title: Inverse relationship between aldosterone and large artery compliance in chronically treated heart failure patients.
abstract: OBJECTIVE
  The purpose of this study was to examine, in chronically treated heart failure patients vs control subjects, the influence of neurohumoral activation and aldosterone escape on arterial elastic behaviour, assessed by non-invasive mathematical lumped-parameter modelling of the compliance of the arterial system.
  
  
  RESULTS
  Radial arterial pulse waves were recorded non-invasively for 30 s with an arterial tonometer sensor array in 13 chronic heart failure patients (mean age, 59 +/- 2.5 years) in New York Heart Association class II. The patients had been taking digoxin, furosemide, captopril and aspirin for more than 3 months. Thirteen healthy subjects (mean age, 50 +/- 4.0 years) acted as controls. Compliance of the proximal (aorta and major branches, C1) and distal parts (C2) of the circulation were derived from a third order four-element modified Windkessel model which can reproduce arterial pressure waveforms, including both exponential and oscillatory sections. Active renin, angiotensin II and aldosterone levels were determined on venous blood samples in the supine position and after 30 min active standing. There was decreased proximal (C1, 1.51 +/- 0.11 ml x mmHg(-1), P<0.01) and distal (C2, 0.050 +/- 0.011 ml x mmHg(-1)) arterial compliance in the chronic heart failure patients vs controls (C1, 1.71 +/- 0.16 ml x mmHg(-1); C2, 0.054 +/- 0.006 ml x mmHg(-1)). The chronic heart failure patients were characterized by an aldosterone escape phenomenon which was inversely correlated with the proximal arterial compliance in both supine (r= - 0.795, P=0.002) and standing (r= - 0.628, P=0.029) positions.
  
  
  CONCLUSIONS
  In chronically treated heart failure patients with full angiotensin-converting enzyme-inhibition and diuretics, there is decreased compliance of the aorta and its major branches, which is inversely correlated with the aldosterone escape phenomenon.
authors.affiliation: Department of Cardiology and Angiology, University Hospital, Gent, Belgium.
authors.forename: D A
authors.initials: DA
authors.lastname: Duprez
authors.forename: M L
authors.initials: ML
authors.lastname: De Buyzere
authors.forename: E R
authors.initials: ER
authors.lastname: Rietzschel
authors.forename: Y
authors.initials: Y
authors.lastname: Taes
authors.forename: D L
authors.initials: DL
authors.lastname: Clement
authors.forename: D
authors.initials: D
authors.lastname: Morgan
authors.forename: J N
authors.initials: JN
authors.lastname: Cohn
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology*; D002908:Chronic Disease; D003187:Compliance / Q000187:drug effects; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D018709:Statistics, Nonparametric; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000450:Aldosterone