title: Cardiorenal anemia syndrome in chronic heart failure contributes to increased sympathetic nerve activity.
abstract: BACKGROUND
  We sought to assess whether cardiorenal anemia syndrome (CRAS) in chronic heart failure (CHF) patients contributes to sympathetic overactivity through modulation of sympathetic reflexes.
  
  
  RESULTS
  We prospectively studied 15 patients with CRAS and CHF and 15 control CHF patients, matched for age, gender distribution, type of cardiomyopathy, left ventricular ejection fraction (LVEF) and BMI. We compared muscle sympathetic nerve activity (MSNA) and the effect of peripheral chemoreflex deactivation on MSNA in both groups. We also compared sympathetic baroreflex function, assessed by the slope of the relationship between MSNA and diastolic blood pressure in both groups and while peripheral chemoreflexes were (by breathing 100% oxygen for 15 min) or not deactivated. Baseline MSNA was significantly elevated in CHF patients with CRAS compared with control CHF patients (83.1 ± 4.6 versus 64.9 ± 2.9 bursts/100 heart beats; P<0.05) and sympathetic baroreflex impaired (2.69 ± 0.44 vs 5.25 ± 0.60%bursts/mmHg; P<0.01). Chemoreflex deactivation with administration of 100% oxygen led to a significant decrease in muscle sympathetic nerve activity (77.8 ± 4.7 versus 82.1 ± 4.9 bursts/100 heart beats; P<0.01) and to an increase in sympathetic baroreflex function (2.77 ± 0.45 vs 5.63 ± 0.73%bursts/mmHg; P<0.01) in patients with CRAS and CHF. In contrast, neither room air nor 100% oxygen changed MSNA, hemodynamic or sympathetic baroreflex function in control CHF patients.
  
  
  CONCLUSIONS
  CRAS in CHF patients is associated with elevated sympathetic activity mediated by both tonic activation of peripheral chemoreflex and baroreflex impairment.
authors: Institut National de la Sante et de la Recherche Médicale, UMR-1048, Institut des Maladies Metaboliques et Cardiovasculaires, Toulouse, France; Department of Forensic Medicine, Centre Hospitalier Universitaire de Toulouse, F-31059 Toulouse, France. Electronic address: franchitto.n@chu-toulouse.fr.
authors: Nicolas
authors: N
authors: Franchitto
authors: Fabien
authors: F
authors: Despas
authors: Marc
authors: M
authors: Labrunee
authors: Angelica
authors: A
authors: Vaccaro
authors: Elisabeth
authors: E
authors: Lambert
authors: Gavin
authors: G
authors: Lambert
authors: Michel
authors: M
authors: Galinier
authors: Jean-Michel
authors: JM
authors: Senard
authors: Atul
authors: A
authors: Pathak
mesh_terms: D000368:Aged; D000740:Anemia / Q000150:complications* / Q000503:physiopathology; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure; D059347:Cardio-Renal Syndrome / Q000209:etiology / Q000503:physiopathology*; D002628:Chemoreceptor Cells / Q000502:physiology; D018450:Disease Progression; D004311:Double-Blind Method; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D016277:Ventricular Function, Left
keywords: Anemia; Chronic heart failure; Chronic kidney disease; Microneurography; Sympathetic nerve activity