Omar Razek1, Lubormira Cermakova2, Hamidreza Armani2, Terry Lee3, Gordon A Francis4, G B John Mancini5, Jiri Frohlich6, Liam R Brunham7. 1. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. 2. Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada. 3. Centre for Health Evaluation and Outcome Sciences, University of British Columbia, Vancouver, British Columbia, Canada. 4. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia, Vancouver, British Columbia, Canada. 5. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada. 6. Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. 7. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Healthy Heart Program Prevention Clinic, St Paul's Hospital, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia, Vancouver, British Columbia, Canada. Electronic address: Liam.brunham@ubc.ca.
Abstract
BACKGROUND: Familial hypercholesterolemia (FH) is the most common inherited dyslipidemia and is characterized by elevated low-density lipoprotein cholesterol (LDL-C) and markedly increased risk for atherosclerotic cardiovascular disease. Lipid-lowering therapy is the mainstay of treatment, but few patients with FH are able to achieve commonly recommended lipid targets. METHODS: We examined changes in LDL-C levels in patients in the British Columbia FH Registry from 2015 to 2017, corresponding to the period immediately before, and the first 2 years after, availability of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in Canada. RESULTS: Among 275 patients with a clinical diagnosis of FH in whom a lipid profile was available between January 1, 2016 and December 31, 2017, 48 had started using a PCSK9 inhibitor. LDL-C decreased in the cohort overall from 2015 to 2017. When patients were stratified according to PCSK9 inhibitor use, the reduction in LDL-C was significantly greater in patients receiving a PCSK9 inhibitor compared with those who did not receive one. Among patients receiving a PCSK9 inhibitor, 85.4% achieved a ≥ 50% reduction in LDL-C or LDL-C < 2 mmol/L, compared with 50.2% of patients not receiving a PCSK9 inhibitor (P < 0.001). CONCLUSIONS: Our results suggest that control of lipid levels in patients with FH has improved and that the achievement of guideline-directed goals has been facilitated by access to PCSK9 inhibitors. These observations provide insight into the real-world effectiveness of PCSK9 inhibitor therapy in patients with FH.
BACKGROUND:Familial hypercholesterolemia (FH) is the most common inherited dyslipidemia and is characterized by elevated low-density lipoprotein cholesterol (LDL-C) and markedly increased risk for atherosclerotic cardiovascular disease. Lipid-lowering therapy is the mainstay of treatment, but few patients with FH are able to achieve commonly recommended lipid targets. METHODS: We examined changes in LDL-C levels in patients in the British Columbia FH Registry from 2015 to 2017, corresponding to the period immediately before, and the first 2 years after, availability of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in Canada. RESULTS: Among 275 patients with a clinical diagnosis of FH in whom a lipid profile was available between January 1, 2016 and December 31, 2017, 48 had started using a PCSK9 inhibitor. LDL-C decreased in the cohort overall from 2015 to 2017. When patients were stratified according to PCSK9 inhibitor use, the reduction in LDL-C was significantly greater in patients receiving a PCSK9 inhibitor compared with those who did not receive one. Among patients receiving a PCSK9 inhibitor, 85.4% achieved a ≥ 50% reduction in LDL-C or LDL-C < 2 mmol/L, compared with 50.2% of patients not receiving a PCSK9 inhibitor (P < 0.001). CONCLUSIONS: Our results suggest that control of lipid levels in patients with FH has improved and that the achievement of guideline-directed goals has been facilitated by access to PCSK9 inhibitors. These observations provide insight into the real-world effectiveness of PCSK9 inhibitor therapy in patients with FH.
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