title: Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures.
abstract: BACKGROUND
  Approximately half of all patients with chronic heart failure (HF) have a decreased ejection fraction (EF) (systolic HF [SHF]); the other half have HF with a normal EF (diastolic HF [DHF]). However, the underlying pathophysiological differences between DHF and SHF patients are incompletely defined. The purpose of this study was to use echocardiographic and implantable hemodynamic monitor data to examine the pathophysiology of chronic compensated and acute decompensated HF in SHF versus DHF patients.
  
  
  RESULTS
  Patients were divided into 2 subgroups: 204 had EF <50% (SHF) and 70 had EF >or=50% (DHF). DHF patients had EF of 58+/-8%, end-diastolic dimension of 50+/-10 mm, estimated resting pulmonary artery diastolic pressure (ePAD) of 16+/-9 mm Hg, and diastolic distensibility index (ratio of ePAD to end-diastolic volume) of 0.11+/-0.06 mm Hg/mL. In contrast, SHF patients had EF of 24+/-10%, end-diastolic dimension of 68+/-11 mm, ePAD of 18+/-7 mm Hg, and diastolic distensibility index of 0.06+/-0.04 mm Hg/mL (P<0.05 versus DHF for all variables except ePAD). In SHF and DHF patients who developed acute decompensated HF, these events were associated with a significant increase in ePAD, from 17+/-7 to 22+/-7 mm Hg (P<0.05) in DHF and from 21+/-9 to 24+/-8 mm Hg (P<0.05) in SHF. As a group, patients who did not have acute decompensated HF events had no significant changes in ePAD.
  
  
  CONCLUSIONS
  Significant structural and functional differences were found between patients with SHF and those with DHF; however, elevated diastolic pressures play a pivotal role in the underlying pathophysiology of chronic compensated and acute decompensated HF in both SHF and DHF.
authors.affiliation: Department of Medicine, Division of Cardiology, Medical University of South Carolina, Charleston, SC 29425, USA. zilem@musc.edu
authors.forename: Michael R
authors.initials: MR
authors.lastname: Zile
authors.forename: Tom D
authors.initials: TD
authors.lastname: Bennett
authors.forename: Martin
authors.initials: M
authors.lastname: St John Sutton
authors.forename: Yong K
authors.initials: YK
authors.lastname: Cho
authors.forename: Philip B
authors.initials: PB
authors.lastname: Adamson
authors.forename: Mark F
authors.initials: MF
authors.lastname: Aaron
authors.forename: Juan M
authors.initials: JM
authors.lastname: Aranda
authors.forename: William T
authors.initials: WT
authors.lastname: Abraham
authors.forename: Frank W
authors.initials: FW
authors.lastname: Smart
authors.forename: Lynne Warner
authors.initials: LW
authors.lastname: Stevenson
authors.forename: Fred J
authors.initials: FJ
authors.lastname: Kueffer
authors.forename: Robert C
authors.initials: RC
authors.lastname: Bourge
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000379:methods / Q000639:trends*