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

Thomas A. Burkart, Matthew J. Scozzaro, Farahnaz R. Angella, Kiran N. Jayaram, Mario D. Gonzalez, Jamie B. Conti, Anne B. Curtis

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)263-266
Number of pages4
JournalClinical Cardiology
Volume25
Issue number6
DOIs
StatePublished - Jan 1 2002

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Adenosine
Atrioventricular Nodal Reentry Tachycardia
Atrioventricular Block
History
Supraventricular Tachycardia
Cardiac Arrhythmias
Confidence Intervals

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Burkart, Thomas A. ; Scozzaro, Matthew J. ; Angella, Farahnaz R. ; Jayaram, Kiran N. ; Gonzalez, Mario D. ; Conti, Jamie B. ; Curtis, Anne B. / Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways : Response of control patients to incremental doses of adenosine. In: Clinical Cardiology. 2002 ; Vol. 25, No. 6. pp. 263-266.
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abstract = "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.",
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Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways : Response of control patients to incremental doses of adenosine. / Burkart, Thomas A.; Scozzaro, Matthew J.; Angella, Farahnaz R.; Jayaram, Kiran N.; Gonzalez, Mario D.; Conti, Jamie B.; Curtis, Anne B.

In: Clinical Cardiology, Vol. 25, No. 6, 01.01.2002, p. 263-266.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways

T2 - Response of control patients to incremental doses of adenosine

AU - Burkart, Thomas A.

AU - Scozzaro, Matthew J.

AU - Angella, Farahnaz R.

AU - Jayaram, Kiran N.

AU - Gonzalez, Mario D.

AU - Conti, Jamie B.

AU - Curtis, Anne B.

PY - 2002/1/1

Y1 - 2002/1/1

N2 - 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.

AB - 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.

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