Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.
OBJECTIVE
To determine whether venous congestion, rather than impairment of cardiac output, is primarily associated with the development of worsening renal function (WRF) in patients with advanced decompensated heart failure (ADHF).


BACKGROUND
Reduced cardiac output is traditionally believed to be the main determinant of WRF in patients with ADHF.


METHODS
A total of 145 consecutive patients admitted with ADHF treated with intensive medical therapy guided by pulmonary artery catheter were studied. We defined WRF as an increase of serum creatinine >/=0.3 mg/dl during hospitalization.


RESULTS
In the study cohort (age 57 +/- 14 years, cardiac index 1.9 +/- 0.6 l/min/m(2), left ventricular ejection fraction 20 +/- 8%, serum creatinine 1.7 +/- 0.9 mg/dl), 58 patients (40%) developed WRF. Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p < 0.001) and after intensive medical therapy (11 +/- 8 mm Hg vs. 8 +/- 5 mm Hg, p = 0.04). The development of WRF occurred less frequently in patients who achieved a CVP <8 mm Hg (p = 0.01). Furthermore, the ability of CVP to stratify risk for development of WRF was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates.


CONCLUSIONS
Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.
Mullens
Wilfried
W
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Abrahams
Zuheir
Z
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Francis
Gary S
GS
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Sokos
George
G
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Taylor
David O
DO
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Starling
Randall C
RC
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Young
James B
JB
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
Tang
W H Wilson
WHW
Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: tangw@ccf.org.
D000368:Aged; D002302:Cardiac Output; D002496:Central Venous Pressure; D003404:Creatinine / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D006940:Hyperemia / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D007674:Kidney Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index
D003404:Creatinine