Abstract
Atherosclerosis is an inflammatory process occurring in arterial tissue, involving the subintimal accumulation of LDL. Measurement of the rate at which LDL and other lipoproteins, such as HDL and VLDL, enter and exit the tissue can provide insight into the mechanisms involved in the development of atherosclerotic lesions. Permeation of VLDL, LDL, HDL, and glucose was measured for both normal and atherosclerotic human carotid endarterectomy tissues (CEA) at 20°C and 37°C using optical coherence tomography (OCT). The rates for LDL permeation through normal CEA tissue were (3.16 ± 0.37) × 10(-5) cm/s at 20°C and (4.77 ± 0.48) × 10(-5) cm/s at 37°C, significantly greater (P < 0.05) than the rates for atherosclerotic CEA tissue at these temperatures [(1.97 ± 0.34) × 10(-5) cm/s at 20°C and (2.01 ± 0.23) × 10(-5) cm/s at 37°C]. This study effectively used OCT to measure the rates at which naturally occurring lipoproteins enter both normal and diseased carotid intimal tissue.
Highlights
Atherosclerosis is an inflammatory process occurring in arterial tissue, involving the subintimal accumulation of low-density lipoproteins (LDL)
Several imaging techniques have been used to study the permeation of analytes in biological tissues, including ultrasound [6], magnetic resonance imaging (MRI) [7], optical projection tomography (OPT) [8], and optical coherence tomography (OCT) [9,10,11,12,13,14]
A significant difference (P < 0.05) between 20°C and 37°C in normal tissue was found for the permeability rate of LDL, (3.16 ± 0.37) × 10Ϫ5 cm/s and (4.77 ± 0.48) × 10Ϫ5 cm/s, respectively, supporting previous suggestions for an arterial transport mechanism specific to LDL
Summary
Atherosclerosis is an inflammatory process occurring in arterial tissue, involving the subintimal accumulation of LDL. Permeation of VLDL, LDL, HDL, and glucose was measured for both normal and atherosclerotic human carotid endarterectomy tissues (CEA) at 20°C and 37°C using optical coherence tomography (OCT). Considerable evidence indicates that initiation of the inflammatory response involves accumulation of lipids and lipoprotein particles, low-density lipoproteins (LDL), beneath the intimal layer of the arterial wall. This accumulation may be attributed to increased influx into and/or decreased efflux out of the intimal layer [4].
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