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1.
J Clin Lipidol ; 17(5): 694-699, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37598001

RESUMO

Elevated lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular disease. However, there are no approved and effective treatments for lowering Lp(a) and the associated cardiovascular risks. Omega-3 fatty acids (ω-3FAs), primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have both triglyceride-lowering and anti-inflammatory properties. This pilot study investigated the effect of high dose ω-3FAs (3.6 g/day) on arterial inflammation in 12 patients with elevated Lp(a) (> 0.5 g/L) and stable coronary artery disease (CAD) receiving cholesterol-lowering treatment. Arterial inflammation was determined using 18F-fluorodexoyglucose positron emission tomography/computed tomography before and after 12-weeks intervention. ω-3FAs significantly lowered plasma concentrations of triglycerides (-17%, p < 0.01), Lp(a) (-5%, p < 0.01) as well as aortic maximum standardized uptake value (SUVmax) (-4%, p < 0.05). The reduction in SUVmax was significantly inversely associated with average on-treatment EPA (r = -0.750, p < 0.01), but not DHA and triglyceride, concentrations. In conclusion, high dose ω-3FAs decrease arterial inflammation in patients with elevated Lp(a) and stable CAD, which may involve a direct arterial effect of EPA.


Assuntos
Arterite , Doença da Artéria Coronariana , Ácidos Graxos Ômega-3 , Humanos , Ácido Eicosapentaenoico/uso terapêutico , Projetos Piloto , Ácidos Graxos Ômega-3/uso terapêutico , Ácidos Docosa-Hexaenoicos/uso terapêutico , Doença da Artéria Coronariana/tratamento farmacológico , Triglicerídeos , Arterite/tratamento farmacológico , Lipoproteína(a)
3.
Am J Physiol Heart Circ Physiol ; 317(5): H923-H938, 2019 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-31469291

RESUMO

Cardiovascular disease (CVD) is the leading cause of death worldwide. The human body is populated by a diverse community of microbes, dominated by bacteria, but also including viruses and fungi. The largest and most complex of these communities is located in the gastrointestinal system and, with its associated genome, is known as the gut microbiome. Gut microbiome perturbations and related dysbiosis have been implicated in the progression and pathogenesis of CVD, including atherosclerosis, hypertension, and heart failure. Although there have been advances in the characterization and analysis of the gut microbiota and associated bacterial metabolites, the exact mechanisms through which they exert their action are not well understood. This review will focus on the role of the gut microbiome and associated functional components in the development and progression of atherosclerosis. Potential treatments to alter the gut microbiome to prevent or treat atherosclerosis and CVD are also discussed.


Assuntos
Artérias/microbiologia , Aterosclerose/microbiologia , Bactérias/metabolismo , Microbioma Gastrointestinal , Intestinos/microbiologia , Animais , Antibacterianos/uso terapêutico , Artérias/metabolismo , Artérias/patologia , Aterosclerose/metabolismo , Aterosclerose/patologia , Aterosclerose/terapia , Dieta Saudável , Suplementos Nutricionais , Disbiose , Transplante de Microbiota Fecal , Interações Hospedeiro-Patógeno , Humanos , Placa Aterosclerótica , Transdução de Sinais
4.
Curr Opin Cardiol ; 28(2): 216-22, 2013 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23370227

RESUMO

PURPOSE OF REVIEW: Despite advanced medical and device-based therapies, congestive heart failure (CHF) remains a major medical problem, associated with significant morbidity and mortality. Vitamin D deficiency is prevalent in CHF and is associated with poor outcomes. In this manuscript we review the evidence linking vitamin D deficiency and CHF and discuss potential mechanisms involved, as well the clinical data on vitamin D supplementation in CHF patients. RECENT FINDINGS: A clear relationship has been established between Vitamin D deficiency and increased mortality and morbidity in CHF. However, the mechanism involved is not clearly understood. Recent clinical and experimental evidence have identified the renin-angiotensin-aldosterone system and inflammatory cytokines as likely mediators that can lead to poor clinical outcomes via the cardiorenal syndrome. Clinical data on vitamin D supplementation also remain unestablished, with potential clinical benefits recently reported in patients with vitamin D deficiency. Nonetheless, large-scale randomized clinical trials are lacking. SUMMARY: Vitamin D is an emerging agent with tremendous potential and may represent a novel target for therapy in CHF. Further studies are needed to identify the mechanism(s) involved in the pathophysiology as well as to adequately examine the role of Vitamin D measurement and supplementation in patients with CHF.


Assuntos
Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/fisiopatologia , Deficiência de Vitamina D/complicações , Vitamina D/fisiologia , Vitaminas/fisiologia , Doença Crônica , Progressão da Doença , Ergocalciferóis/administração & dosagem , Insuficiência Cardíaca/tratamento farmacológico , Humanos , Vitamina D/uso terapêutico , Deficiência de Vitamina D/fisiopatologia , Vitaminas/administração & dosagem , Vitaminas/uso terapêutico
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