ArticleLife (Basel, Switzerland)2020
Higher Responsiveness to Rosuvastatin in Polygenic versus Monogenic Hypercholesterolaemia: A Propensity Score Analysis.
Article in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Trial
- Clinical and biochemical features of atherogenic hyperlipidemias with different genetic basis: A comprehensive comparative study.PloS one · 2024Article
- Familial Hypercholesterolemia: Pitfalls and Challenges in Diagnosis and Treatment.Reviews in cardiovascular medicine · 2023Review
- The Clinical Importance of Differentiating Monogenic Familial Hypercholesterolemia from Polygenic Hypercholesterolemia.Current cardiology reports · 2022Review
- Polygenic risk score for hypercholesterolemia in a Brazilian familial hypercholesterolemia cohort.Atherosclerosis plus · 2022Article
- Monogenic Versus Polygenic Forms of Hypercholesterolemia and Cardiovascular Risk: Are There Any Differences?Current atherosclerosis reports · 2022Review
- Management of dyslipidemia in Poland: Interdisciplinary Expert Position Statement endorsed by the Polish Cardiac Society Working Group on Cardiovascular Pharmacotherapy. The Fourth Declaration of Sopot.Cardiology journal · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Background
methodsFH Individuals were tested for mutations in LDLR and APOB genes
resultsMonogenic subjects had higher mean (±SD) baseline LDL-C when compared to polygenic (7.6 ± 1.5 mmol/L vs. 6.2 ± 1.2 mmol/L; p < 0.001). Adjusted model showed a lower percentage of change in LDL-C after rosuvastatin treatment in monogenic patients vs. polygenic subjects (45.9% vs. 55.4%, p < 0.001). The probability of achieving LDL-C targets in monogenic FH was lower than in polygenic subjects (0.075 vs. 0.245, p = 0.004). Polygenic patients were more likely to achieve LDL-C goals, as compared to those monogenic (OR 3.28; 95% CI: 1.23-8.72).
conclusionOur findings indicate an essentially higher responsiveness to rosuvastatin in FH patients with a polygenic cause, as compared to those carrying monogenic mutations.
Indexed as
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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.