Electrophysiologic studies in 2 patients with persistent atrial tachycardia suggest an ectopic atrial focus is responsible, showing relative immunity to overdrive pacing up to 600 beats/min.
Case Report (n=2)
Electrophysiologic studies in patients with refractory persistent atrial tachycardia suggest an ectopic atrial focus mechanism with distinct responses to overdrive pacing compared to the sinoatrial node.
Clinical and electrophysiologic studies in two patients with chronic persistent atrial tachycardia unresponsive to drug or electroconversion therapy are reported. In both, exercise increased the atrial rate and decreased the atrioventricular nodal conduction time. The opposite effect occurred after β-adrenergic blockade. Single electrically-induced atrial depolarizations (A 2 ) at progressively premature times resulted in a linear increase in the return cycle (A 2 A 3 ) until plateau levels were achieved but failed to produce sinus rhythm. Abrupt cessation of continuous atrial pacing at rates up to 600 beats/min in one patient and up to 300 beats/min in the other resulted in a pause that was similar to the plateau levels of A 2 A 3 achieved during atrial scanning with single impulses. Our findings suggest that an ectopic atrial focus is responsible for this arrhythmia. The electrophysiologic properties of the ectopic pacemaker appear to be similar to the sinoatrial node in some respects but to differ in terms of spontaneous rate and in relative immunity from the effects of overdrive pacing.
Scheinman et al. (1974) conducted a case report in chronic persistent atrial tachycardia (n=2). Electrophysiologic studies was evaluated on Electrophysiologic response to pacing and pharmacological interventions. Electrophysiologic studies in 2 patients with persistent atrial tachycardia suggest an ectopic atrial focus is responsible, showing relative immunity to overdrive pacing up to 600 beats/min.