Progression and regression of atherosclerotic lesions: monitoring with serial noninvasive magnetic resonance imaging.
BACKGROUND
Modification or stabilization of atherosclerotic plaques has been proposed as the mechanism responsible for the beneficial clinical effect of lipid-lowering therapies. An imaging modality able to quantify atherosclerotic plaque composition could potentially allow not only the identification of these vulnerable atherosclerotic lesions, but also monitoring of the effects of therapeutic interventions on plaque composition. Our aim was to monitor changes in burden and composition of atherosclerotic plaques in a rabbit model of complex atherosclerosis using serial noninvasive magnetic resonance imaging (MRI).


RESULTS
Aortic atherosclerotic lesions were induced in rabbits and the animals randomized to continue an atherogenic diet (atherosclerosis progression) or resume normal chow (atherosclerosis regression) for 6 months. MRI of the aorta was performed at 3 time points in each rabbit, as follows: baseline, after atherosclerosis induction (9 months old), and after atherosclerosis regression or progression (15 months old). Histopathologic correlation with MRI was performed. There was a significant (P<0.0001) reduction in atherosclerotic burden in the regression group, and an increase in the progression group. There was a significant (P<0.001) reduction in the lipidic component of plaques in the regression group, and an increase in the progression group. A small, nonsignificant increase in the fibrotic plaque components was noted in the regression group, but a significant decrease in the fibrotic composition of lesions in the progression group. A significant correlation (P<0.001) was found between MRI and histopathology for atherosclerotic burden and plaque composition.


CONCLUSIONS
These findings indicate that serial noninvasive MRI can monitor changes in atherosclerotic plaque composition under conditions of atherosclerotic progression and regression.
Helft
Gérard
G
Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, New York, NY 10029-6574, USA.
Worthley
Stephen G
SG
Fuster
Valentin
V
Fayad
Zahi A
ZA
Zaman
Azfar G
AG
Corti
Roberto
R
Fallon
John T
JT
Badimon
Juan J
JJ
D000375:Aging; D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology*; D001161:Arteriosclerosis / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D004035:Diet Therapy; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D018450:Disease Progression; D005355:Fibrosis / Q000150:complications / Q000175:diagnosis; D016014:Linear Models; D050356:Lipid Metabolism; D008055:Lipids / Q000032:analysis; D008279:Magnetic Resonance Imaging; D011237:Predictive Value of Tests; D011817:Rabbits; D012075:Remission, Spontaneous; D018570:Risk Assessment; D014654:Vascular Patency
D008055:Lipids