A controlled clinical trial of vitamin E supplementation in patients with congestive heart failure

Keith, Mary; Jeejeebhoy, Khursheed N.; Langer, Anatoly; Kurian, Regina; Barr, Aiala; O’Kelly, Brian; Sole, Michael J.

doi:10.1093/ajcn/73.2.219

Cited by 104 publications

(52 citation statements)

References 29 publications

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“…In normal subjects expired pentane decreased (Lemoyne et al, 1987) but TBARS in urine were unaffected when measured by HPLC (Kosugi et al, 1995) or decreased when measured by fluorometry (Cadenas et al, 1996). In smokers, plasma TBARS and conjugated dienes decreased (Brown et al, 1994), but in patients with congestive heart failure there was no effect on markers of oxidative stress (Keith et al, 2001). The impact of intervention studies on cardiovascular disease is even more controversial (Stephens et al, 1996;Heart Outcomes Prevention Evaluation Study Investigation, 2000) in spite of convincing epidemiological evidence on the protective role vitamin E intake on disease (Stampfer et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effects of intravenous supplementation with α-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides

et al. 2002

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Objective: To compare the effects of a lipid emulsion containing medium-chain triglycerides (MCT) and supplemented with atocopherol to a conventional long-chain triglyceride (LCT) emulsion. Design: Randomised double blind study. Setting: Department of Internal Medicine, Antwerp University Hospital. Subjects and interventions: Twenty-four patients with an indication for total parenteral nutrition for a minimum of 10 days were randomly assigned to two groups: group E received as lipid source MCT=LCT (50=50) suplemented with 100 mg DL-atocopherol=day and group C received LCT. Blood samples were analysed at inclusion, after 4 -6 and after 9 -11 days. Results: In group E, serum a-tocopherol doubled from 11.4 AE 6.9 at inclusion to 20.9 AE 7.9 and to 23.8 AE 8.8 mg=ml after 4 and 9 days, respectively, but did not change in group C (P ¼ 0.008). Production of thiobarbituric acid-reacting substances (TBARS) after 120 min incubation with copper decreased from 66 AE 34 at inclusion to 29 AE 25 nmol MDA=mg LDL and VLDL-cholesterol after 4 and to 42 AE 17 after 9 days (P ¼ 0.022 when compared to group C, which underwent no significant changes). Velocity of production of fluorescent products decreased in group E but not in group C (P ¼ 0.026). Conclusions: Supplementation of TPN containing MCT=LCT with 100 mg DL-a-tocopherol=day leads to a doubling in serum atocopherol and to a decrease in the susceptibility of LDL and VLDL to peroxidation in vitro.

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Section: Discussionmentioning

confidence: 99%

Effects of intravenous supplementation with α-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides

et al. 2002

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“…5,14,32 However, the effectiveness of antioxidants for human patients with heart failure has not been clarified. Keith et al 33 reported that supplementation with vitamin E did not result in any significant improvement in patients with heart failure. In this study, we have reported the reduction of harmful HNE by carvedilol treatment.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol Decreases Elevated Oxidative Stress in Human Failing Myocardium

et al. 2002

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Background-Oxidative stress has been implicated in the pathogenesis of heart failure. However, direct evidence of oxidative stress generation in the human failing myocardium has not been obtained. Furthermore, the effect of carvedilol, a vasodilating ␤-blocker with antioxidant activity, on oxidative stress in human failing hearts has not been assessed. This study was therefore designed to determine whether levels of lipid peroxides are elevated in myocardia of patients with dilated cardiomyopathy (DCM) and whether carvedilol reduces the lipid peroxidation level. Methods and Results-Endomyocardial biopsy samples obtained from 23 patients with DCM and 13 control subjects with normal cardiac function were studied immunohistochemically for the expression of 4-hydroxy-2-nonenal (HNE)-modified protein, which is a major lipid peroxidation product. Expression of HNE-modified protein was found in all myocardial biopsy samples from patients with DCM. Expression was distinct in the cytosol of cardiac myocytes. Myocardial HNE-modified protein levels in patients with DCM were significantly increased compared with the levels in control subjects (PϽ0.0001). Endomyocardial biopsy samples from 11 patients with DCM were examined before and after treatment (mean, 9Ϯ4 months) with carvedilol (5 to 30 mg/d; mean dosage, 22Ϯ8 mg/d). After treatment with carvedilol, myocardial HNE-modified protein levels decreased by 40% (PϽ0.005) along with amelioration of heart failure. Conclusions-Oxidative stress is elevated in myocardia of patients with heart failure. Administration of carvedilol resulted in a decrease in the oxidative stress level together with amelioration of cardiac function.

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“…One trial of 56 patients with advanced heart failure indicated that supplementation with vitamin E did not result in any significant improvements in prognostic or functional indexes of heart failure or in quality of life [91]. On the other hand Horning et al were the first to show that acute intra-arterial administration or oral intake of vitamin C over a period of 4 weeks significantly improved flow-mediated dilatation by about 50% in patients with CHF [92].…”

Section: No In Chf-effects Of Carvedilolmentioning

confidence: 99%

Nitric Oxide and its Role in Cardiovascular Diseases

Dobutović¹

2011

TONOJ

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Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.

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A controlled clinical trial of vitamin E supplementation in patients with congestive heart failure

Abstract: Supplementation with vitamin E did not result in any significant improvements in prognostic or functional indexes of heart failure or in the quality of life of patients with advanced heart failure.

Cited by 104 publications

References 29 publications

Effects of intravenous supplementation with α-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides

Effects of intravenous supplementation with α-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides

Carvedilol Decreases Elevated Oxidative Stress in Human Failing Myocardium

Nitric Oxide and its Role in Cardiovascular Diseases

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