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. 1995 Oct;15(10):1533-42.

T2-weighted contrast for NMR characterization of human atherosclerosis

Affiliations
  • PMID: 7583524

T2-weighted contrast for NMR characterization of human atherosclerosis

J F Toussaint et al. Arterioscler Thromb Vasc Biol. 1995 Oct.

Abstract

We sought to determine whether 1H NMR images without chemical-shift selection can adequately characterize the components of human atheromatous arteries. NMR, as a nondestructive, biochemical imaging tool, has the potential to identify lipids in atherosclerotic plaques but has not yet produced detailed images of atheroma components. Using 1H NMR spectroscopy at 9.4 T, we examined microdissected components of diseased and normal arteries to determine water relaxation constants (T1 and T2) as well as the relative content of mobile lipid. Relaxation times were also measured at 1.5 and 4.7 T. Sections of arteries with atherosclerotic lesions of graded severity were imaged at 1.5 and 9.4 T. The contrast-to-noise ratio (CNR) was used to assess lesion conspicuity. In the atheromatous core, the water NMR signal predominates over that of lipid (lipid-to-water ratio, 0.11). At 9.4 T, T2 is 20.2 ms for the atheromatous core, 30.1 ms for the collagenous cap, and 29.5 ms for normal media. This results in a high CNR on T2-weighted (T2w) images for atheromatous core compared with the collagenous cap and normal media. A similar contrast was measured at lower field strength. Calcifications do not generate appreciable signal due to their low water content but can be detected on T1-weighted (T1w) images. The water T2 contrast allows discrimination of the atheromatous lipid core from collagenous regions. The combination of T1w and T2w sequences permits in vitro identification of the atheromatous core, collagenous cap, calcifications, media, adventitia, and perivascular fat. The discrimination of collagen fibers that overlie lipid deposits permits study of plaque protection and stability at all field strengths and may provide the basis for in vivo microscopy of human atherosclerosis.

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