title: Clinical predictors and hemodynamic consequences of elevated peripheral chemosensitivity in optimally treated men with chronic systolic heart failure.
abstract: OBJECTIVE
  Augmented peripheral chemoreflex response is an important mechanism in the pathophysiology of chronic heart failure (CHF). This study characterizes prevalence and clinical predictors of this phenomenon in optimally managed male CHF patients, and seeks to describe the hemodynamic consequences of chemoreceptor hypersensitivity.
  
  
  RESULTS
  Thirty-four optimally managed CHF patients and 16 control subjects were prospectively studied. Hypoxic ventilatory response (HVR)-a measure of peripheral chemosensitivity-was calculated with the use of short nitrogen gas administrations. Systolic blood pressure (SBP) and heart rate (HR) following transient hypoxic challenges were recorded with a Nexfin monitor. Hemodynamic responses to hypoxia were expressed by the linear slopes between oxygen saturation (%) and SBP (mm Hg) or HR (beats/min). Elevated HVR was present in 15 (44%) of the CHF patients. Patients with elevated HVR exhibited higher levels of N-terminal pro-B-type natriuretic peptide, lower left ventricular ejection fraction, and higher prevalence of atrial fibrillation. CHF patients with elevated HVR had significantly greater SBP and HR responses to hypoxia than CHF patients with normal HVR.
  
  
  CONCLUSIONS
  Despite comprehensive pharmacotherapy, elevated HVR is prevalent in CHF patients, related to severity of the disease and associated with augmented hemodynamic responses to hypoxia. CHF patients with elevated HVR may be prone to unfavorable hemodynamic changes.
authors.affiliation: Department of Cardiology, Center for Heart Disease, 4th Military Hospital, Wroclaw, Poland. pnsky@wp.pl
authors.forename: Piotr
authors.initials: P
authors.lastname: Niewinski
authors.forename: Zoar J
authors.initials: ZJ
authors.lastname: Engelman
authors.forename: Marat
authors.initials: M
authors.lastname: Fudim
authors.forename: Stanislaw
authors.initials: S
authors.lastname: Tubek
authors.forename: Bartlomiej
authors.initials: B
authors.lastname: Paleczny
authors.forename: Ewa A
authors.initials: EA
authors.lastname: Jankowska
authors.forename: Waldemar
authors.initials: W
authors.lastname: Banasiak
authors.forename: Paul A
authors.initials: PA
authors.lastname: Sobotka
authors.forename: Piotr
authors.initials: P
authors.lastname: Ponikowski
mesh_terms: D001281:Atrial Fibrillation / Q000453:epidemiology; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D002628:Chemoreceptor Cells / Q000502:physiology*; D006325:Heart Atria / Q000000981:diagnostic imaging; D054143:Heart Failure, Systolic / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology; D014463:Ultrasonography
chemical_list: D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain