title: Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study.
abstract: OBJECTIVE
  Elevated levels of the mineralocorticoid hormone aldosterone are recognized as a modifiable contributor to the pathophysiology of select cardiovascular diseases due to left heart failure. In pulmonary arterial hypertension (PAH), pulmonary vascular remodelling induces right ventricular dysfunction and heart failure in the absence of left ventricular (LV) dysfunction. Hyperaldosteronism has emerged as a promoter of pulmonary vascular disease in experimental animal models of PAH; however, the extent to which hyperaldosteronism is associated with PAH in patients is unknown. Thus, the central aim of the current study is to determine if hyperaldosteronism is an unrecognized component of the PAH clinical syndrome.
  
  
  RESULTS
  Plasma aldosterone levels and invasive cardiopulmonary haemodynamic measurements were obtained for 25 patients referred for evaluation of unexplained dyspnoea or pulmonary hypertension. Compared with controls (n = 5), patients with PAH (n = 18) demonstrated significantly increased plasma aldosterone levels (1200.4 ± 423.9 vs. 5959.1 ± 2817.9 pg/mL, P < 0.02), mean pulmonary artery pressure (21.4 ± 5.0 vs. 45.5 ± 10.4 mmHg, P < 0.002), and pulmonary vascular resistance (PVR) (1.41 ± 0.6 vs. 7.3 ± 3.8 Wood units, P < 0.003) without differences in LV ejection fraction or pulmonary capillary wedge pressure between groups. Among patients not prescribed PAH-specific pharmacotherapy prior to cardiac catheterization, a subgroup of the cohort with severe pulmonary hypertension, aldosterone levels correlated positively with PVR (r = 0.72, P < 0.02) and transpulmonary gradient (r = 0.69, P < 0.02), but correlated inversely with cardiac output (r = -0.79, P < 0.005).
  
  
  CONCLUSIONS
  These data demonstrate a novel cardiopulmonary haemodynamic profile associated with hyperaldosteronism in patients: diminished cardiac output due to pulmonary vascular disease in the absence of LV heart failure.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. bmaron@partners.org
authors.forename: Bradley A
authors.initials: BA
authors.lastname: Maron
authors.forename: Alexander R
authors.initials: AR
authors.lastname: Opotowsky
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Landzberg
authors.forename: Joseph
authors.initials: J
authors.lastname: Loscalzo
authors.forename: Aaron B
authors.initials: AB
authors.lastname: Waxman
authors.forename: Jane A
authors.initials: JA
authors.lastname: Leopold
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000097:blood*; D006328:Cardiac Catheterization; D002303:Cardiac Output, Low / Q000097:blood / Q000150:complications* / Q000000981:diagnostic imaging; D016022:Case-Control Studies; D015331:Cohort Studies; D004452:Echocardiography; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000150:complications* / Q000000981:diagnostic imaging; D006976:Hypertension, Pulmonary / Q000097:blood / Q000150:complications* / Q000000981:diagnostic imaging; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011669:Pulmonary Wedge Pressure; D014655:Vascular Resistance; D018497:Ventricular Dysfunction, Right / Q000097:blood / Q000150:complications*
chemical_list: D000450:Aldosterone