Liver elastography (LE) provides information on the degree of hepatic fibrosis and steatosis as well as the consequences of venocapillary congestion due to heart failure (HF). LE may aid in the prognostic assessment of patients with HF. Finding methods to complement this evaluation in patients with HF is crucial, as it is a common disease, more prevalent in older patients, and one of the leading causes of hospitalization (2.6%) and death (6%) in Brazil, consuming 3% of the total public resources allocated to the Brazilian Unified Health System (SUS).
HF can secondarily affect the function of various organs and systems, especially the liver, through venous congestion.
LE allows for the assessment of biomechanical properties of tissues and can be considered a virtual palpation. Under stress, stiffer tissues exhibit less axial displacement and greater transverse displacement velocity, which implies the propagation of shear waves. Shear waves can be generated by applying mechanical stress externally to the body or by applying the Acoustic Radiation Force Impulse (ARFI) of the ultrasound (US) beam directly to the body, which applies high concentrated energy to create tissue compression (stress) and generate shear waves. Shear wave elastography (SWE) describes any technique that generates shear waves and measures their velocity. This includes vibration controlled transient elastography (VCTE), ARFI, and magnetic resonance elastography. ARFI-SWE includes point SWE (pSWE) and 2D-SWE.
The term shear wave LE refers to techniques based on both types of stress, namely VCTE and ARFI-based techniques. In the latter, shear wave velocity/stiffness is assessed at a single point (approximately 1 cc), as in pSWE, or using multiple ARFI lines, where it is possible to obtain quantitative color-coded images of elasticity, as in 2D-SWE.
The FibroScan® device evaluates the elasticity of liver tissue using a 5 MHz US transducer. The device emits low-frequency vibrations (50 Hz), and the shear waves propagating through the tissue are detected and their velocity measured by US. The stiffer the liver parenchyma (i.e., the higher the degree of inflammation), the faster the vibrations propagate. This velocity represents the mean liver elasticity, measured in kilopascals (kPa).
Liver changes caused by decompensated HF, in addition to neuroendocrine factors, lead to an increase in canalicular enzymes (e.g., alkaline phosphatase and gamma-glutamyl transpeptidase) and bilirubin and/or ischemia with elevation of transaminases, which may progress to so-called "cardiac cirrhosis".
There is a significant correlation between liver stiffness and markers of increased venocapillary pressure.
Gamma-glutamyl transpeptidase and direct bilirubin are laboratory tests that are frequently elevated in patients with HF, correlating with the degree of systemic congestion and greater severity.
Most patients with acute HF had elevated liver stiffness values above 7.65 kPa and NT-proBNP levels, which tended to decrease with clinical improvement.
A recent meta-analysis confirmed that liver stiffness is associated with a worse prognosis in patients with acute decompensated HF.
In a study of 52 patients with acute decompensated HF, excluding those with associated liver disease, LE was performed to assess outcomes of left ventricular assist device (LVAD) use, heart transplantation, or death. Median liver elasticity was increased in patients who received an LVAD or heart transplant within 30 days compared with those who did not (median [IQR] = 55.6 [22.5-63.4] vs. 13.8 [9.5-40.3] kPa, P = 0.049). In addition, the risk of the composite outcome was higher in the third tertile (> 39.8 kPa vs. the first and second tertiles combined, HR 2.83, 95% CI 1.20-6.67, P = 0.02). Each 1 kPa increase in LSM was associated with a 1% increase in the incidence of readmission (IRR 1.01, 95% CI 1.00-1.02, P = 0.01), confirming LE as a useful tool for prognostic assessment.
There are several limitations to LE testing. First, it is necessary to achieve a signal acquisition success rate. This success rate requires proper training and depends on patient-related factors. Besides, there is still no standardization in the evaluation of variables in patients with HF.
Literature indicates that although different LE techniques show a strong linear correlation with increasing stages of liver fibrosis, LSM values obtained with ARFI-SWE techniques are lower than those obtained with VCTE. This difference increases at more advanced stages of liver fibrosis. Besides, different US systems provide different LSMs in the same individuals; therefore, the cutoff points for accurate staging of fibrosis that mimic histologic classifications cannot be used interchangeably between US systems, and the same US system should be used for follow-up measurements in the same patient. Therefore, the US system used to measure liver stiffness should be reported.
Each organ has its own elasticity, and this examination uses sound vibrations and the propagation of waves in tissue to provide measurements that can indicate tissue damage. Besides the liver, elastography is performed on the breast, thyroid, and heart to assess myocardial stiffness. Mechanical waves propagate along the heart wall at speeds related to stiffness and are associated with increased fibrosis, filling pressures and diastolic dysfunction. Because of the thin wall geometry of the heart and its complex material properties, a proper understanding of the various factors that influence wave propagation is still required to correctly interpret the results.
Renal elastography was also evaluated with the prospect of assessing fibrosis and potentially avoiding pretransplant renal biopsy, although more data are needed. There was a moderate correlation between renal stiffness measured by SWE and biopsy results.