title: Noninvasive Assessment of Atrioventricular Nodal Function: Effect of Rate-Control Drugs during Atrial Fibrillation.
abstract: BACKGROUND
  During atrial fibrillation (AF), conventional electrophysiological techniques for assessment of refractory period or conduction velocity of the atrioventricular (AV) node cannot be used. We aimed at evaluating changes in AV nodal properties during administration of tecadenoson and esmolol using a novel ECG-based method.
  
  
  METHODS
  Fourteen patients (age 58 ± 8 years, 10 men) with AF were randomly assigned to either 75 or 300 μg intravenous tecadenoson. After tecadenoson wash-out, patients received esmolol continuously (100 μg/kg per min for 10 mins, then 50 μg/kg per min for 50 mins). Atrial fibrillatory rate (AFR) and heart rate (HR) were assessed in 15-min segments. Using the novel method, we assessed the absolute refractory periods of the slow and fast pathways (aRPs and aRPf) of the AV node to produce an estimate of the functional refractory period.
  
  
  RESULTS
  During esmolol infusion, AFR and HR were significantly decreased and the absolute refractory period was significantly prolonged in both pathways (aRPs: 387 ± 73 vs 409 ± 62 ms, P < 0.05; aRPf: 490 ± 80 vs 529 ± 58 ms, P < 0.05). During both tecadenoson doses, HR decreased significantly and AFR was unchanged. Both aRPs and aRPf were prolonged for a 75 μg dose (aRPs: 322 ± 97 vs 476 ± 75 ms, P < 0.05; aRPf: 456 ± 102 vs 512 ± 55 ms, P < 0.05) whereas a trend toward prolongation was observed for a 300 μg dose.
  
  
  CONCLUSIONS
  The estimated parameters reflect expected changes in AV nodal properties, i.e., slower conduction through the AV node for tecadenoson and prolongation of the AV node refractory period for esmolol. Thus, the proposed approach may be used to assess drug effects on the AV node in AF patients.
authors.affiliation: Department of Electronics, Information and Bioengineering, Politecnico of Milano, Italy.
authors.forename: Valentina D A
authors.initials: VD
authors.lastname: Corino
authors.affiliation: Department of Biomedical Engineering and Center for Integrative Electrocardiology at Lund University (CIEL), Lund University, Lund, Sweden.
authors.forename: Frida
authors.initials: F
authors.lastname: Sandberg
authors.affiliation: Department of Electronics, Information and Bioengineering, Politecnico of Milano, Italy.
authors.forename: Luca T
authors.initials: LT
authors.lastname: Mainardi
authors.affiliation: Center for Integrative Electrocardiology at Lund University (CIEL) and Arrhythmia Clinic, Skåne University Hospital, Lund, Sweden.
authors.forename: Pyotr G
authors.initials: PG
authors.lastname: Platonov
authors.affiliation: Department of Biomedical Engineering and Center for Integrative Electrocardiology at Lund University (CIEL), Lund University, Lund, Sweden.
authors.forename: Leif
authors.initials: L
authors.lastname: Sörnmo
mesh_terms: D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy*; D001283:Atrioventricular Node / Q000187:drug effects*; D005260:Female; D005663:Furans / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D011412:Propanolamines / Q000494:pharmacology / Q000627:therapeutic use; D058906:Purinergic P1 Receptor Agonists / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D000889:Anti-Arrhythmia Agents; D005663:Furans; D011412:Propanolamines; D058906:Purinergic P1 Receptor Agonists; C118601:tecadenoson; D000241:Adenosine; C036604:esmolol
keywords: atrial fibrillation; atrioventricular node; esmolol; functional refractory period; tecadenoson