title: A disproportionate elevation in right ventricular filling pressure, in relation to left ventricular filling pressure, is associated with renal impairment and increased mortality in advanced decompensated heart failure.
abstract: BACKGROUND
  Discordance between left- and right-sided filling pressures occurs in a subset of patients presenting with acute decompensated heart failure (ADHF). We hypothesized that a disproportionately increased right atrial pressure (RAP) relative to the pulmonary capillary wedge pressure (PCWP) would be associated with both renal dysfunction and mortality in ADHF.
  
  
  METHODS
  A total of 367 patients admitted with ADHF with elevated intracardiac filling pressures were treated with intensive medical therapy guided by invasive hemodynamic monitoring. Baseline characteristics, hemodynamics, and renal function at admission were stratified by RAP/PCWP quartiles. The association of RAP/PCWP quartile with all-cause mortality after a median follow-up of 2.4 years was assessed in univariable and multivariable models, which included adjustment for the RAP.
  
  
  RESULTS
  The median RAP/PCWP was 0.58 (interquartile range 0.43-0.75). Increasing RAP/PCWP was inversely associated with estimated glomerular filtration rate at baseline and with treatment (P < .0001) independently of RAP. High RAP/PCWP was associated with increased mortality (quartile 4 vs 1: hazard ratio [95% CI] 2.1 [1.3-3.5], P = .002). The association of RAP/PCWP with mortality persisted after adjustment for age, gender, mean arterial pressure, RAP, cardiac index, pulmonary vascular resistance, and estimated glomerular filtration rate (hazard ratio 2.4 [1.4-3.9], P = .007).
  
  
  CONCLUSIONS
  A disproportionate increase in right to left ventricular filling pressures is associated with renal dysfunction and mortality, independently of the right atrial pressure.
authors.affiliation: Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH.
authors.forename: Justin L
authors.initials: JL
authors.lastname: Grodin
authors.affiliation: Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
authors.forename: Mark H
authors.initials: MH
authors.lastname: Drazner
authors.affiliation: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Hasselt University, Diepenbeek, Belgium.
authors.forename: Matthias
authors.initials: M
authors.lastname: Dupont
authors.affiliation: Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium; Hasselt University, Diepenbeek, Belgium.
authors.forename: Wilfried
authors.initials: W
authors.lastname: Mullens
authors.affiliation: Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH.
authors.forename: David O
authors.initials: DO
authors.lastname: Taylor
authors.affiliation: Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH.
authors.forename: Randall C
authors.initials: RC
authors.lastname: Starling
authors.affiliation: Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH. Electronic address: tangw@ccf.org.
authors.forename: W H Wilson
authors.initials: WH
authors.lastname: Tang
mesh_terms: D000368:Aged; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000401:mortality* / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology*; D017725:Ventricular Pressure / Q000502:physiology*