Oxidized low‐density lipoprotein and high‐density lipoprotein cholesterol modulate coronary arterial remodeling: An intravascular ultrasound study

Background: Oxidized low-density lipoprotein (oxLDL) not only plays an important role in plaque formation, but also impairs the endothelium-dependent relaxation. Constrictive remodeling rather than intimal hyperplasia mainly contributes to restenosis after balloon angioplasty. Probucol (powerful antioxidant) reduced restenosis rate by improving constrictive remodeling. Thus, oxLDL may modulate coronary arterial remodeling. Hypothesis: The study was designed for using intravascular ultrasound to test the hypothesis that arterial constrictive remodeling (CR) was associated with oxLDL in patients with coronary artery disease. Methods: Intravascular ultrasound was performed in 36 patients with de novo atherosclerotic coronary. Remodeling was defined and evaluated as follows: remodeling index (RI) = lesion vessel area (VA)/(proximal reference VA + distal reference VA)/2. Constrictive remodeling (CR) was defined as remodeling index (RI) < 0.9. Neutral and expansive remodeling (NER) was defined as RI ≥0.9. The level of plasma ox-LDL was measured by sandwich ELISA using the monoclonal antibody (DLH3)-recognized oxidatively modified lipoproteins and the antihuman apoprotein B monoclonal antibody. Results: Neutral and expansive remodeling was found in 24 lesions, and CR in 12 lesions. Remodeling index was significantly lower in the CR group than in the NER group (0.8 ± 0.1 vs. 1.0 ± 0.1, p< 0.001). The level of oxLDL in the CR group was significantly higher than that in the NER group (24.0 ± 12.1 vs. 16.4 ± 6.2 U/ml, p < 0.05). The level of high-density lipoprotein-cholesterol (HDL-C) in the CR group was significantly lower than that in the NER group (40.5 ± 4.8 vs. 46.2 ± 10.6 mg/ml, p < 0.05). There was a statistically significant correlation between the value of HDL-C/ ox-LDL and the RI (r = -0.48, p< 0.005). Conclusions: Oxidized LDL and HDL-C were associated with arterial remodeling in de novo atherosclerotic lesions.