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Rapid pacing from the high right atrium was performed in 7 patients with atrial flutter in whom potentials with multicomponent high-frequency deflections were recorded at the high right atrium to examine the origin of these potentials during transient entrainment in atrial flutter. In all of the patients with relatively slow rapid pacing, the potentials were captured orthodromically through the atrial flutter reentry circuit with a long conduction time. With more rapid pacing, the potentials were split into 2 associated components: P1 and P2. P1 was captured antidromically with a short conduction time whereas P2 was captured persistently in an orthodromic direction through the reentry circuit with a progressively long conduction time. In 3 of the 7 patients, atrial flutter was converted into another atrial flutter by rapid pacing. During this other atrial flutter, the potentials at the high right atrium were split from the beginning to form double potentials: D1 and D2. During rapid pacing, D1 and D2 were fused, and D1 was captured antidromically whereas D2 was captured orthodromically through the reentry circuit. In sinus rhythm, the potentials at the high right atrium formed fractionated potentials. These findings suggest that 1) fractionated potentials may represent 2 atrial regions with different conductivity properties, 2) fractionated potentials may be able to change into double potentials, and 3) double potentials may be attributable to their conductivity properties rather than refractoriness.

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We evaluated the patterns of interruption of atrial flutter (AFl) induced by rapid atrial pacing in 10 patients using standard electrophysiologic techniques. We observed 3 patterns of interruption of AFl: 1) interruption resulting from block of an orthodromic wavefront within the reentry loop in 5 patients; 2) interruption when pacing impulses no longer captured all of the recording sites in the atrium during rapid atrial pacing in 2 patients, and 3) interruption with 1 echo wave after the cessation of pacing in 3 patients. These findings suggest that there are patterns of interruption of AFl other than that resulting from a simple block of an orthodromic wavefront within the reentry loop.

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We present a case treated with aprindine and metoprolol combined with a DDD type pacemaker for repetitive monomorphic ventricular tachycardia. A 50-year-old man was admitted because of palpitation and near syncope attack. Electrocardiogram showed repetitive monomorphic ventricular tachycardias (RBBB LAD type) and R-R interval of about 440 msec and I degree A-V block in sinus rhythm. Electrophysiologic study disclosed that overdrive pacing in HRA suppressed ventricular tachycardias. Left ventriculography revealed a dilated left ventricular and decreased contractility. Antiarrhythmic agents such as quinidine sulfate, procainamide, disopyramide, mexiletine, lidocaine and propranolol were not effective. But, the combination of propranolol and aprindine decreased the rate of the ventricular tachycardia. With aprindine 60 mg/day and metoprolol 60 mg/day combined with the atrioventricular sequential pacing at 85/min, ventricular tachycardia completely disappeared.

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To investigate the genesis of the double potential (DP), which is two separate waves, and its role in the reentry circuit of atrial flutter (AF), we performed overdrive pacing (ODP) from the high right atrium (HRA) in six cases of spontaneous AF in which the DP was recorded in the HRA. In four of the six cases, when the DP was arbitrarily designated D1 and D2, D1 and D2 showed progressive fusion during ODP. In addition, the D1 return cycle, immediately after the termination of ODP, corresponded to the AF cycle, and the D2 return cycle corresponded to the pacing cycle. This may indicate that the DP is caused by the collision of two directional waves. Furthermore, it is suggested that the HRA plays an important role in preventing a possible shortcutting of reentry waves and in stabilizing the reentry circuit of AF.

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Paroxysmal tachycardia with widened QRS complexes was found in a 46-year-old woman. In sinus rhythm, the patient had electrocardiographic evidence of type B preexcitation with a left bundle branch block pattern. The resting PR interval (160 msec) and A-H interval (100 msec) were within normal limits, but the H-V interval (10 msec) was abnormally short. Programmed atrial extrastimuli at progressively shorter coupling intervals resulted in sudden prolongation of the A-H interval from 120 msec to 250 msec, and the His bundle activities became incorporated just after initiation of the QRS complexes. The QRS morphology was changed but the change was minimal, and atrial echo beats or sustained tachycardia with wide and preexcited QRS complexes were elicited. It is postulated that the site of reentry is within the AV node with preexcitation occurring as the result of conduction in an anomalous nodoventricular pathway.

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Atrial reentrant tachycardia (ART) which demonstrated transient entrainment shifted to an uncommon type of atrial flutter (AF) with premature atrial stimulation, and then returned to ART spontaneously. Subsequently, this ART shifted to a common type of AF by rapid atrial pacing, which was further transformed into an uncommon type of AF and finally terminated by rapid atrial pacing. The mechanism of AF in clinical cases is still controversial, but in this case, AF, both uncommon and common types, is considered due to macro-reentry within the atria. To explain the shift of ART to AF and mutual transformation between common and uncommon type of AF, we made a schematic figure of reentry loop within the atria of ART and AF.

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