Feasibility of 4D MRI for Assessment of Regional Hepatic Blood Flow
Eric James Keller1, Laura Kulik2, James C. Carr1, Michael Markl1,3, and Jeremy Douglas Collins1

1Radiology, Northwestern University, Chicago, IL, United States, 2Gastroenterology and Hepatology, Northwestern University, Chicago, IL, United States, 3Biomedical Engineering, Northwestern University, Evanston, IL, United States


The success of surgical and transarterial therapies for hepatocellular carcinoma relies on hepatic hemodynamics. Non-contrast 4D flow MRI can quantify hepatic blood flow at the lobar arterial and portal vein levels with a low relative error and clearly evaluate portosystemic shunts; however, segmental flow quantification remains limited. By pairing 4D flow MRI with HCC surveillance MR imaging, lobar flow per volume can also be assessed, providing valuable information for surgical planning.


Liver cancer is the 3rd leading cause of cancer-related deaths worldwide. Hepatocellular carcinoma (HCC) accounts for 90% of these cancers and often arises in the setting of liver cirrhosis. Treatment of HCC can vary significantly depending on patient and disease characteristics, but surgical resection, liver transplantation, and locoregional therapies are common therapeutic approaches for early and intermediate HCC1. The success of these therapies share a common reliance on hepatic hemodynamics2,3, which have been challenging to assess non-invasively prior to the development of 4D flow MRI. Although 4D flow MRI has been used previously to characterize abdominal hemodynamics4,5, hepatic lobar and segmental flow are seldom assessed. Thus, we sought to investigate the feasibility of non-invasively quantifying hepatic lobar and segmental flow as well as the percent of hepatopedal flow in patients with cirrhosis and imaging evidence of portal hypertension.


The study cohort consisted of 7 prospectively recruited patients (age=55±11yrs, 2 women) with cirrhosis (4 Child-Pugh Grade A; 3 Grade B) and sequelae of portal hypertension (splenomegaly and/or portosystemic shunts) identified on HCC surveillance imaging. All subjects fasted prior to undergoing non-contrast 4D flow MRI at 3T (MAGNETOM Skyra, Siemens Medical Systems, Erlangen, Germany) with ECG- and respiratory navigator gating in an oblique axial imaging volume to include the hepatic and splenic vasculature with the navigator positioned at the lung-spleen interface. Pulse sequence parameters: spatial res=2.1-2.4 x 2.1-2.4 x 2.5-2.7mm; temporal res=40.8-44.0ms; flip angle=7°; TE=2.6-3.1ms; k-t-GRAPPA R=5; VENC=50cm/s. Scan data were first corrected for background phase offset errors using MatLab (the MathWorks, Natick, MA, USA). A PC-MRA was generated to permit 3D segmentation of the abdominal vasculature in Mimics (Materialise, Leuven, Belgium) that was used to restrict the velocity field to the vasculature for visualization and quantification of the liver hemodynamics in EnSight (CEI, Apex, NC, USA). Flow quantification was assessed using relative error in flow input and output at lobar and segmental branch points in arterial and portal systems. Percent hepatopedal flow was calculated by dividing non-portosystemic shunt flow by the total flow entering the portal system via the superior mesenteric and splenic veins. Hepatic lobar volumes were also measured on 3D T1-weighted gradient recalled echo (GRE) imaging. The sum of left and right lobar arterial and portal flow was indexed to 100 mL liver volume and compared via two-tailed t-tests.


Intra-hepatic portal and arterial blood flows were clearly visualized for all patients without the use of contrast. Example portal flow visualization and relative error calculation is provided in Figure 1. Relative error in flow quantification was low (<10%) for lobar portal and arterial divisions [5.8±2.0% (arterial); 8.8±8.7% (portal)], but significantly higher for segmental arterial and portal divisions [21.9±18.5% (arterial); 30±14.7% (portal)]. Hepatopedal flow ranged from 11-100%, capturing shunt flows ranging from 0.57-14.63ml/cycle (Figure 2). No significant difference was found between right and left lobar flow (ml/min) per 100ml liver volume [49.0±42.6 (right) v. 38.6±20.0 (left); p=0.60]; however, there was heterogeneity of flow with lobar flow indices ranging from 25.5-134.0 for the right lobe and 18.2-75.4 for the left lobe (Figure 3).


These results illustrate the potential of non-contrast abdominal 4D flow MRI to quantify blood flow at the lobar arterial and portal vein level with a low relative error, and clearly evaluate portosystemic shunts. Such information may be useful for HCC treatment planning. For example, the significant variance in right and left lobar flow per volume suggests liver parenchymal perfusion may not be as uniform as previously thought. By combining 4D flow MRI with surveillance MR imaging for HCC, lobar flow indices could be assessed and the extent of systemic shunting quantified to guide surgical planning. In terms of future research, one could use this level of hemodynamic detail to understand whether a higher lobar flow index predicts better survival of smaller grafts, differential lobar arterial flow predicts success of transarterial therapies, or certain portal flow patterns proceed portal vein thrombosis. Finally, it is also worth noting that 4D flow MRI assessment of segmental flow remains limited and will likely require better spatial resolution to achieve that level of detail.


Accurate, non-invasive assessment of hepatic lobar arterial and portal blood flow has the potential to help predict complications which arise in the setting of cirrhosis and guide surgical and transarterial therapies for HCC. Such hemodynamic detail can be achieved by pairing non-contrast 4D flow MRI with HCC surveillance MR imaging in this patient population. Although segmental flow quantification is possible with 4D flow MRI, its lower internal consistency is a limiting factor.


This work was funded by the Radiological Society of North America Research & Education Foundation (Seed Grant #1218).


1. European Association For The Study Of The L, European Organisation For R, Treatment Of C. EASL-EORTC clinical practice guidelines: management of hepatocellular carcinoma. Journal of hepatology. Apr 2012;56(4):908-943.

2. Ben-Haim M, Emre S, Fishbein TM, et al. Critical graft size in adult-to-adult living donor liver transplantation: impact of the recipient's disease. Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. Nov 2001;7(11):948-953.

3. Lewandowski RJ, Geschwind JF, Liapi E, Salem R. Transcatheter intraarterial therapies: rationale and overview. Radiology. Jun 2011;259(3):641-657.

4. Roldan-Alzate A, Frydrychowicz A, Said A, et al. Impaired regulation of portal venous flow in response to a meal challenge as quantified by 4D flow MRI. Journal of magnetic resonance imaging : JMRI. Oct 2015;42(4):1009-1017.

5. Stankovic Z, Csatari Z, Deibert P, et al. Normal and altered three-dimensional portal venous hemodynamics in patients with liver cirrhosis. Radiology. Mar 2012;262(3):862-873.


Figure 1: Example of portal blood flow visualization and relative error calculations at lobar and segmental branch points.

Figure 2: Patients’ calculated hepatopedal flow and relative error in lobar and segmental flow quantification.

Figure 3: Patients’ measured liver volumes and calculated lobar flow indices. *At the time of this scan, Patient #2 had been diagnosed with HCC and underwent Y90 radioembolization affecting flow.

Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)