title: Atrial septostomy decreases sympathetic overactivity in pulmonary arterial hypertension.
abstract: BACKGROUND
  We have reported previously that the sympathetic nervous system is activated in patients with pulmonary arterial hypertension (PAH), and that this is only partly explained by a decrease in arterial oxygenation. Possible causes for increased muscle sympathetic nerve activity (MSNA) in patients with PAH include right atrial distension and decreased cardiac output. Both may be improved by atrial septostomy, but this intervention also further decreases arterial oxygenation. In the present study, we wanted to investigate the effect of atrial septostomy on MSNA in patients with PAH.
  
  
  METHODS
  We recorded BP, heart rate (HR), arterial O2 saturation (SaO2), and MSNA before and after atrial septostomy in PAH patients (mean [+/- SE] age, 48 +/- 5 years) and in closely matched control subjects. Measurements were also performed after septostomy, while SaO2 was brought to the preprocedure level by supplemental O2 therapy.
  
  
  RESULTS
  Compared to the control subjects (n = 10), the PAH patients (n = 11) had a lower mean BP (75 +/- 2 vs 96 +/- 3 mm Hg, respectively; p < 0.001), lower mean SaO2 (92 +/- 1% vs 97 +/- 0%, respectively; p < 0.001), increased mean HR (84 +/- 4 vs 68 +/- 3 beats/min; p < 0.01), and markedly increased mean MSNA (76 +/- 5 vs 29 +/- 2 bursts per minute; p < 0.001). Atrial septostomy decreased mean SaO2 (to 85 +/- 2%; p < 0.001) and mean MSNA (to 69 +/- 4 bursts per minute; p < 0.01), but did not affect HR or BP. Therapy with supplemental O2 did not affect MSNA, BP, or HR. The decrease in MSNA was correlated to the decrease in right atrial pressure (r = 0.62; p < 0.05).
  
  
  CONCLUSIONS
  Atrial septostomy in PAH patients decreases sympathetic hyperactivity despite an associated decrease in arterial oxygenation, and this appears to be related to decreased right atrial distension.
authors.affiliation: Department of Cardiology, Erasme Univerisy Hospital, 808, Lennik Rd, 1070 Brussels, Belgium. Agnieszka.Ciarka@ulb.ac.be
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Ciarka
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Vachièry
authors.forename: Anne
authors.initials: A
authors.lastname: Houssière
authors.forename: Marko
authors.initials: M
authors.lastname: Gujic
authors.forename: Eric
authors.initials: E
authors.lastname: Stoupel
authors.forename: Sonia
authors.initials: S
authors.lastname: Velez-Roa
authors.forename: Robert
authors.initials: R
authors.lastname: Naeije
authors.forename: Philippe
authors.initials: P
authors.lastname: van de Borne
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D005260:Female; D006325:Heart Atria / Q000294:innervation / Q000601:surgery*; D006339:Heart Rate / Q000502:physiology; D006346:Heart Septum / Q000294:innervation / Q000601:surgery*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D013564:Sympathetic Nervous System / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology
chemical_list: D000450:Aldosterone; D010100:Oxygen; D009638:Norepinephrine