Liver stiffness is directly influenced by central venous pressure
Received 28 May 2009; received in revised form 27 July 2009; accepted 30 July 2009. published online 03 December 2009.
Background & Aims
Liver stiffness (LS) as measured by transient elastography [Fibroscan] offers a novel non-invasive approach to assess liver cirrhosis. Since Fibroscan seems to be unreliable in patients with congestive heart failure, it remains to be determined whether hemodynamic changes affect LS irrespective of fibrosis.
Methods & results
Using landrace pigs, we studied the direct relationship between the central venous pressure and LS measured by Fibroscan. Clamping of the inferior caval vein increased LS from 3.1 to 27.8kPa while reopening reversed LS within 5min to almost normal values of 5.1kPa. We then studied LS as a function of venous pressure in the isolated pig liver by clamping the upper and lower caval, portal vein and hepatic artery. The stepwise increase of intravenous pressure to 36cm of water column (3.5kPa) linearly and reversibly increased LS to the upper detection limit of 75kPa. We finally measured LS in 10 patients with decompensated congestive heart failure before and after recompensation. Initial LS was elevated in all patients, in 8 of them to a degree that suggested liver cirrhosis (median 40.7kPa). Upon recompensation with a median weight loss of 3.0kg, LS decreased in all 10 patients down to a median LS of 17.8kPa. Inflammation could not account for increased LS since initial liver enzyme counts were only slightly elevated and did not change significantly.
Conclusion
LS is a direct function of central venous pressure which should be considered when assessing the degree of fibrosis.
1Department of Medicine and Center for Alcohol Research, Liver Disease and Nutrition, Salem Medical Center, University of Heidelberg, Zeppelinstraße 11 – 33, 69121 Heidelberg, Germany
2Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany
Corresponding author. Address: Department of Internal Medicine, Salem Medical Center, University of Heidelberg, Zeppelinstraße 11 – 33, 69121 Heidelberg, Germany. Tel.: +49 06221 483 210; fax: +49 06221 484 494.
ABSTRACT