A 49 years old Chinese male patient had a history of paroxysmal palpitation for 25 years, and recurred more frequently in the month before admission. Tachycardia usually burst on and off suddenly. The duration of the development was from a few minutes to 10 hours. A history of hypertension was for 4 years. Physical examinations show no abnormal physical signs. Ultrasound examination met with high blood pressure heart changes: mild expansion of the ascending aorta, normal left ventricular systolic function and diastolic dysfunction. Electrocardiogram (ECG) showed no abnormity under sinus rhythm; on paroxysmal tachycardia outburst [Figure 1], narrow QRS complex presenting together with heart rate (HR) 178/ min, interval from QRS wave to P wave (RP interval) was 120ms and RP interval < PR interval (interval from P wave to QRS wave). It's difficult to distinguish it from atrioventricular reentrant tachycardia.
Intracardiac electrophysiological examination: right atrial programmed basic stimulus coupled with cycle length decreasing extrastimulus (S1S2) at 500/280ms induced a narrow QRS complex tachycardia, but it was not accompanied by atrioventricular conduction jump phenomena [Figure 2]. Ventricular wave (V) and atrial wave (A) did not interfuse. VA interval = 120ms. It seems to be a side pathway, but right ventricular grading frequency increment stimulation showed ventricle to atrium decline conduction as well as Wenckebach phenomenon. Tachycardia could not be terminated by ventricular premature beat [Figure 3]. This suggested that there was no atrioventricular side pathway and atrioventricular nodal reentry was very likely. While we tried to improve atrioventricular node by ablating the slow pathway in lower region, atrioventricular junctional rhythm occurred, and the junctional beats decreased with the process of ablation. Subsequent repeated electrophysiological examination showed that under almost the same condition, right atrial programmed S1S2 at 550/270 ms induced atrioventricular conduction jump phenomenon, and the same paroxysmal tachycardia been induced [Figure 4]. We continued to improve atrioventricular node till to the jump phenomenon disappeared. After that not only repeatedly grading frequency increment stimulation but also programmed S1S2 could not induce tachycardia. Then, we repeated these stimulations after intravenous infusion of isoproterenol, still, no tachycardia and atrioventricular conduction jump phenomenon recurred. These electrophysiological examination suggested the success of ablation.