Reevaluation of enhanced atrioventricular nodal conduction: Evidence to suggest a continuum of normal atrioventricular nodal physiology

W. M. Jackman, E. N. Prystowsky, G. V. Naccarelli, N. S. Fineberg, G. T. Rahilly, J. J. Heger, D. P. Zipes

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) ≤ 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) ≤ 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (ΔAH) ≤ 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and ΔAH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR ≤ 60 msec, 36 (23%) shortest PCL 1:1 ≤ 300 msec, 76 (48%) ΔAH ≤ 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither ΔAH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and ΔAH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.

Original languageEnglish (US)
Pages (from-to)441-448
Number of pages8
JournalCirculation
Volume67
Issue number2
StatePublished - 1983
Externally publishedYes

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Atrioventricular Block
Cluster Analysis

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Jackman, W. M., Prystowsky, E. N., Naccarelli, G. V., Fineberg, N. S., Rahilly, G. T., Heger, J. J., & Zipes, D. P. (1983). Reevaluation of enhanced atrioventricular nodal conduction: Evidence to suggest a continuum of normal atrioventricular nodal physiology. Circulation, 67(2), 441-448.

Reevaluation of enhanced atrioventricular nodal conduction : Evidence to suggest a continuum of normal atrioventricular nodal physiology. / Jackman, W. M.; Prystowsky, E. N.; Naccarelli, G. V.; Fineberg, N. S.; Rahilly, G. T.; Heger, J. J.; Zipes, D. P.

In: Circulation, Vol. 67, No. 2, 1983, p. 441-448.

Research output: Contribution to journalArticle

Jackman, WM, Prystowsky, EN, Naccarelli, GV, Fineberg, NS, Rahilly, GT, Heger, JJ & Zipes, DP 1983, 'Reevaluation of enhanced atrioventricular nodal conduction: Evidence to suggest a continuum of normal atrioventricular nodal physiology', Circulation, vol. 67, no. 2, pp. 441-448.
Jackman WM, Prystowsky EN, Naccarelli GV, Fineberg NS, Rahilly GT, Heger JJ et al. Reevaluation of enhanced atrioventricular nodal conduction: Evidence to suggest a continuum of normal atrioventricular nodal physiology. Circulation. 1983;67(2):441-448.
Jackman, W. M. ; Prystowsky, E. N. ; Naccarelli, G. V. ; Fineberg, N. S. ; Rahilly, G. T. ; Heger, J. J. ; Zipes, D. P. / Reevaluation of enhanced atrioventricular nodal conduction : Evidence to suggest a continuum of normal atrioventricular nodal physiology. In: Circulation. 1983 ; Vol. 67, No. 2. pp. 441-448.
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AU - Jackman, W. M.

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AU - Naccarelli, G. V.

AU - Fineberg, N. S.

AU - Rahilly, G. T.

AU - Heger, J. J.

AU - Zipes, D. P.

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N2 - The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) ≤ 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) ≤ 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (ΔAH) ≤ 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and ΔAH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR ≤ 60 msec, 36 (23%) shortest PCL 1:1 ≤ 300 msec, 76 (48%) ΔAH ≤ 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither ΔAH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and ΔAH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.

AB - The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) ≤ 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) ≤ 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (ΔAH) ≤ 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and ΔAH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR ≤ 60 msec, 36 (23%) shortest PCL 1:1 ≤ 300 msec, 76 (48%) ΔAH ≤ 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither ΔAH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and ΔAH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.

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