A new method for induction of atrioventricular nodal reentrant tachycardia in non-inducible cases.

AIM: In some patients with clinical paroxysmal supraventricular tachycardia (PSVT), who are candidates for radiofrequency (RF) catheter ablation, attempts for the induction of arrhythmia during the electrophysiological study (EPS) fail despite different stimulation protocols even during the isoproterenol infusion and atropine injection. The presence of an atrial-His interval (AH) jump during decremental pre-mature atrial stimulation is the only clue for slow pathway ablation in these patients; in occasional patients, however, the AH jump is an accidental finding and the real arrhythmia is not atrioventricularnodal reentrant tachycardia (AVNRT). We aimed to introduce a new method for the induction of AVNRT in these patients. METHODS AND RESULTS: Ten patients (50% male, mean age=44.40 ± 12.80 years) with clinical PSVT who were referred to our department for the EPS and RF catheter ablation were selected. These patients had documented clinical PSVT with non-inducible arrhythmia during the EPS with different stimulation protocols even during the isoproterenol infusion and atropine injection but they only showed an AH jump. To induce AVNRT, low-watt (15-20), low-temperature (40-45°C) RF currents were delivered into the slow pathway area for a maximum of 40 s. Atrioventricularnodal reentrant tachycardia was inducible in five cases (50%, three male, mean age=45.80 ± 9.65 years). Induction of AVNRT occurred either during the RF current application after the occurrence of junctional ectopic beats or after another stimulation protocol. CONCLUSION: A low-watt, low-temperature RF current application into the slow pathway area can be a provocative method for the induction of AVNRT probably by AV-junction warming and conduction-velocity augmentation.

Definition of the reentry circuit with demonstration of a low frequency diastolic potential in a patient with verapamil-sensitive idiopathic left ventricular tachycardia.

A low frequency slow potential preceding the Purkinje spike was recorded at the midseptum during tachycardia in a 69-year-old man with verapamil-sensitive left ventricular tachycardia. This potential was characteristically absent during sinus rhythm before radiofrequency ablation, but became evident following the QRS complex after successful ablation at the tachycardia exit site. Induction of tachycardia with programmed stimulation was dependent on emergence of this slow potential. Decremental conduction was noted between the QRS complex and the slow potential. Further energy application at a site proximal to where the slow potential was initially recorded totally eliminated the slow potential.

Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: response of control patients to incremental doses of adenosine.

BACKGROUND: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electrophysiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. HYPOTHESIS: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. METHODS: Thirty-seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. RESULTS: The mean (+/- standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 +/- 3.9 and 7.4 +/- 4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0-8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. CONCLUSION: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.

Differential effects of atropine and isoproterenol on inducibility of atrioventricular nodal reentrant tachycardia.

BACKGROUND: Radiofrequency ablation of the "slow pathway" in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. METHODS: 80 patients (57 women, 23 men, age 50+/-14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01 mg/kg atropine or 0.5-1.0 microg/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. RESULTS: Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300+/-48 ms vs. 374+/-113 ms, P=0.012). CONCLUSION: Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.