Abstract
ObjectivesLow-density lipoprotein (LDL) is an important risk factor for coronary artery disease. However, its localization in human coronary plaques is not well understood. The present study was performed to visualize LDL in human coronary artery wall.Methods(1) The fluorescence characteristic of LDL was investigated by color fluorescent microscopy (CFM) with excitation at 470-nm and emission at 515-nm using Nile blue dye (NB) as a biomarker. (2) Native LDL in 40 normal segments, 42 white plaques and 35 yellow plaques (20 with necrotic core) of human coronary arteries was investigated by color fluorescent angioscopy (CFA) and CFM.Results(1) NB elicited a brown, golden and red fluorescence characteristic of LDL, apolipoprotein B-100, and lysophosphatidylcholine/triglyceride, respectively. (2) The % incidence of LDL in normal segments, white, and yellow plaques was 25, 38 and 14 by CFA and 42, 42 and 14 by CFM scan of their luminal surface, respectively, indicating lower incidence (p<0.05) of LDL in yellow plaques than white plaques, and no significant differences in detection sensitivity between CFA and CFM. By CFM transected surface scan, LDL deposited more frequently and more diffusely in white plaques and yellow plaques without necrotic core (NC) than normal segments and yellow plaques with NC. LDL was localized to fibrous cap in yellow plaques with NC. Co-deposition of LDL with other lipid components was observed frequently in white plaques and yellow plaques without NC.Conclusions(1) Taken into consideration of the well-known process of coronary plaque growth, the results of the present study suggest that LDL begins to deposit before plaque formation; increasingly deposits with plaque growth, often co-depositing with other lipid components; and disappears after necrotic core formation. (2) CFA is feasible for visualization of LDL in human coronary artery wall.
Highlights
Low-density lipoprotein (LDL) is a pro-atherogenic agent that is converted by oxidation to oxidized low-density lipoprotein, which plays an important role in the initiation, progression and destabilization of atherosclerotic plaques [1,2,3,4].LDL is itself a clinically proven risk factor for ischemic vascular events; coronary heart disease is associated with higher serum levels of LDL [5], the incidence of silent myocardial ischemia is higher in type II diabetic patients with high levels of serum LDL [6]; and LDL is a predictor of future cardiovascular events in statin-treated patients [7]
Conclusions: (1) Taken into consideration of the well-known process of coronary plaque growth, the results of the present study suggest that LDL begins to deposit before plaque formation; increasingly deposits with plaque growth, often codepositing with other lipid components; and disappears after necrotic core formation
All these data have been obtained by measuring the serum levels of LDL, not that which is deposited in the coronary arterial wall, and treatment has been directed to lowering the plasma levels of this substance in anticipation of reducing its content in the coronary arterial wall
Summary
LDL is itself a clinically proven risk factor for ischemic vascular events; coronary heart disease is associated with higher serum levels of LDL [5], the incidence of silent myocardial ischemia is higher in type II diabetic patients with high levels of serum LDL [6]; and LDL is a predictor of future cardiovascular events in statin-treated patients [7] All these data have been obtained by measuring the serum levels of LDL, not that which is deposited in the coronary arterial wall, and treatment has been directed to lowering the plasma levels of this substance in anticipation of reducing its content in the coronary arterial wall. We have succeeded in imaging the native lipid components, such as oxLDL, and lysophosphatidylcholine (LPC), of human coronary plaques by using CFA in vitro and/or in vivo, but have not attempted imaging of LDL because of the lack of an appropriate, biocompatible marker [15,16,17,18]
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