AJP - Heart Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 297: H2136-H2143, 2009. First published October 9, 2009; doi:10.1152/ajpheart.00712.2009
0363-6135/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Table
Right arrow Buy
Right arrow All Versions of this Article:
297/6/H2136    most recent
00712.2009v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Tadros, R.
Right arrow Articles by Billette, J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tadros, R.
Right arrow Articles by Billette, J.

Rate-dependent AV nodal refractoriness: a new functional framework based on concurrent effects of basic and pretest cycle length

Rafik Tadros and Jacques Billette

Département de physiologie, Faculté de médecine, Université de Montréal, Montreal, Canada

Submitted July 30, 2009 ; accepted in final form October 4, 2009

The atrioventricular (AV) node filters atrial impulses. Underlying rate-dependent refractory properties are assessed with the effective (ERPN; longest nonconducted atrial cycle length) and functional (FRPN; shortest His bundle cycle) refractory period determined with premature protocols at different basic rates. Fast rates prolong ERPN and shorten FRPN, but these effects vary with subjects, age, and species. We propose that these opposite and variable effects reflect the net sum of concurrent cumulative and noncumulative effects associated with basic (BCL) and pretest cycle length (PTCL), respectively. To test this hypothesis, we assessed selective and combined effects of five BCL (S1S1) and six PTCL (S1S2) on ERPN, FRPN, and their subintervals (ERPN = A2H2 + H2A3 and FRPN = H2A3 + A3H3, where A is atrium and H is His bundle) with S1S2S3 protocols in six rabbit heart preparations. At control BCL, PTCL shortenings prolonged ERPN (113 ± 12 vs. 101 ± 14 ms, P < 0.01) as a net result of prolonged A2H2 and curtailed H2A3. At control PTCL, BCL shortenings increased ERPN (127 ± 20 vs. 101 ± 14 ms, P < 0.01) by prolonging A2H2. FRPN did not vary with BCL but decreased (163 ± 6 vs. 175 ± 10 ms, P < 0.01) with PTCL that curtailed H2A3. Equal BCL and PTCL shortenings as in standard protocols prolonged ERPN but left FRPN unchanged. Notably, ERPN and FRPN significantly correlated through their H2A3 subinterval. In conclusion, BCL and PTCL are both important determinants of AV nodal refractoriness and together account for rate-induced changes in ERPN and FRPN observed during standard premature protocols. ERPN and FRPN are related variables. Similar functional rules may govern nodal refractory behavior during supraventricular tachyarrhythmias.

atrioventricular node; heart rate; effective refractory period; functional refractory period; rate dependence



Address for reprint requests and other correspondence: J. Billette, Département de physiologie, Faculté de médecine, Université de Montreal, CP 6128 Succ CV, Montréal, Quebec, Canada H3C 3J7 (e-mail: jacques.billette{at}umontreal.ca).







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.