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Open AccessArticle

Higher Responsiveness to Rosuvastatin in Polygenic versus Monogenic Hypercholesterolemia: A Propensity Score Analysis

1
Department of Cardiology I, Medical University of Gdansk, Dębinki 7, 80-211 Gdańsk, Poland
2
Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London WC1E 6BT, UK
3
Department of Clinical Chemistry, Medical University of Gdansk, Dębinki 7, 80-211 Gdańsk, Poland
4
Institute of Statistics, Department of Economic Sciences, Faculty of Management and Economics, Gdansk University of Technology, 80-233 Gdańsk, Poland
5
Department of Biology and Genetics, Medical University of Gdansk, Dębinki 1, 80-211 Gdańsk, Poland
6
Centre for Cardiovascular Genetics, British Heart Foundation Laboratories, Institute of Cardiovascular Science, the Rayne Building University College London, London WC1E 6JF, UK
*
Author to whom correspondence should be addressed.
Life 2020, 10(5), 73; https://doi.org/10.3390/life10050073
Received: 22 April 2020 / Revised: 14 May 2020 / Accepted: 16 May 2020 / Published: 20 May 2020
(This article belongs to the Section Medical Research)
Background: The monogenic defect in familial hypercholesterolemia (FH) is detected in ∼40% of cases. The majority of mutation-negative patients have a polygenic cause of high LDL-cholesterol (LDL-C). We sought to investigate whether the underlying monogenic or polygenic defect is associated with the response to rosuvastatin. Methods: FH Individuals were tested for mutations in LDLR and APOB genes. A previously established LDL-C-specific polygenic risk score (PRS) was used to examine the possibility of polygenic hypercholesterolemia in mutation-negative patients. All of the patients received rosuvastatin and they were followed for 8 ± 2 months. A propensity score analysis was performed to evaluate the variables associated with the response to treatment. Results: Monogenic 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). Conclusion: Our findings indicate an essentially higher responsiveness to rosuvastatin in FH patients with a polygenic cause, as compared to those carrying monogenic mutations. View Full-Text
Keywords: polygenic hypercholesterolemia; monogenic hypercholesterolemia; rosuvastatin; propensity score polygenic hypercholesterolemia; monogenic hypercholesterolemia; rosuvastatin; propensity score
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Mickiewicz, A.; Futema, M.; Ćwiklinska, A.; Kuchta, A.; Jankowski, M.; Kaszubowski, M.; Chmara, M.; Wasąg, B.; Fijałkowski, M.; Jaguszewski, M.; Humphries, S.E.; Gruchała, M. Higher Responsiveness to Rosuvastatin in Polygenic versus Monogenic Hypercholesterolemia: A Propensity Score Analysis. Life 2020, 10, 73.

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