The physiologic basis of reciprocal rhythm*

An 84-year-old male had experienced palpitations. He was transported to our hospital for treatment of palpitations. A 12-lead electrocardiogram (ECG) showed regular tachycardia with a wide QRS complex of 153 bpm, and the P wave was not clear. The ECG after the tachycardia stopped showed a sinus rhythm, and there was a prolonged PR interval of 312 ms and complete right bundle branch block. We recorded a prolonged AH interval (235 ms) in electrophysiology study (EPS). As for the St-A interval (185 ms) by consecutive pacing from the right ventricular apex, it was short in comparison with the anterograde conduction. As a result of detailed EPS, we diagnosed the tachycardia as slow–fast atrioventricular nodal reentrant tachycardia. The anterograde conduction depended on the slow pathway (SP), and the fast pathway (FP) was considered to have only retrograde conduction. It was thought that a complete atrioventricular block been caused by the SP ablation. Therefore we carried out FP ablation with three-dimensional computed tomography and the EnSite NavX mapping system (St. Jude Medical, St Paul, MN, USA), which was superior in space resolution power, and were able to effect a radical cure without complications.

Supraventricular tachycardias (SVTs) affect all age groups and are a source of significant morbidity. They are frequently encountered in otherwise healthy individuals without structural heart disease. Advances in the understanding of their mechanisms and anatomical locations have led to highly effective pharmacologic and nonpharmacologic treatment strategies. Recognition, identification, and differentiation of the various SVTs are of great importance in formulating an effective treatment strategy. Developments over the past four decades have made possible the accurate diagnosis of SVTs. Today, advances in catheter design, energy delivery systems, mapping systems, and remote navigation systems have rendered the ablation of most SVTs safe and effective. This monograph provides an in-depth discussion of the history, presentation, mechanism, and treatment strategies of the most commonly encountered SVTs. The monograph is divided into two parts. The first part is presented here.

An electrocardiogram was obtained that was characterized by sinus rhythm with progressive prolongation of the PR interval not followed by a blocked sinus impulse. After a critically long PR interval, the QRS complex was followed by a premature P′ wave, representing an echo beat, a manifest reentry in the atrioventricular (AV) node. The pause, occasioned by the premature P′ wave, was at times interrupted by an AV junctional escape beat, occurring with an escape interval of 1.21–1.24 seconds. On other occasions, however, the escape beat did not manifest on schedule, even though the pause was markedly longer than the escape cycle. This suggested that the manifest reentry was followed by a further concealed reentry, resulting in inapparent discharge of the AV junctional escape pacemaker, whose firing was postponed, thereby allowing the sinus impulse to capture the ventricles.

Atrioventricular (AV) nodal reentrant tachycardia and atrial flutter are considered 2 distinct supraventricular tachycardias. Recent clinical and experimental data suggest that both these tachycardias include an area in the lower right atrial septum in their reentrant pathways. This study was designed to test the hypothesis that there is an association between the mechanisms of AV nodal reentrant tachycardia and atrial flutter because of a shared pathway of reentry. Consecutive patients referred for evaluation and management of supraventricular tachycardia, thought to be due to AV nodal reentry, underwent electrophysiologic testing protocols designed to induce both AV nodal reentrant tachycardia and atrial flutter, if present. Fifteen of 29 patients (52%) had both AV nodal reentrant tachycardia and atrial flutter induced during eloctrophysiologic testing. Seven of these 15 patients (47%) underwent transcatheter radiofrequency current application (mean power 34 ± 4 W) against the tricuspid annulus above the coronary sinus. In each patient, neither AV nodal reentrant tachycardia nor atrial flutter could be induced after the procedure. Repeat study after successful ablation (mean 6 days) showed no inducible supraventricular arrhythmia of either type at baseline study or during isoproterenol infusion.

Atrial flutter occurs frequently (15 of 29 patients; 52%) in patients with AV nodal reentrant tachycardia, because of a shared pathway in their reentry circuits. Because of this shared pathway, both arrhythmias can be ablated at the same site. These observations promote new insights into the mechanism and therapeutics of supraventricular tachycardias.