ArticleCJC open2019
Efficacy of Evolocumab in Monogenic vs Polygenic Hypercholesterolemia.
Article in CJC open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Six years' experience with LipidSeq: clinical and research learnings from a hybrid, targeted sequencing panel for dyslipidemias.BMC medical genomics · 2020Trial
- Does Genotype Affect the Efficacy of PCSK9 Inhibitors in the Treatment of Familial Hypercholesterolemia?Cardiovascular drugs and therapy · 2025Review
- The Clinical Importance of Differentiating Monogenic Familial Hypercholesterolemia from Polygenic Hypercholesterolemia.Current cardiology reports · 2022Review
- Monogenic Versus Polygenic Forms of Hypercholesterolemia and Cardiovascular Risk: Are There Any Differences?Current atherosclerosis reports · 2022Review
- Clinical Implications of Monogenic Versus Polygenic Hypercholesterolemia: Long-Term Response to Treatment, Coronary Atherosclerosis Burden, and Cardiovascular Events.Journal of the American Heart Association · 2021Observational
- Role of PCSK9 Inhibitors in Patients with Familial Hypercholesterolemia.Endocrinology and metabolism (Seoul, Korea) · 2021Article
- The need for polygenic score reporting standards in evidence-based practice: lipid genetics use case.Current opinion in lipidology · 2021Review
- Higher Responsiveness to Rosuvastatin in Polygenic versus Monogenic Hypercholesterolaemia: A Propensity Score Analysis.Life (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhibitors of proprotein convertase subtilisin kexin 9 are indicated in Canada for treatment of patients with familial hypercholesterolemia (FH). Classically, FH is considered to be a monogenic condition caused by rare pathogenic mutations; however, some patients have hypercholesterolemia on a polygenic basis. Whether the effect of proprotein convertase subtilisin kexin 9 inhibitor treatment differs between patients with monogenic hypercholesterolemia and patients with polygenic hypercholesterolemia is unclear.
methodsWe performed retrospective chart reviews on patients treated with evolocumab 140 mg subcutaneously biweekly from the Lipid Genetics Clinic, London Health Sciences Centre. Evolocumab-treated patients with hypercholesterolemia were grouped into monogenic or polygenic categories on the basis of their genotype determined by targeted next-generation sequencing. Absolute and relative changes in low-density lipoprotein cholesterol (LDL-C) levels before and after evolocumab treatment were studied.
resultsIn 32 patients with monogenic heterozygous FH and 7 patients with polygenic hypercholesterolemia treated with evolocumab, absolute incremental reductions in LDL-C were 2.94 ± 1.22 mmol/L and 3.15 ± 0.90 mmol/L, respectively (
conclusionAlthough the sample size is small, the findings suggest comparable biochemical responsiveness to evolocumab in both monogenic (heterozygous) and polygenic hypercholesterolemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.