Liver MRI: From basic protocol to advanced techniques

Abstract

A B S T R A C TLiver MR is a well-established modality with multiparametric capabilities. However, to take advantage of its full capacity, it is mandatory to master the technique and optimize imaging protocols, apply advanced imaging concepts and understand the use of different contrast media. Physiologic artefacts although inherent to upper abdominal studies can be minimized using triggering techniques and new strategies for motion control. For standardization, the liver MR protocol should include motion-resistant T2-w sequences, in-op phase GRE T1 and T2-w fast spin echo sequences with fat suppression. Diffusion-weighted imaging (DWI) is mandatory, especially for detection of sub-centimetre metastases. Contrast-enhanced MR is the cornerstone of liver MR, especially for lesion characterization. Although extracellular agents are the most extensively used contrast agents, hepatobiliary contrast media can provide an extra-layer of functional diagnostic information adding to the diagnostic value of liver MR. The use of high field strength (3T) increases SNR but is more challenging especially concerning artefact control. Quantitative MR belongs to the new and evolving field of radiomics where the use of emerging biomarkers such as perfusion or DWI can derive new information regarding disease detection, prognostication and evaluation of tumour response. This information can overcome some of the limitations of current tests, especially when using vascular disruptive agents for oncologic treatment assessment. MR is, today, a robust, mature, multiparametric imaging modality where clinical applications have greatly expanded from morphology to advanced imaging. This new concept should be acknowledged by all those involved in producing high quality, high-end liver MR studies.

Recent advances in non-invasive magnetic resonance imaging assessment of hepatocellular carcinoma

“…Generally, DCE-MRI consists of acquisition of T1-weighted MR images before, during, and after intravenous injection of a gadolinium-based contrast agent[ 40 ]. The contrast agent extravasates at level of tumor tissue, from intravascular to the extravascular extracellular space (EES) with increased T1-w signal[ 43 , 54 , 55 ]. This extravasation to EES in the tumor tissue depends on vessel leakiness (permeability) and blood flow (perfusion), and so the signal measured with DCE-MRI could be sensitive to alterations in vascular permeability, EES, and blood flow[ 43 , 54 ].…”

“…DCE-MRI signals can be quantified using a semi-quantitative (model free) or quantitative (model based) analysis[ 56 ]. Both analysis methods have several parameters related with tumor angiogenesis[ 54 , 57 ] and can give different information on liver and tumor perfusion[ 56 ]. Briefly, with the semi-quantitative analysis, all perfusion parameters are extracted directly from time-signal intensity (SI) curves [ e.g ., AUC, maximum SI or peak enhancement ratio, wash-in slope, mean transit time (MTT)], derived from different dynamic contrastographic sequences.…”

“…Quantitative analysis depends on fitting the time SI curves with the changes in concentration of the contrast agent using pharmacokinetic techniques using several kinetics models based on different physiological assumptions made[ 56 ]. These kinetics models can be bi-compartmental models (taking into account vessels and EES) or mono-compartmental (taking into account the vascular space because of the typical architecture of the liver)[ 56 ], with a double or single input system (arterial and portal or arterial alone), conventional compartment (CC) models vs distributed parameters (DP) models[ 54 , 56 ].…”

“…Several parameters extracted with quantitative analysis are related to the influx of contrast agent from the intravascular space to the EES (K trans) and its reverse (Kep), the volume fraction of EES (Ve), which is an indirect expression of the cellular density of the tissue[ 43 , 54 , 56 ].…”

“…Moreover, numerous pharmacokinetic models have been proposed by Tofts et al[ 58 ], Brix et al[ 59 ], and Larsson et al[ 60 ], using a single arterial input function[ 43 ]. Because HCC receives major blood supply from hepatic neo-arteries and often arise from a cirrhotic liver, the single input model (considering only the arterial input) and the dual compartment model (because of the alteration in the EES) are frequently both used in the literature[ 54 , 56 ].…”