Electrophysiologic close attention was performed in a 52-year-old man with stamp A ventricular preexcitation.

Electrophysiologic close attention was performed in a 52-year-old man with stamp A ventricular preexcitation. An accessory atrioventricular pathway with no ventriculoatrial conduction was localized to the posteroseptal region. "Fatigue phenomenon," defined as suppression of atrioventricular conduction following rapid pacing, was observ to be provok by way of atrial pacing in a rate- and duration-dependent manner. Administration of 5 mg of intravenous verapamil during sinus rhyme abolished the delta waves. These observations may indicate that pathologic changes in the accessory pathway are responsible for these phenomena.

Depression of atrioventricular conduction following rapid pacing has been defined as the "fatigue phenomenon."[1] This phenomenon has been demonstrated in the abnormal conduction system[1-3] Verapamil, a calcium-channel blocker has essentially no electrophysiologic power on an accessory pathway made up of sodium-channel-dependent myocardium.[4] Suppression of conduction with a calcium-channel-blocking medicine would indicate the presence of a dead inward calcium-sensitive current. In this report, we describe a case in which verapamil abolished anterograde conduction of an accessory pathway that exhibited the fatigue phenomenon.

CASE REPORT

A 52-year-old man was admitted for evaluation of elision He had long-standing ECG evidence of mark A ventricular preexcitation. There was no documentation of intermittent preexcitation. He had no organic heart disease as assessed clinically and echocardiographically. Electrophysiologic consideration was performed with the patient in the mildly sedated, postabsorptive state after informed approval had been obtained. The patient was receiving no antiarrhythmic medicines at the time of the research The techniques for electrophysiologic reflection have been described previously.[5]

Quadripolar electrode catheters were positioned in the high right atrium, coronary sinus, and right ventricular apex and across the tricuspid valve to record the His budget potential. Intracardiac electrograms and multiple surface ECG leads were displayed simultaneously. The heart was stimulated at twice the diastolic commencement current with a pulse width of 2 m Sinus node retrieval times and the refractory periods of the right atrium, the atrioventricular node, and the right ventricle were normal. There was no ventriculoatrial conduction at any round of years length tested. An accessory atrioventricular pathway capable of anterograde conduction solely was localized to the posteroseptal region. At pacing period lengths of 600 and 500 m the anterograde effective refractory periods of the accessory pathway were 360 and 390 m respectively. During incremental atrial pacing, 1:1 conduction athwart the accessory pathway persisted to 460 m with conduction shut up in the pathway at 450 m The interval between the pacing stimulus and a delta wave was always constant without any evidence of "decremental properties" in the accessory pathway.[6] Intermittent preexcitation none developed (sinus cycle lengths = 750 to 800 ms) in the bridle state. Fatigue phenomenon was observ following rapid atrial pacing (Fig 1) During and after atrial pacing at a period length of 660 ms for 30 s delta waves persisted. However, three consecutive normal QR complexe were noted with termination of atrial pacing at a period length of 400 ms for 30 s Furthermore, atrial pacing at a revolution of time length of 320 ms for 30 s was followed by 12 consecutive normal QR complexe The los of delta waves was also related to the duration of the atrial pacing. Pacing at comparable round of years lengths for 5 s or les was followed by dint of no more than two normal QR complexe However, it was not related to the sinus period length. Ventricular pacing failed to stimulate this phenomenon. Subsequently, 5 mg of verapamil was administered intravenously during sinus periodical emphasis Approximately 2 min later, the delta waves were abolished (Fig 2) Repeat atrial stimulation showed no evidence of anterograde accessory pathway conduction at any rate.

DISCUSSION

In a previous contemplation Narula and Runge[1] showed that the fatigue phenomenon, defined as suppression of atrioventricular conduction following rapid pacing, was observ in the diseased His-Purkinje arrangement Fisch[2] demonstrated three cases of package branch block due to ventricular tachycardia and speculated that the phenomenon may be related to "fatigue" or "overdrive suppression." All of his patients had advanced heart disease. Ohe and his colleagues[3] reported a similar phenomenon in an accessory pathway elicited according to rapid ventricular pacing in a 43-year-old man with the Wolff-Parkinson-White syndrome As in our case, the anterograde electrophysiologic properties of the accessory pathway were moderately postponeed To the best of our knowledge, their case is the alone one in which this phenomenon occurr in an accessory pathway. Our case stretch outs their observation and demonstrates that this phenomenon can also be provok into an accessory pathway on atrial pacing in a rate-and duration-dependent manner. Since all QR complexe normalized during rapid atrial pacing (Fig 1) united can postulate that this phenomenon was also the accrue of repetitive retrograde concealed conduction into the accessory pathway via the atrioventricular node. There was no evidence of ventriculoatrial conduction in our case. Retrograde concealed conduction has been demonstrated to be met with even in the accessory pathway capable of anterograde conduction only[7] However, failure to kindle the fatigue phenomenon with ventricular pacing in our case intimates that anterograde input into the accessory pathway might be largely responsible for this phenomenon for at least sinus period lengths tested. Additional pacing modalities, as it was as atrial pacing after ventricular pacing, might have been of help in further elucidating the contribution of retrograde concealment for other settings. Additionally, stable sinus revolution of time lengths after pacing may assign bradycardia-dependent block in the accessory pathway les likely as the mechanism. Whatever the mechanisms involved, it appears that this phenomenon is associated with the diseased atrioventricular conduction system[1-3]

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