Amirhossein Sahebkar1, Maria-Corina Serban2, Dimitri P Mikhailidis3, Peter P Toth4, Paul Muntner5, Sorin Ursoniu6, Svetlana Mosterou7, Stephen Glasser8, Seth S Martin9, Steven R Jones10, Manfredi Rizzo11, Jacek Rysz12, Allan D Sniderman13, Michael J Pencina14, Maciej Banach15. 1. Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Metabolic Research Centre, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia. Electronic address: amir_saheb2000@yahoo.com. 2. Department of Epidemiology, University of AL at Birmingham, Birmingham, AL, USA; Department of Functional Sciences, Discipline of Pathophysiology, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania. Electronic address: dr.corinaserban@yahoo.com. 3. Department of Clinical Biochemistry, Royal Free Campus, University College London Medical School, University College London (UCL), London, UK. Electronic address: mikhailidis@aol.com. 4. Preventive Cardiology, CGH Medical Center, Sterling, IL, USA; The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. Electronic address: Peter.Toth@cghmc.com. 5. Department of Epidemiology, University of AL at Birmingham, Birmingham, AL, USA. Electronic address: pmuntner@uab.edu. 6. Department of Functional Sciences, Discipline of Public Health, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania. Electronic address: sursoniu@yahoo.com. 7. Institute for Cardiovascular Medicine Timisoara, Cardiology Department, University of Medicine and Pharmacy "Victor Babes" Timisoara, Romania. Electronic address: tanaliliana@yahoo.co.uk. 8. Department of Preventive Medicine, University of AL at Birmingham, Birmingham, AL, USA. Electronic address: sglasser@uabmc.edu. 9. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. Electronic address: smart100@jhmi.edu. 10. The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. Electronic address: sjones64@jhmi.edu. 11. Biomedical Department of Internal Medicine and Medical Specialties, University of Palermo, Italy. Electronic address: manfredi.rizzo@unipa.it. 12. Department of Nephrology, Hypertension and Family Medicine, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland. Electronic address: jacek.rysz@umed.lodz.pl. 13. Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada. Electronic address: allansniderman@hotmail.com. 14. Duke Clinical Research Institute, Department of Biostatistics and Bioinformatics, Duke University, Durham, NC, USA. Electronic address: michal.pencina@duke.edu. 15. Department of Hypertension, Chair of Nephrology and Hypertension, Medical University of Lodz, Poland. Electronic address: maciejbanach@aol.co.uk.
Abstract
BACKGROUND: Several studies suggest differences between fibrates and statins in lowering plasma fibrinogen (Fib) concentrations, but the evidence is not definitive. Therefore, the aim of this meta-analysis of head-to-head randomized trials was to compare the efficacy of statins and fibrates on plasma Fib concentrations. METHODS: The literature search included Medline, Scopus, and Web of Science up to February 1st, 2015, to identify head-to-head comparative randomized trials investigating the efficacy of fibrates vs statins on plasma Fib concentrations. RESULTS: In total 22 trials with 2762 participants were included to the meta-analysis. Random-effect meta-analysis suggested a significantly greater effect of fibrates vs statins in lowering plasma Fib concentrations (weighted mean difference [WMD]: -40.7mg/dL, 95% confidence interval [CI]: -55.2, -26.3, p<0.001). When the analysis was stratified according to the type of fibrate administered, there were significant Fib-lowering effects with both bezafibrate (n=8 treatment arms; WMD: -23.7mg/dL, 95% CI: -41.8, -5.7, p=0.01) and fenofibrate (n=15 treatment arms; WMD: -43.7mg/dL, 95% CI: -61.3, -26.2, p<0.001). Overall, there was a numerically greater effect in the subgroup of trials with ≥12 weeks duration (n=17 treatment arms; WMD: -42.7mg/dL, 95% CI: -60.3, -25.1, p<0.001) compared with the subgroup of trials lasting <12 weeks (n=7 treatment arms; WMD: -36.7mg/dL, 95% CI: -52.0, -21.4, p<0.001). CONCLUSIONS: Monotherapy with either fibrates or statins suggested a significantly greater effect of fibrates in lowering plasma Fib concentrations. According to these findings, mechanisms associated with fibrinogen metabolism might be responsible for the distinct effects of statins and fibrates in reducing cardiovascular endpoints.
BACKGROUND: Several studies suggest differences between fibrates and statins in lowering plasma fibrinogen (Fib) concentrations, but the evidence is not definitive. Therefore, the aim of this meta-analysis of head-to-head randomized trials was to compare the efficacy of statins and fibrates on plasma Fib concentrations. METHODS: The literature search included Medline, Scopus, and Web of Science up to February 1st, 2015, to identify head-to-head comparative randomized trials investigating the efficacy of fibrates vs statins on plasma Fib concentrations. RESULTS: In total 22 trials with 2762 participants were included to the meta-analysis. Random-effect meta-analysis suggested a significantly greater effect of fibrates vs statins in lowering plasma Fib concentrations (weighted mean difference [WMD]: -40.7mg/dL, 95% confidence interval [CI]: -55.2, -26.3, p<0.001). When the analysis was stratified according to the type of fibrate administered, there were significant Fib-lowering effects with both bezafibrate (n=8 treatment arms; WMD: -23.7mg/dL, 95% CI: -41.8, -5.7, p=0.01) and fenofibrate (n=15 treatment arms; WMD: -43.7mg/dL, 95% CI: -61.3, -26.2, p<0.001). Overall, there was a numerically greater effect in the subgroup of trials with ≥12 weeks duration (n=17 treatment arms; WMD: -42.7mg/dL, 95% CI: -60.3, -25.1, p<0.001) compared with the subgroup of trials lasting <12 weeks (n=7 treatment arms; WMD: -36.7mg/dL, 95% CI: -52.0, -21.4, p<0.001). CONCLUSIONS: Monotherapy with either fibrates or statins suggested a significantly greater effect of fibrates in lowering plasma Fib concentrations. According to these findings, mechanisms associated with fibrinogen metabolism might be responsible for the distinct effects of statins and fibrates in reducing cardiovascular endpoints.
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