title: Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension.
abstract: OBJECTIVE
  This study sought to investigate the influence of right ventricular (RV) hemodynamic variables and function on the secretion of brain natriuretic peptide (BNP) in patients with isolated RV overload.
  
  
  BACKGROUND
  Plasma BNP is known to increase in proportion to the degree of left ventricular (LV) overload. However, whether BNP secretion is also regulated in the presence of RV overload remains unknown.
  
  
  METHODS
  Plasma BNP and atrial natriuretic peptide (ANP) levels in the pulmonary artery were measured in 44 patients with RV overload: 18 with RV volume overload (RVVO) due to atrial septal defect and 26 with RV pressure overload (RVPO) due to primary or thromboembolic pulmonary hypertension. Right heart catheterization was performed in all patients. RV and LV ejection fraction, myocardial mass and volume of the four chambers were determined by using electron beam computed tomography.
  
  
  RESULTS
  Although both plasma BNP and ANP levels were significantly elevated in patients with RV overload compared with values in control subjects, plasma BNP and the BNP/ANP ratio were significantly higher in patients with RVPO than with RVVO (BNP 294 +/- 72 vs. 48 +/- 14 pg/ml; BNP/ANP 1.6 +/- 0.2 vs. 0.8 +/- 0.2, both p < 0.05). Plasma BNP correlated positively with mean pulmonary artery pressure (r = 0.73), total pulmonary resistance (r = 0.79), mean right atrial pressure (r = 0.79), RV end-diastolic pressure (r = 0.76) and RV myocardial mass (r = 0.71); it correlated negatively with cardiac output (r = -0.33) and RV ejection fraction (r = -0.71). Plasma BNP significantly decreased from 315 +/- 120 to 144 +/- 54 pg/ml with long-term vasodilator therapy (total pulmonary resistance decreased from 23 +/- 4 to 15 +/- 3 Wood U).
  
  
  CONCLUSIONS
  Plasma BNP increases in proportion to the extent of RV dysfunction in pulmonary hypertension.
authors.affiliation: Department of Internal Medicine, and Research Institute, National Cardiovascular Center, Suita, Osaka, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Nagaya
authors.forename: T
authors.initials: T
authors.lastname: Nishikimi
authors.forename: Y
authors.initials: Y
authors.lastname: Okano
authors.forename: M
authors.initials: M
authors.lastname: Uematsu
authors.forename: T
authors.initials: T
authors.lastname: Satoh
authors.forename: S
authors.initials: S
authors.lastname: Kyotani
authors.forename: S
authors.initials: S
authors.lastname: Kuribayashi
authors.forename: S
authors.initials: S
authors.lastname: Hamada
authors.forename: M
authors.initials: M
authors.lastname: Kakishita
authors.forename: N
authors.initials: N
authors.lastname: Nakanishi
authors.forename: M
authors.initials: M
authors.lastname: Takamiya
authors.forename: T
authors.initials: T
authors.lastname: Kunieda
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
authors.forename: K
authors.initials: K
authors.lastname: Kangawa
mesh_terms: D000328:Adult; D000368:Aged; D009320:Atrial Natriuretic Factor / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000097:blood*; D014057:Tomography, X-Ray Computed / Q000379:methods; D018497:Ventricular Dysfunction, Right / Q000097:blood*
chemical_list: D009419:Nerve Tissue Proteins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor