title: Cardiac hemodynamics and proinflammatory cytokines during biatrial and right atrial appendage pacing in patients with interatrial block.
abstract: OBJECTIVE
  Interatrial block (IAB) frequently coexists with sinus node disease and is considered a risk factor of left atrial dysfunction, atrial arrhythmias, and heart failure development. Conventional right atrial appendage (RAA) pacing impairs intra- and interatrial conductions and consequently prolongs P wave duration. Biatrial (BiA) pacing helps correct IAB, but its advantageous influence remains controversial. The aim of the study was to compare the effects of BiA and RAA pacing on cardiac hemodynamics and serum concentrations of inflammatory markers and neuropeptides.
  
  
  METHODS
  Twenty-eight patients with IAB and preserved atrio-ventricular conduction treated with BiA pacing were studied. Standard invasive hemodynamic measurements were performed during BiA and RAA pacings. Furthermore, the influence of 1 week of BiA and RAA pacing on neuropeptides: atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) and markers of inflammation: high sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and neopterin was examined.
  
  
  RESULTS
  BiA pacing resulted in significant increase of cardiac output (CO) and reduction of pulmonary capillary wedge pressure. We demonstrated significantly lower concentrations of ANP, hs-CRP, IL-6, and neopterin after 1 week of BiA in comparison to RAA pacing. BNP levels remained unchanged.
  
  
  CONCLUSIONS
  BiA pacing in comparison to RAA pacing improves hemodynamic performance in patients with IAB and preserved atrio-ventricular conduction. BiA pacing is associated with reduction of ANP and markers of inflammation (hs-CRP, IL-6, and neopterin).
authors.affiliation: Department of Cardiology, Medical University of Lublin, 8 Jaczewskiego Str, Lublin, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Rubaj
authors.forename: Piotr
authors.initials: P
authors.lastname: Rucinski
authors.forename: Andrzej
authors.initials: A
authors.lastname: Kutarski
authors.forename: Alicja
authors.initials: A
authors.lastname: Dabrowska-Kugacka
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Oleszczak
authors.forename: Barbara
authors.initials: B
authors.lastname: Zimon
authors.forename: Michal
authors.initials: M
authors.lastname: Trojnar
authors.forename: Tomasz
authors.initials: T
authors.lastname: Zapolski
authors.forename: Jakub
authors.initials: J
authors.lastname: Drozd
authors.forename: Adam
authors.initials: A
authors.lastname: Tarkowski
authors.forename: Andrzej
authors.initials: A
authors.lastname: Wysokinski
mesh_terms: D000368:Aged; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control*; D020517:Atrial Appendage / Q000503:physiopathology*; D053840:Brugada Syndrome; D000075224:Cardiac Conduction System Disease; D002302:Cardiac Output; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D003326:Coronary Circulation; D016207:Cytokines / Q000097:blood*; D005260:Female; D006329:Heart Conduction System / Q000002:abnormalities* / Q000503:physiopathology; D006801:Humans; D008297:Male; D009205:Myocarditis / Q000209:etiology / Q000503:physiopathology*; D013318:Stroke Volume; D016896:Treatment Outcome
chemical_list: D016207:Cytokines