Intravascular ultrasound evaluation of coronary plaque regression by low density lipoprotein-apheresis in familial hypercholesterolemia

Matsuzaki, Masunori; Hiramori, Katsuhiko; Imaizumi, Tsutomu; Kitabatake, Akira; Hishida, Hitoshi; Nomura, Masatoshi; Fujii, Takashi; Sakuma, Ichiro; Fukami, Kenichi; Honda, Takashi; Ogawa, Hiroshi; Yamagishi, Masakazu

doi:10.1016/s0735-1097(02)01955-1

Cited by 153 publications

(81 citation statements)

References 25 publications

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“…39 Moreover, aggressive lipidlowering therapy, ie, LDL cholesterol removal, with LDL apheresis produced remarkable regression of coronary atherosclerotic plaques. 40 Here, in LOX-1 mice, atherosclerotic progression was completely inhibited despite a very transient oxLDL decrease, suggesting not only preventive but also therapeutic effects of oxLDL removal. In addition, smooth muscle cells persisted in plaques, particularly in plaque surface areas of LOX-1 mice.…”

Section: Discussionmentioning

confidence: 83%

Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis

Ishigaki

Katagiri²,

Gao³

et al. 2008

Circulation

159

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Background-Several clinical studies of statin therapy have demonstrated that lowering low-density lipoprotein (LDL) cholesterol prevents atherosclerotic progression and decreases cardiovascular mortality. In addition, oxidized LDL (oxLDL) is suggested to play roles in the formation and progression of atherosclerosis. However, whether lowering oxLDL alone, rather than total LDL, affects atherogenesis remains unclear. Methods and Results-To clarify the atherogenic impact of oxLDL, lectin-like oxLDL receptor 1 (LOX-1), an oxLDL receptor, was expressed ectopically in the liver with adenovirus administration in apolipoprotein E-deficient mice at 46 weeks of age. Hepatic LOX-1 expression enhanced hepatic oxLDL uptake, indicating functional expression of LOX-1 in the liver. Although plasma total cholesterol, triglyceride, and LDL cholesterol levels were unaffected, plasma oxLDL was markedly and transiently decreased in LOX-1 mice. In controls, atherosclerotic lesions, detected by Oil Red O staining, were markedly increased (by 38%) during the 4-week period after adenoviral administration. In contrast, atherosclerotic progression was almost completely inhibited by hepatic LOX-1 expression. In addition, plasma monocyte chemotactic protein-1 and lipid peroxide levels were decreased, whereas adiponectin was increased, suggesting decreased systemic oxidative stress. Thus, LOX1 expressed in the livers of apolipoprotein E-deficient mice transiently removes oxLDL from circulating blood and possibly decreases systemic oxidative stress, resulting in complete prevention of atherosclerotic progression despite the persistence of severe LDL hypercholesterolemia and hypertriglyceridemia. Conclusions-OxLDL has a major atherogenic impact, and oxLDL removal is a promising therapeutic strategy against atherosclerosis. Clinical Perspective p 83Oxidative stress might play critical roles in many diseases. In particular, oxidation of LDL might be a key step in the development of atherosclerosis. 4 -6 Oxidized LDL (oxLDL) has been proposed to be involved in many atherogenic changes in the vascular wall such as expression of adhesion molecules, migration of macrophages and smooth muscle cells, release of chemokines, 7 and impairment of endothelial nitric oxide production. 8 Importantly, oxLDL is incorporated into macrophages via receptor-mediated endocytosis, leading to macrophage transformation into foam cells and thus the plaque formation of atherosclerotic lesions. Furthermore, oxLDL itself reportedly induces oxidative stress in endothelial cells, smooth muscle cells, and macrophages, resulting in a vicious cycle of atherogenic plaque formation. 9 the effectiveness of antioxidant therapy against atherosclerosis is controversial. 10 -15 In addition, antioxidants may inhibit not only oxLDL formation but also many other oxidationsensitive pathways. Therefore, it is unclear that the antiatherogenic effects of antioxidants, if any, are due to inhibition of oxLDL formation. Thus, whether lowering oxLDL alone, rather than total LDL, affects ...

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Section: Discussionmentioning

confidence: 83%

Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis

Ishigaki

Katagiri²,

Gao³

et al. 2008

Circulation

159

View full text Add to dashboard Cite

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“…Angiographic and intravascular ultrasound investigations revealed the regression of coronary atherosclerosis after LDL-apheresis. [25][26][27] Morita, et al described the effectiveness of LDL apheresis in bypass grafts. 28) Our results also suggest that intensive cholesterol-lowering is effective at preventing graft occlusion.…”

Section: Discussionmentioning

confidence: 99%

Ten-year Follow-up of Familial Hypercholesterolemia Patients After Intensive Cholesterol-lowering Therapy

Masaki

Tatami²,

Kumamoto³

et al. 2005

Int. Heart J.

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SUMMARYTo prevent coronary artery disease, it is necessary for patients with familial hypercholesterolemia (FH) to maintain a low cholesterol level. Recently a combination therapy of low-density lipoprotein (LDL) apheresis and statins has been used for FH patients, but their long-term prognosis over 10 years is unknown.In this single center prospective report, 18 FH patients with severe coronary stenosis received LDL apheresis every 2 or 4 weeks and statin therapy for 9.8 ± 3.0 years. Probucol was given to 17 of the 18 patients. We observed their clinical events as well as coronary stenosis findings and ejection fractions for 10.7 ± 2.6 years.Total and LDL cholesterol levels before therapy were 345 ± 46 and 277 ± 48 mg/ dL, respectively. Immediately following LDL-apheresis, these levels decreased to 104 ± 7.5 and 66 ± 16 mg/dL, respectively. There were no cardiac deaths and 4 patients were free from any coronary events. There was one noncardiac death. Nonfatal myocardial infarction occurred in 2 patients and coronary bypass surgery was required in one patient. Twelve patients received additional coronary angioplasty. There was little change in coronary stenosis and ejection fraction following 10 years of the combination therapy. Univariate Cox regression analysis revealed that the calculated mean LDL cholesterol level was the predictive value of treatment efficacy (mean LDL cholesterol < 140 mg/dL, hazard ratio 0.23, P = 0.028). The combination therapy of LDL-apheresis and antilipid drugs delayed the progression of coronary atherosclerosis and prevented a major cardiac event, although complete inhibition was limited to a small group. Additional coronary angioplasty is likely to be required for a favorable clinical outcome in FH patients. (Int Heart J 2005; 46: 833-843)

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“…However, lipid-lowering therapy using the combination of LDL apheresis and lipid-lowering drugs may have a long-term potential role to ameliorate atherosclerotic injury in hyperlipidemic patients. 36 Three lipid peroxidation products, MDA, PCOOH, and oxidized phosphatidylcholine (oxPC), in plasma are generally correlated well with the degree of LDL oxidation. 10,22,37 Among these molecules, oxPC is the key molecule in oxLDL, is capable of inducing monocyte adhesion to endothelial cells and PMN migration, and is directly involved in the early development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

Chien

Chang

Chen

et al. 2004

ATVB

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Objective-The effect of ascorbate treatment on apheresis-induced oxidative stress in uremic and dyslipidemic patients was evaluated. Methods and Results-We developed a chemiluminescence-emission spectrum and high-performance liquid chromatography analysis to assess the effect of ascorbate supplement on plasma reactive oxygen species (ROS) scavenging activity and oxidized lipid/protein production in hyperlipidemic and uremic patients undergoing apheresis. Apheresis was efficient in reduction of atherogenic lipoproteins, complement, fibrinogen, soluble intercellular adhesion molecule-1, and oxidative parameters including phosphatidylcholine hydroperoxide (PCOOH), malonaldehyde, methylguanidine, and diotyrosine. Apheresis itself, however, activated leukocytes to increase ROS activity and reduced the plasma ROS scavenging activity. Ascorbate administration selectively diminished apheresis-enhanced H 2 O 2 and inflammatory mediators such as tumor necrosis factor alpha (TNF-␣) and monocyte chemoattractant protein-1. Chronically dyslipidemic and uremic patients undergoing biweekly apheresis plus ascorbate treatment had lower levels of C-reactive protein and PCOOH than did those without ascorbate treatment during a 6-month follow-up study period. Conclusions-We

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Intravascular ultrasound evaluation of coronary plaque regression by low density lipoprotein-apheresis in familial hypercholesterolemia

Abstract: These results suggest that aggressive lipid-lowering therapy using the combination of LDL-A and lipid-lowering drugs may induce regression of coronary atherosclerotic plaque in FH patients.

Cited by 153 publications

References 25 publications

Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis

Impact of Plasma Oxidized Low-Density Lipoprotein Removal on Atherosclerosis

Ten-year Follow-up of Familial Hypercholesterolemia Patients After Intensive Cholesterol-lowering Therapy

Ascorbate Supplement Reduces Oxidative Stress in Dyslipidemic Patients Undergoing Apheresis

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