title: A possible role for systemic hypoxia in the reactive component of pulmonary hypertension in heart failure.
abstract: BACKGROUND
  The mechanisms underlying the reactive component of pulmonary hypertension (PH) in heart failure (HF) are unclear. We examined whether resting systemic oxygen levels are related to pulmonary hemodynamics in HF.
  
  
  RESULTS
  Thirty-nine HF patients underwent right heart catheterization. Subsequently, patients were classified as having: 1) no PH (n = 12); 2) passive PH (n = 10); or 3) reactive PH (n = 17). Blood was drawn from the radial and pulmonary arteries for the determination of PaO(2), SaO(2), PvO(2), SvO(2), and vasoactive neurohormones. PaO(2) and PvO(2) were lower in reactive PH versus no PH and passive PH patients (65.3 ± 8.6 vs 78.3 ± 11.4 mm Hg and 74.5 ± 14.0 mm Hg; 29.2 ± 4.1 vs 36.2 ± 2.8 mm Hg and 33.4 ± 2.3 mm Hg; P < .05). SaO(2) and SvO(2) were lower in reactive PH versus no PH patients (93 ± 3% vs 96 ± 3%; 51 ± 11% vs 68 ± 4%; P < .05), but not different versus passive PH patients. The transpulmonary pressure gradient (TPG) was inversely related to PaO(2), PvO(2), SaO(2), and SvO(2) in the reactive PH patients only (r ≤ -0.557; P < .05). Similarly, plasma endothelin-1 correlated with PaO(2), PvO(2), SvO(2) (r ≤ -0.495), and TPG (r = 0.662; P < .05) in reactive PH patients only.
  
  
  CONCLUSIONS
  Systemic hypoxia may play a role in the reactive component of PH in HF, potentially via a hypoxia-induced increase in endothelial release of the vasoconstrictor endothelin-1.
authors.affiliation: Division of Cardiovascular Diseases, College of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. taylor.bryan@mayo.edu
authors.forename: Bryan J
authors.initials: BJ
authors.lastname: Taylor
authors.forename: Cesar R
authors.initials: CR
authors.lastname: Mojica
authors.forename: Thomas P
authors.initials: TP
authors.lastname: Olson
authors.forename: Paul R
authors.initials: PR
authors.lastname: Woods
authors.forename: Robert P
authors.initials: RP
authors.lastname: Frantz
authors.forename: Bruce D
authors.initials: BD
authors.lastname: Johnson
mesh_terms: D000328:Adult; D000368:Aged; D001784:Blood Gas Analysis; D006328:Cardiac Catheterization / Q000379:methods; D002303:Cardiac Output, Low / Q000503:physiopathology*; D015331:Cohort Studies; D018450:Disease Progression; D019332:Endothelin-1 / Q000032:analysis / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000401:mortality / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000401:mortality / Q000503:physiopathology; D000860:Hypoxia / Q000097:blood / Q000175:diagnosis* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D018377:Neurotransmitter Agents / Q000032:analysis / Q000097:blood; D010100:Oxygen / Q000097:blood*; D011379:Prognosis; D011446:Prospective Studies; D012044:Regression Analysis; D018570:Risk Assessment; D012720:Severity of Illness Index; D015996:Survival Rate; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D019332:Endothelin-1; D018377:Neurotransmitter Agents; D010100:Oxygen