OMEGA-3 POLYUNSATURATED FATTY ACIDS MAY FAVORABLY AFFECT INFLAMMATORY BIOMARKERS & NOVEL INDICES OF LEFT VENTRICLE FUNCTION IN PATIENTS WITH HEART FAILURE

Purpose: To examine long-term survival after angioplasty and stenting of atherosclerotic renal artery stenosis (RAS). Methods: Over a 5-year period, 241 consecutive patients (153 men; mean age 67±9 years, range 44–84) were treated with angioplasty and stent implantation for 355 ostial renal stenoses >70%. The procedures were performed in standard fashion using a variety of stents. For survival analysis, the patients were divided into 3 groups based on baseline creatinine levels: group 1: 115 (48%) patients with normal renal function (creatinine <1.2 mg/dL); group 2: 93 (39%) patients with moderately impaired renal function (creatinine 1.2 to 2.5 mg/dL); and group 3: 33 (13%) patients with severely impaired renal function (creatinine >2.5 mg/dL). Results: All patients were treated successfully without any procedure-related mortality. The 30-day mortality was 0.4% (1/241). Twenty-two patients died during a follow-up of 27±15 months (range 1–60) (overall survival 91%). The causes of death were cardiac (congestive heart failure or myocardial infarction, 73%), stroke (13.5%), and malignant disease (13.5%). The survival rate was significantly lower (29.6%) in patients with a baseline serum creatinine >2.5 mg/dL (p<0.0001) than in groups 2 (89.1%) or 1 (95.4%). Long-term survival without hemodialysis or restenosis was 66.6% at 48 months. Independent predictors for a reduced survival were left ventricle function (HR 2.59, 95% CI 1.45 to 4.63, p=0.001 for each 15% incremental decrease), age (HR 1.13, 95% CI 1.03 to 1.25, p=0.011), and baseline renal function (HR 1.58, 95% CI 1.10 to 2.29, p=0.014). Conclusions: Survival after successful stenting for severe ostial RAS depends on baseline serum creatinine and left ventricle function. Efforts must be made to avoid the development of advanced ischemic nephropathy and congestive heart failure.

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Effects of supplementation with polyunsaturated fatty acids in patients with heart failure

Internal and Emergency Medicine ◽

10.1007/s11739-011-0671-y ◽

2011 ◽

Vol 6 (S1) ◽

pp. 37-44 ◽

Cited By ~ 6

Author(s):

Savina Nodari ◽

Marco Triggiani ◽

Alessandra Manerba ◽

Giuseppe Milesi ◽

Livio Dei Cas

Keyword(s):

Heart Failure ◽

Fatty Acids ◽

Polyunsaturated Fatty Acids ◽

Patients With Heart Failure

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Omega-3 Fatty Acids Improve Lipid Metabolism and Inflammatory Markers in Patients with Heart Failure Undergoing Exercise Training

International Journal of Food and Nutritional Science ◽

10.15436/2377-0619.15.016 ◽

2015 ◽

Vol 2 (2) ◽

pp. 1-6

Author(s):

Edson Luiz da Silva ◽

Keyword(s):

Heart Failure ◽

Fatty Acids ◽

Lipid Metabolism ◽

Exercise Training ◽

Inflammatory Markers ◽

Omega 3 Fatty Acids ◽

Omega 3 ◽

Patients With Heart Failure

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Maresin‐1 Activates Resolution Sensor and Improves Left Ventricle Function In Acute Heart Failure

The FASEB Journal ◽

10.1096/fasebj.2018.32.1_supplement.718.2 ◽

2018 ◽

Vol 32 (S1) ◽

Author(s):

Ganesh V. Halade ◽

Roman Travis ◽

Vasundhara Kain ◽

Jeevan Kumar Jadapalli

Keyword(s):

Heart Failure ◽

Left Ventricle ◽

Acute Heart Failure ◽

Left Ventricle Function ◽

Maresin 1 ◽

Ventricle Function

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Dose-dependent decrease of platelet activation and tissue factor by omega-3 polyunsaturated fatty acids in patients with advanced chronic heart failure

Thrombosis and Haemostasis ◽

10.1160/th11-03-0169 ◽

2011 ◽

Vol 106 (09) ◽

pp. 457-465 ◽

Cited By ~ 24

Author(s):

Rudolf Berger ◽

Alexandra Hammer ◽

Raisa Hutuleac ◽

Renate Koppensteiner ◽

Christoph Kopp ◽

...

Keyword(s):

Heart Failure ◽

Fatty Acids ◽

Chronic Heart Failure ◽

Polyunsaturated Fatty Acids ◽

Platelet Activation ◽

Interleukin 6 ◽

Omega 3 ◽

Chemotactic Protein ◽

Dose Dependent Decrease ◽

Dose Dependent

SummaryChronic heart failure (CHF) is characterised by activation of neuroendocrine and inflammatory pathways, and both are linked to a prothrombotic state. Treatment with omega-3 polyunsaturated fatty acids (n3-PUFA) showed significant benefits including mortality reduction in CHF, but exact mechanisms of action are still unclear. We investigated the effects of n3-PUFA on markers of platelet activation and thrombogenesis in patients with severe CHF. Thirty-six patients with non-ischaemic CHF (LVEF<35%, NYHA class>2) under optimised therapy were randomised to supplementation with 1g/day or 4g/day n3-PUFA, or placebo for 12 weeks. Using whole-blood flow cytometry, monocyteplatelet aggregates characterised by CD14+/CD42b+ co-expression and monocytic tissue factor (TF) were determined. Plasma levels of P-selectin, sCD40L, fibrinogen, prothrombin fragment F1.2, TF and proinflammatory markers (high sensitive[hs] interleukin-6, hsCRP, hsTNFalpha, monocyte chemotactic protein-1) were measured by immunoassay. Supplementation with 1g/day and 4g/day n3-PUFA but not placebo significantly reduced monocyte-platelet aggregates in a dose-dependent manner (p for trend=0.02 across the groups). A dose of 4g/day but not 1g/day n3-PUFA significantly decreased P-selectin (p=0.03). Plasma TF decreased dose-dependently upon n3-PUFA supplementation (p for trend=0.02), paralleled by a significant decrease of TF+-monocytes (p for trend=0.01). The amount of 4g/day n3-PUFA exhibited modest anti-inflammatory effects with a significant reduction of hs interleukin-6 (p<0.01) and a trend-wise reduction of hsTNF-alpha (p=0.09). No changes were seen for sCD40L, fibrinogen, hsCRP and monocyte chemotactic protein-1, while F1.2 was decreased by 4g/day n3-PUFA (P=0.03). In patients with severe non-ischaemic CHF, treatment with n3-PUFA leads to a dose-dependent decrease of platelet activation and TF. Higher dosage exhibits also anti-inflammatory effects.* ClinicalTrials.gov registration number: NCT00149409

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