In this study, we performed a comparative analysis of clinical data and MRI findings of CHF across patients with different underlying causes. Patients with CHF had a median age of 55 years, with 68% being female. Most CHF lesions were distributed near the second hepatic hilum, predominantly revealing radial and wedge-shaped patterns, and delayed enhancement on contrast-enhanced MRI. Most CHF lesions showed hypointensity on T1WI, while they appeared mild to moderate hyperintense on T2WI, DWI, and ADC maps. The CHF lesions were often accompanied by obvious liver cirrhosis and capsular retraction.
In our study, drug-induced liver injury and autoimmune hepatitis predominated among liver diseases, a finding partially consistent with prior research [15]. However, Ohtomo et al. reported that viral hepatitis was the primary etiology of liver cirrhosis, which led to a larger proportion (14%) of CHF in their study [4]. Therefore, we suppose that the differences of study subjects and enrolled patients make the results deviate. The patients with primary sclerosing cholangitis had a relatively small sample size in our study, which limited further comparison.
It is well-known that males are more susceptible to alcoholic liver disease and chronic hepatitis B [16], consistent with our findings. Our study also showed that the drug-induced liver injury group was predominantly composed of older females. Bilaj et al. reported that in their study, six CHF lesions were found in 32 patients with autoimmune hepatitis [17]. It is known that autoimmune hepatitis can lead to chronic liver disease. Notably, our study found a higher proportion of younger females among autoimmune hepatitis patients, in line with other research [18].
In terms of location and morphology, our findings indicated that CHF lesions predominantly appeared as patches, radially distributed around the second hepatic hilum, and were primarily located in the left medial lobe and right anterior lobe. These two lobes are within the drainage area of the middle hepatic vein (MHV). The MHV has a shorter length, smaller proximal diameter and larger drainage flow, which may lead to higher retro-sinusoidal pressure from regenerating nodules [19]. However, some lesions also showed diffuse distribution around the vascular structures and beneath the hepatic capsule. Histopathological examination typically revealed an abundance of macrophages, as well as varying degrees of hepatocyte necrosis, and increased steatosis [20]. Some CHF lesions exhibited a cord-like shape, suggesting end-stage of fibrosis. As the lesions showed more extensive confluent patterns, their size increased. When multiple lesions of CHF were present, they showed a focal distribution pattern and uneven thickness, with these characteristics occurring in specific areas of the liver rather than being diffusely distributed throughout the entire liver. While the imaging of diffuse fibrosis revealed a reticular pattern of fine fibrotic bands that were slightly hyperintense on the fat-suppressed T2WI sequence, with homogeneous thickness and delayed enhancement. Regenerative nodules were observed within these fibrotic bands [21].
On conventional MRI, most lesions exhibited low T1WI signal and mild to moderate hyperintensity on T2WI, without hemorrhage or cystic areas, consistent with previous studies [22]. In DWI sequences, CHF showed slightly restricted diffusion, with ADC values higher than the surrounding liver parenchyma, suggesting potential collagen bundle loosening within the lesions [23]. This distinct pattern may help differentiate CHF from infiltrative HCC, which typically exhibits lower ADC values [24].
On the late arterial phase, approximately half of CHF lesions showed mild-to-moderate enhancement, indicating immature fibrosis with significant inflammatory infiltration on microscopy [25]. On the portal venous phase, most CHF lesions exhibited high signal enhancement. On the delayed phase, all CHF lesions demonstrated predominantly uniform high signal, suggesting fibrosis characteristics. These features help to differentiate CHF from non-neoplastic lesions such as vascular hepatic perfusional changes. The typical manifestations of vascular hepatic perfusional changes display patchy areas with relatively hypo-enhancement or hyper-enhancement observed on the arterial phase, and appeared isointense on the portal venous phase or delayed phase compared with the surrounding normal hepatic parenchyma with blood vessels running through [26]. Hepatobiliary contrast agents provide no significant advantage over conventional agents, as both CHF and many neoplastic lesions typically show low signal in the hepatobiliary phase due to absence of functioning hepatocytes [27, 28].
In terms of accompanied findings, most cases showed obvious liver cirrhosis with capsular retraction, also observed in other liver diseases [29]. The degree of capsular retraction correlated with cirrhosis progression [30]. Early fibrosis appears as patches, while advanced fibrosis presents as patches and streaks near the liver capsule, leading to retraction and volume loss. Additionally, some livers of our patients had smooth borders, suggesting potential differences in CHF mechanisms between hepatitis and cirrhosis. Further research is needed to explore this.
Based on previous literatures, the diagnosis of CHF should be differentiated from infiltrative HCC and ICC. Infiltrative HCC lesions typically exhibit imaging features such as significant nonrim arterial phase hyperenhancement, wash-out on portal venous or delayed phase, a lower ADC value, satellite nodules, and the formation of tumor thrombus within the portal vein [31, 32]. In contrast, CHF lesions show no or mild-moderate enhancement on the arterial phase, hyperenhancement on the delayed phase relative to the background parenchyma, as well as hepatic volume loss, slightly narrowed intrahepatic vessels, but no tumor thrombus. ICC lesions usually present as target masses, with rim arterial phase hyperenhancement, peripheral washout, delayed central enhancement, targetoid restriction on DWI and ADC map, and associate with capsule contraction at the periphery and distal bile duct dilation [33]. Early-stage CHF lesions may show no or mild-moderate enhancement on the arterial phase, lack capsule contraction, and have a relatively high ADC value. These key imaging discriminators can guide clinical decisions, such as avoiding biopsy for typical CHF or performing a biopsy if the enhancement pattern is atypical.
Building on the preceding discussion and in accordance with the Liver Imaging Reporting and Data System version (LI-RADS) v2018 [34], we recommend the following MRI sequences for evaluating CHF: T1WI in-phase and out-of-phase, T2WI, DWI, late arterial phase, portal venous phase, and delayed phase enhanced imaging. If feasible, the hepatobiliary phase and magnetic resonance elastography can also be included.
This study has several limitations. First, its retrospective, single-center design introduced inherent selection bias. Additionally, the sample size particularly in subgroup analyses was insufficient, which may have biased the results. Variations in MRI scanners and contrast agents could have contributed to image heterogeneity. Furthermore, the lack of biopsy for pathological confirmation in CHF cases may have resulted in misclassification bias. Future studies should include a larger, more diverse cohort to address these limitations.
