Liver stiffness (Fibroscan®) is directly controlled by venous pressure

Background and aims: Measurement of liver stiffness (LS) by transient elastography [Fibroscan] is a non-invasive tool to assess liver fibrosis/cirrhosis. However, LS seems to be unreliable in patients with congestive heart failure suggesting that an increased central venous pressure may affect LS.

Methods and results: Using landrace pigs, we here studied the direct relationship between the pressure in the caval vein and liver stiffness measured by Fibroscan. Clamping of the caval vein for 5min increased LS from 3.1. kPa to 27.8 kPa while reopening reversed LS within 5min to almost normal values of 5.1 kPa. We then studied LS as a function of venous pressure in the isolated pig liver by clamping upper and lower caval and the portal vein. Complete stop of blood flow at 0 kPa hydrostatic pressure increased LS to 9.7 kPa. Stepwise increase of intravenous pressure to 36cm of water column (3.5 kPa) linearly and reversibly increased LS to the upper detection limit of 75 kPa. We finally measured LS in 10 patients with decompensated congestive heart failure before and after recompensation over a mean observation interval of 7.2 days. Initial LS was elevated in all patients in 8 of them to a degree that suggested advanced liver cirrhosis (median 40.7 kPa). Upon recompensation with a median weight loss of 3.0kg, LS decreased in all 10 patients by 54% down to a median LS of 17.8 kPa. Initial liver enzyme counts were only slightly elevated and did not change significantly.

Conclusion: Liver stiffness is a direct function of venous pressure which should be considered when assessing the degree of fibrosis. In the absence of liver disease, LS could be used as noninvasive surrogate for systemic venous pressure.