Double Hepatic Arterial Phase MRI of the Liver with Switching of Reversed Centric and Centric K-Space Reordering
Masayuki Kanematsu1,2,
Satoshi Goshima2,
Hiroshi Kondo2,
Ryujiro Yokoyama1,
Kimihiro Kajita1,
Hiroaki Hoshi2,
Minoru Onozuka3,
Atsushi Nozaki4,
Masaya Hirano4,
Yoshimune Shiratori5 and
Noriyuki Moriyama6
1 Department of Radiology Services, Gifu University Hospital, 1-1 Yanagido, Gifu
501-1193, Japan.
2 Department of Radiology, Gifu University School of Medicine, Gifu,
Japan.
3 Department of Physiology and Neuroscience, Kanagawa Dental College, Yokosuka,
Japan.
4 Imaging Application Technology Center, GE Yokogawa Medical Systems, Tokyo,
Japan.
5 Department of Medical Informatics, Gifu University School of Medicine, Gifu,
Japan.
6 Research Center for Cancer Prevention and Screening, National Cancer Center
Hospital, Tsukiji, Japan.
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Fig. 1 —Drawing shows timing scheme of double hepatic arterial phase
(HAP) imaging. K-space lines for early HAP imaging are filled with echo data
from k-space margins to center, and those for other phase imaging are filled
from center to margins. Eight dummy excitation pulses are given for first
second. K-space centers are filled 10, 21, 49, and 181 seconds after arrival
of contrast medium in abdominal aorta. Practical imaging delay (D)
for early HAP imaging is determined as follows: D =
TV-A - 8, where TV-A is aortic transit
time in test bolus imaging. Eight seconds is subtracted so that end of first
HAP imaging (k-space center) comes 10 seconds after arrival of contrast medium
in abdominal aorta. Late HAP imaging begins automatically after 10-second
breathing interval after early HAP imaging. Portal venous phase imaging is
started 10 seconds after late HAP imaging. Equilibrium phase imaging is
initiated so that k-space lines are filled at 181 seconds.
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Fig. 2 —Graph shows contrast phase versus mean signal intensity for
abdominal aorta and spleen. Signal intensity of abdominal aorta peaks in early
hepatic arterial phase (HAP) and then decreases over time. Significant
differences in mean signal intensity (p < 0.005) exist between all
phases but not between late HAP and portal venous phase (PVP). Signal
intensity of spleen is high in early HAP, late HAP, and portal venous phase
and then decreases slightly in equilibrium phase (EP). Significant differences
in mean signal intensity (p < 0.0001) exist between all phases but
not between early HAP and equilibrium phase or between late HAP and portal
venous phase. Pre = before contrast injection.
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Fig. 3 —Graph shows contrast phase versus mean signal intensity for
portal trunk, liver parenchyma, and hepatic veins. Signal intensity of portal
trunk increases steeply over late hepatic arterial phase (HAP) and then
decreases gradually. Significant differences in mean signal intensity
(p < 0.05) exist between all phases but not between late HAP and
portal venous phase (PVP). Signal intensity of liver parenchyma increases
constantly over portal venous phase and then decreases slightly in equilibrium
phase (EP). Significant differences in mean signal intensity (p <
0.05) exist between all phases but not between late HAP and equilibrium phase
or between portal venous and equilibrium phases. Signal intensity of hepatic
veins increases steeply over portal venous phase and then decreases slightly
in equilibrium phase. Significant differences in mean signal intensity exist
between all phases (p < 0.005). Pre = before contrast
injection.
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Fig. 4 —Graph shows contrast phase versus tumor-to-liver contrast.
Tumor-to-liver contrast peaks in early hepatic arterial phase (HAP) and then
decreases rapidly. This value turns negative during portal venous phase (PVP)
and equilibrium phase (EP). Significant differences in mean tumor-to-liver
contrast (p < 0.005) exist between all phases but not between
unenhanced and portal venous phases, unenhanced and equilibrium phases, or
portal venous and equilibrium phases. Pre = before contrast injection.
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Fig. 5A —63-year-old man with developing hypervascular hepatocellular
carcinoma (HCC) and cirrhosis due to type C viral hepatitis. Unenhanced
spoiled gradient-recalled echo axial image (TR/TE, 155/1.5) shows hepatic
nodule (arrow) with 3-cm area of mixed signal intensity in posterior
segment of liver.
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Fig. 5B —63-year-old man with developing hypervascular hepatocellular
carcinoma (HCC) and cirrhosis due to type C viral hepatitis. Early hepatic
arterial phase (HAP) spoiled gradient-recalled echo axial image (155/1.5)
obtained with reversed centric k-space reordering and for which central
k-space lines were filled 10 seconds after arrival of contrast medium in
abdominal aorta shows intensely enhanced abdominal aorta (asterisk)
and proximal hepatic arteries (arrowheads), splenic moiré
pattern enhancement (curved arrow), and HCC as area of homogeneous
enhancement (straight arrow).
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Fig. 5C —63-year-old man with developing hypervascular hepatocellular
carcinoma (HCC) and cirrhosis due to type C viral hepatitis. Late HAP spoiled
gradient-recalled echo axial image (155/1.5) obtained with centric k-space
reordering and for which central k-space lines were filled 21 seconds after
arrival of contrast medium in abdominal aorta shows intensely enhanced
proximal portal veins (arrowheads) and HCC as mixed area of
persistent enhancement (arrow) and washout. Splenic enhancement is
more intense than hepatic parenchymal enhancement.
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Fig. 5D —63-year-old man with developing hypervascular hepatocellular
carcinoma (HCC) and cirrhosis due to type C viral hepatitis. Portal venous
phase spoiled gradient-recalled echo axial image (155/1.5) obtained with
centric k-space reordering and for which central k-space lines were filled 49
seconds after arrival of contrast medium in abdominal aorta shows HCC as mixed
area of mild washout (arrow). Hepatic parenchymal enhancement is as
intense as splenic enhancement.
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Fig. 5E —63-year-old man with developing hypervascular hepatocellular
carcinoma (HCC) and cirrhosis due to type C viral hepatitis. Equilibrium phase
spoiled gradient-recalled echo axial image (155/1.5) obtained with centric
k-space reordering and for which central k-space lines were filled at 181
seconds after contrast arrival in abdominal aorta shows HCC as area of clear
washout (arrow).
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Fig. 6A —64-year-old man with surgically proven 12-mm hypervascular
hepatocellular carcinoma (HCC) and cirrhosis due to type B viral hepatitis.
Early hepatic arterial phase (HAP) spoiled gradient-recalled echo axial image
(TR/TE, 155/1.5) obtained with reversed centric k-space reordering and for
which central k-space lines were filled 10 seconds after arrival of contrast
medium in abdominal aorta shows HCC as area of homogeneous enhancement
(arrow).
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Fig. 6B —64-year-old man with surgically proven 12-mm hypervascular
hepatocellular carcinoma (HCC) and cirrhosis due to type B viral hepatitis.
Late HAP spoiled gradient-recalled echo axial image (155/1.5) obtained with
centric k-space reordering and for which central k-space lines were filled 21
seconds after arrival of contrast medium in abdominal aorta shows HCC as area
of ringlike coronal enhancement (arrow).
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Fig. 6C —64-year-old man with surgically proven 12-mm hypervascular
hepatocellular carcinoma (HCC) and cirrhosis due to type B viral hepatitis.
Portal venous phase spoiled gradient-recalled echo axial image (155/1.5)
obtained using centric k-space reordering and for which central k-space lines
were filled 49 seconds after arrival of contrast medium in abdominal aorta
shows HCC as area of subtly persistent coronal enhancement
(arrow).
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Fig. 6D —64-year-old man with surgically proven 12-mm hypervascular
hepatocellular carcinoma (HCC) and cirrhosis due to type B viral hepatitis.
Equilibrium phase spoiled gradient-recalled echo axial image (155/1.5)
obtained with centric k-space reordering and for which central k-space lines
were filled 181 seconds after arrival of contrast medium in abdominal aorta
shows almost no abnormal imaging findings for HCC. Ringlike coronal
enhancement in B is crucial in differential diagnosis between
hypervascular HCC and early enhancing pseudolesion, because equilibrium phase
image shows no abnormal imaging findings such as tumor washout or delayed
enhancement of fibrous pseudocapsules.
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Fig. 7 —Graph shows contrast phase versus degree of hepatic arterial
enhancement or washout of hepatocellular carcinoma. Degree peaked in early
hepatic arterial phase (HAP) and then decreased rapidly. Degree turned
negative over portal venous phase (PVP) and equilibrium phase (EP).
Significant differences in mean degree (p < 0.05) exist between
all phases. Qualitative results correspond well with quantitative results in
Figure 4.
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Copyright © 2006 by the American Roentgen Ray Society.
