Lipoprotein Apheresis and Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors in Patients With Heterozygous Familial Hypercholesterolemia: A One Center Study
| Autor: | Genovefa Kolovou, Niki Katsiki, Andreas Melidonis, Athanasios J. Manolis, Nikoletta Karampetsou, Dimitri P. Mikhailidis, Stamatis S. Makrygiannis, Vana Kolovou, Sophie Mavrogieni |
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| Rok vydání: | 2020 |
| Předmět: |
Adult
Male Heterozygote medicine.medical_specialty Serine Proteinase Inhibitors Time Factors Familial hypercholesterolemia 030204 cardiovascular system & hematology Antibodies Monoclonal Humanized Hyperlipoproteinemia Type II 03 medical and health sciences 0302 clinical medicine Internal medicine Humans Medicine Genetic Predisposition to Disease Pharmacology (medical) In patient 030212 general & internal medicine PCSK9 Inhibitors Aged Pharmacology Greece business.industry Anticholesteremic Agents Subtilisin Cholesterol LDL Middle Aged Proprotein convertase medicine.disease Combined Modality Therapy Phenotype Treatment Outcome Endocrinology Receptors LDL Mutation Blood Component Removal Kexin Female Proprotein Convertase 9 Cardiology and Cardiovascular Medicine business Lipoprotein apheresis Biomarkers |
| Zdroj: | Journal of Cardiovascular Pharmacology and Therapeutics. 26:51-58 |
| ISSN: | 1940-4034 1074-2484 |
| DOI: | 10.1177/1074248420943079 |
| Popis: | Aim:We evaluated the lipid-lowering (LL) effect of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) in patients with heterozygous familial hypercholesterolemia (HeFH) treated with LL-drugs and lipoprotein apheresis (LA).Patients and Methods:The PCSK9i treatment (evolocumab 420 mg/4 weeks, alirocumab 150 mg/2 weeks, or alirocumab 75 mg/2 weeks: 9, 6, and 2 patients, respectively) was initiated in patients with HeFH (n = 17; aged 35-69 years, 10 men, previously treated with statins + ezetimibe ± colesevelam and LA sessions for 2-12 years). A lipid profile was obtained before and immediately after the LA session and before, 1 and 2 months after switching to PCSK9i treatment. The duration of PCSK9i therapy ranged from 3 to 18 months.Results:Median total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) levels before LA were 268, 198, 46, and 126 mg/dL, respectively, and decreased (at the end of the LA session) to 117, 50, 40, and 51 mg/dL, respectively ( P < .001 for TC and P = .001 for all other comparisons). The median time-averaged LDL-C levels following LA were 155 (121, 176; median [25th, 75th percentile]) mg/dL. Median TC, LDL-C, and TG levels before PCSK9i therapy were 269, 190, and 127 mg/dL and decreased to 152, 100, and 95 mg/dL, respectively ( P = .002, P < .002, and P < .03, respectively). Steady LDL-C levels with PCSK9i treatment were significantly lower compared with time-averaged LDL-C levels following LA (median value: 100 vs 155 mg/dL; P = .008). With PCSK9i, from 13 patients with CHD, 6 (46.1%) patients achieved LDL-C Conclusions:PCSK9i can reduce LDL-C more consistently over time compared with a transient decrease following LA in HeFH patients. PCSK9i therapy may reduce the frequency of LA. Larger trials are required to establish the clinical implications of PCSK9i in patients previously on LA. |
| Databáze: | OpenAIRE |
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