Specific Lp(a) apheresis: A tool to prove lipoprotein(a) atherogenicity

• Published in: Atherosclerosis. Supplements 2017-11, Vol.30, p.166-173
• Main Authors: Pokrovsky, S.N., Afanasieva, O.I., Safarova, M.S., Balakhonova, T.V., Matchin, Yu.G., Adamova, I.Y.u., Konovalov, G.A., Ezhov, M.V.
• Format: Article
• Language: English
• Subjects: Atherosclerosis; Atorvastatin Calcium - therapeutic use; Biomarkers - blood; Blood Component Removal - methods; Carotid Artery Diseases - blood; Carotid Artery Diseases - diagnostic imaging; Carotid Artery Diseases - therapy; Carotid Intima-Media Thickness; Cholesterol, LDL - blood; Coronary Angiography; Coronary Artery Disease - blood; Coronary Artery Disease - diagnostic imaging; Coronary Artery Disease - therapy; Coronary Stenosis - blood; Coronary Stenosis - diagnostic imaging; Coronary Stenosis - therapy; Dyslipidemias - blood; Dyslipidemias - diagnosis; Dyslipidemias - therapy; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Inflammation Mediators - blood; Intravascular ultrasound; Lipoprotein(a); Lipoprotein(a) - blood; Male; Middle Aged; Plaque, Atherosclerotic; Prospective Studies; Quantitative coronary angiography; Regression; Risk Factors; Specific Lp(a) apheresis; Targeted therapy; Time Factors; Treatment Outcome; Ultrasonography, Interventional
• ISSN: 1567-5688; 1878-5050
• DOI: 10.1016/j.atherosclerosissup.2017.05.004

An elevated lipoprotein(a) (Lp(a)) level is observed in more than 30% of patients with stable ischemic heart disease (SIHD). We conducted an investigation of the effects of specific Lp(a) apheresis on the progression of atherosclerosis in SIHD patients with Lp(a) levels greater than 50 mg/dL. We prospectively enrolled 15 patients diagnosed with SIHD based on symptom-driven coronary angiography findings, with Lp(a) ≥50 mg/dL and a low density lipoprotein cholesterol (LDL-C) ≤2.5 mmol/L, who were on long-term statin therapy. They underwent weekly Lp(a) apheresis using Lp(a) Lipopak® adsorption columns which contain monospecific sheep polyclonal antibodies against human Lp(a). Fifteen age and gender matched SIHD patients receiving atorvastatin monotherapy served as controls. At baseline and 18 months post-treatment, quantitative coronary angiography, intracoronary ultrasound with virtual histology and carotid ultrasound were performed. Lipid profile, including Lp(a), was measured at the scheduled visits, and before and after each apheresis procedure. Levels of high-sensitivity C-reactive protein (hsCRP), matrix metalloproteinases (MMP)-7 and 9, and tissue inhibitor of matrix metalloproteinases (TIMP)-1 and 2 were determined at baseline and at the end of the study period. Each specific Lp(a) apheresis procedure was carried out with two adsorption columns resulting in an average acute decrease in Lp(a) levels of 75% (from 110 ± 22 to 29 ± 16 mg/dL) without significant changes in other plasma components. Lp(a) reduction over the course of 18 months was associated with a decrease in the mean percent diameter stenosis of 5.05% and an increase in minimal lumen diameter of 14%; the mean total atheroma volume was reduced by 4.60 mm3 (p