Treatment with high-dose n-3 PUFAs has no effect on platelet function, coagulation, metabolic status or inflammation in patients with atherosclerosis and type 2 diabetes

Cardiovascular Diabetology

Original Investigation

Maciej Haberka¹  Krzysztof Piotr Malinowski²  Malgorzata Poreba³  Aleksander Siniarski³  Renata Golebiowska-Wiatrak³  Ewa Konduracka⁴  Grzegorz Gajos⁴  Jadwiga Nessler⁴  Magdalena Mostowik⁵  Anetta Undas⁶ 

[1] Department of Cardiology, School of Health Science, Medical University of Silesia, Katowice, Poland;Institute of Public Health, Faculty of Health Science, Jagiellonian University Medical College, Kraków, Poland;John Paul II Hospital, Pradnicka 80, 31-202, Kraków, Poland;John Paul II Hospital, Pradnicka 80, 31-202, Kraków, Poland;Department of Coronary Disease and Heart Failure, Institute of Cardiology, Faculty of Medicine, Jagiellonian University Medical College, Pradnicka 80, 31-202, Kraków, Poland;John Paul II Hospital, Pradnicka 80, 31-202, Kraków, Poland;Department of Medical Education, Jagiellonian University Medical College, Kraków, Poland;John Paul II Hospital, Pradnicka 80, 31-202, Kraków, Poland;Institute of Cardiology, Jagiellonian University Medical College, Pradnicka 80, 31-202, Kraków, Poland;

关键词: Cardiovascular disease;    Atherosclerosis;    Diabetes type 2;    Omega-3 polyunsaturated fatty acids;   

DOI  :  10.1186/s12933-017-0523-9

 received in 2017-01-31, accepted in 2017-03-19,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundDespite numerous studies on cardioprotective effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs), there is limited evidence for n-3 PUFA-mediated effects, especially at its higher dose, on cardiovascular risk in patients with type 2 diabetes (DM2) and established atherosclerosis.PurposeTo investigate the effect of daily treatment with a higher dose (2 g) of n-3 PUFAs on platelet function, coagulation parameters, fibrin clot properties, markers of systemic inflammation and metabolic status, in patients with atherosclerotic vascular disease and DM2 who receive optimal medical therapy.MethodsWe conducted a prospective, double-blind, placebo-controlled, randomized, double-center study, in which thrombin generation (plasma thrombogenic potential from automated thrombogram), fibrin clot properties (plasma fibrin clot permeability; lysis time), platelet aggregation (light transmission aggregometry with adenosine diphosphate and arachidonic acid used as agonists), HbA1c, insulin level, lipid profiles, leptin and adiponectin levels, as well as markers of systemic inflammation (i.e., hsCRP, IL-6, TNF-α, ICAM-1, VCAM-1, and myeloperoxidase) were determined at baseline and at 3 months after treatment with 2 g/day of n-3 PUFAs (n = 36) or placebo (n = 38). Moreover, we assessed serum fatty acids of the phospholipid fraction by gas chromatography both at baseline and at the end of the study.ResultsMajority of patients were treated with optimal medical therapy and achieved recommended treatment targets. Despite higher serum levels of eicosapentaenoic acid (EPA) (by 204%; p < 0.001) and docosahexaenoic acid (DHA) (by 62%; p < 0.0001) in n-3 PUFA group at the end of treatment no changes in platelet aggregation, thrombin generation, fibrin clot properties or markers of systemic inflammation were observed. No intergroup differences in the insulin, HbA1c and lipid levels were found at the end of the study. There was no change in adiponectin and leptin in interventional group, however leptin increased in control group (p = 0.01), therefore after study period leptin levels were lower in the interventional group (p = 0.01). Additionally, resolvin D1 did not differ between interventional and control group.ConclusionsIn conclusion, our study demonstrated that in patients with long-standing, well-controlled DM2 and atherosclerotic disease the treatment with a high dose of n-3 PUFAs (namely, 1 g/day of EPA and 1 g/day of DHA for 3 months) does not improve coagulation, metabolic, and inflammatory status when measured with the specified tests.The study was registered in ClinicalTrials.gov; identifier: NCT02178501. Registration date: April 12, 2014

【 授权许可】

CC BY   
© The Author(s) 2017