title: Reduction of charge-modified LDL by statin therapy in patients with CHD or CHD risk factors and elevated LDL-C levels: the SPECIAL Study.
abstract: Various forms of atherogenic modified low-density lipoprotein (LDL) including oxidized LDL and small, dense LDL have increased negative charge as compared to normal LDL. Charge-modified LDL (electronegative LDL) and normal LDL subfractions in plasma are analyzed by capillary isotachophoresis (cITP) as fast-migrating LDL (fLDL) and slow-migrating LDL (sLDL). We examined the effects of pravastatin and simvastatin on charge-based LDL subfractions as determined by cITP in patients with hypercholesterolemia. Patients (n=72) with CHD or CHD risk factors and elevated LDL cholesterol (LDL-C) levels were randomly assigned to receive pravastatin or simvastatin. After treatment with statins for 3 and 6 months, both cITP fLDL and sLDL were reduced (p<0.05) from the baseline, but the effects did not differ between treatment with pravastatin and simvastatin. At baseline and after treatment for 3 months, cITP sLDL was correlated with LDL-C, but fLDL was correlated with inflammatory markers, high-sensitive C-reactive protein and LDL-associated platelet-activating factor acetylhydrolase, and atherogenic lipoproteins, remnant-like particle cholesterol and small, dense LDL cholesterol. In conclusion, cITP fLDL was related to inflammatory markers and atherogenic lipoproteins and was reduced by treatment with statins. Charge-modified LDL subfraction could be a potential marker for atherosclerosis and a target for therapy.
authors.affiliation: Department of Cardiology, Fukuoka University School of Medicine, Fukuoka, Japan. bozhang@fukuoka-u.ac.jp
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Daizaburo
authors.initials: D
authors.lastname: Yanagi
authors.forename: Keita
authors.initials: K
authors.lastname: Noda
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Nishikawa
authors.forename: Akira
authors.initials: A
authors.lastname: Matsunaga
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shirai
authors.forename: Atsushi
authors.initials: A
authors.lastname: Iwata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yoshinaga
authors.forename: Hisashi
authors.initials: H
authors.lastname: Adachi
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Keijiro
authors.initials: K
authors.lastname: Saku
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism*; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use; D012307:Risk Factors; D019821:Simvastatin / Q000627:therapeutic use; D016896:Treatment Outcome; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D014280:Triglycerides; D002097:C-Reactive Protein; D019821:Simvastatin; D017035:Pravastatin