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MRI and NMR spectroscopy of the lipids of atherosclerotic plaque in rabbits and humans
Author(s) -
Trouard Theodore P.,
Altbach Maria I.,
Hunter Glenn C.,
Eskelson Cleamond D.,
Gmitro Arthur F.
Publication year - 1997
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1910380105
Subject(s) - in vivo , cholesterol , aorta , chemistry , linoleic acid , nuclear magnetic resonance spectroscopy , cholesteryl ester , magnetic resonance imaging , atheroma , pathology , nuclear magnetic resonance , lipoprotein , fatty acid , medicine , biochemistry , biology , radiology , physics , microbiology and biotechnology , organic chemistry
The early stages of atherosclerosis are characterized by the deposition of cholesteryl esters and triglycerides into the arterial wall. In the excised human atherosclerotic plaque these lipids are in a liquid‐like state at body temperature and observable via MRI and NMR spectroscopy. To assess the ability of MRI to quantitatively image the lipids of atherosclerotic plaque in vivo , we have investigated eight New Zealand White rabbits fed atherogenic diets (2 weight (wt)% cholesterol, 1 wt% cholesterol + 6 wt% peanut oil, and 1 wt% cholesterol + 6 wt% corn oil). Postmortem examination indicated that all rabbits developed atherosclerosis in the aorta. Except for one animal, magnetic resonance angiography showed no noticeable obstruction in the aorta. MRI was carried out in an attempt to image atherosclerotic plaque lipids directly, but no signal was detected in vivo. However, a plaque lipid signal was observed from excised tissue using a small diameter RF coil. 1 H NMR spectroscopy of the atherosclerotic plaque from excised aortas indicated that the major fraction of plaque lipids in rabbits is not in a liquid state at physiological temperature and are only marginally MRI‐visible compared to human plaque lipid. The differences in the MRI characteristics of rabbit and human plaque are due to differences in the fatty acid profile of the cholesteryl esters, chiefly a decrease of linoleic acid in rabbit lesions.