responsible for subsidiary pacemaker automaticity. Pacemaker action potentials exhibited two phases of diastolic depolarization: an initial steeper slope (D,) followed by a more gradual slope (D2). Cesium (1 mM) decreased D, (-45.6%) to a significantly greater extent than D 2 (-33.6%) and increased spontaneous cycle length (SCL) (+37.7%). Tetrodotoxin (10"' M) had no effect on maximum rate of rise of upstroke, although it increased SCL (+23. M ost of our understanding of atrial pacemaker function has been gained from experiments on primary pacemakers of the sinoatrial (S-A) node. These experiments indicate that several mechanisms may contribute to primary pacemaker automaticity, including 1) timedependent decay of potassium conductance, 2) timedependent inward pacemaker current and 3) slow inward calcium current.1 In addition, there is evidence that a secondary, slower component of the slow inward current, mediated via intracellular calcium release, may bring the final phase of the diastolic potential to threshold. Portions of this work have been presented in abstract form (Lipsius SL, Rubenstein DS: Slow inward current and intracellular calcium mediate subsidiary atrial pacemaker automaticity in the cat. J Physiol [Lond] 1985,371:239P).