Liver stiffness is associated with right heart dysfunction, cardiohepatic syndrome, and prognosis in pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) can lead to congestive hepatopathy, known as cardiohepatic syndrome (CHS). Hepatic congestion is associated with increased liver stiffness, which can be quantified using shear wave elastography. We aimed to investigate whether hepatic shear wave elastography detects patients at risk in the early stages of PH. METHODS: Sixty-three prospectively enrolled patients undergoing right heart catheterization (52 diagnosed with PH and 11 with invasive exclusion of PH) and 52 healthy volunteers underwent assessments including echocardiography and hepatic shear wave elastography. CHS was defined as increased levels of ≥2 of the following: gamma-glutamyl transferase, alkaline phosphatase, and bilirubin. Liver stiffness was defined as normal (≤5.0 kPa) or high (>5.0 kPa). RESULTS: Compared with normal liver stiffness, high liver stiffness was associated with impaired right ventricular (RV) and right atrial (RA) function (median [interquartile range] RV ejection fraction: 54 [49; 57]% vs 45 [34; 51]%, p < 0.001; RA reservoir strain: 49 [41; 54]% vs 33 [22; 41]%, p < 0.001), more severe tricuspid insufficiency (p < 0.001), and higher prevalence of hepatovenous backflow (2% vs 29%, p < 0.001) and CHS (2% vs 10%, p = 0.038). In the patient subgroup with precapillary PH (n = 48), CHS and high liver stiffness were associated with increased European Society of Cardiology/European Respiratory Society 2022 risk scores (p = 0.003). CONCLUSIONS: Shear wave liver elastography yields important information regarding right heart function and may complement risk assessment in patients with (suspected) PH.

Spontaneous echo contrast videodensity is flow-related and is dependent on the relative concentrations of fibrinogen and red blood cells.

OBJECTIVES: The purposes of the present study were to: 1) determine whether fibrinogen (Fg) is the plasma protein responsible for spontaneous echo contrast (SEC), and 2) investigate modulators of SEC. BACKGROUND: Spontaneous echo contrast has been linked to the development of thromboemboli. The blood products and their interaction responsible for SEC formation have not been fully elucidated. METHODS: Blood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model. Human blood samples were analyzed in a manner to methodically eliminate individual blood components from whole blood to determine which components are responsible for the formation of SEC. RESULTS: The videodensity (VD) of whole blood was found to be flow-dependent, with higher VD at lower flow rates, and correlated with visually dense SEC. The following blood products produced faint VD values: washed red blood cells (wRBCs), platelet-depleted plasma, Fg, defibrinated plasma, wRBCs plus defibrinated plasma, and physiologic saline. The VD of wRBCs increased incrementally as increasing concentrations of Fg were added. At each hematocrit (Hct) range, as Fg concentration increased, the SEC became denser, and the VD level also increased until a plateau level was reached that was distinct for each Hct. The addition of sialic acid, which inhibits RBC-RBC aggregation, decreased the amount of SEC, even in the presence of Fg. CONCLUSION: These results demonstrated that Fg-mediated RBC aggregation may be responsible for SEC generation. Furthermore, a unique stoichiometric relationship exists between Fg and RBC concentrations that is necessary for blood echogenicity.