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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indirect observations are compatible with cardiac vitamin C deficiency as one contributory factor to oxidative stress in heart failure, but data on ventricular vitamin C content are lacking. Here, we used the well established model of aortic-banded rats at the stage of compensated hypertrophy (6 weeks after banding) and at the transition to cardiac failure (22 weeks after banding) to analyze vitamin C, vitamin E, protein carbonyls and malondialdehyde tissue content together with the respective plasma concentrations. Furthermore, we investigated the expression of the vitamin C transporters SVCT1 and SVCT2 in the left ventricle (LV). Aortic-banded rats, independently from their age, had higher malondialdehyde and protein carbonyl levels in plasma and LV tissue compared to sham-operated animals indicating increased oxidative stress. Plasma vitamin C remained unaffected from cardiac overload, while LV vitamin C was elevated in both stages of hypertrophy together with an increased expression of the vitamin C transporter SVCT2 suggesting increased vitamin C uptake. The levels of antioxidants and lipid peroxides were similar 6 and 22 weeks after aortic banding. Therefore, the accumulation of vitamin C in compensated hypertrophy and in decompensated failure excludes cardiac vitamin C deficiency as a primary factor to oxidative stress in this model.
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PMID:Enhanced myocardial vitamin C accumulation in left ventricular hypertrophy in rats is not attenuated with transition to heart failure. 1828 1

Downregulation of FKBP12.6 and sarcoplasmic reticulum Ca(2+) ATPase (SERCA2a) contributes to sudden cardiac death and heart failure. We aimed to test the hypothesis that (i) downregulation of FKBP12.6 and SERCA2a can be taken as molecular markers for drug interventions and (ii) such downregulation is produced by crosstalk between endothelin-reactive oxygen species and beta-adrenoceptors stimulation, mediated by hyperphosphorylation of protein kinase Cvarepsilon (PKCvarepsilon). Rat cardiomyocytes were incubated with isoproterenol (1 microM), endothelin-1 (0.1 microM) or hydrogen peroxide (10 microM) for 18 h, resulting in downregulation of mRNA and protein of FKBP12.6 and SERCA2a, as well as upregulation of PKCvarepsilon mRNA and phosphorylated PKCvarepsilon protein. These changes were reversed by an application of either propranolol (1 microM), endothelin receptor antagonist CPU0213 (1 microM) or vitamin E (1 microM). As indicated by the fluorescent dye Fluo3, diastolic [Ca(2+)](i) in rat ventricular myocytes was increased after incubation with isoproterenol (0.1 microM). The increased [Ca(2+)](i) in diastole was dramatically decreased by CPU0213. Thus, the downregulation of FKBP12.6 and SERCA2a, and hyperphosphorylation of PKCvarepsilon, appear to be related to crosstalk between over-activated endothelin-reactive oxygen species and a beta-adrenoceptor pathway. CPU0213 is beneficial in treating cardiac insufficiency and preventing cardiac arrhythmias possibly by normalizing hyperphosphorylation of PKCvarepsilon and abnormal FKBP12.6 and SERCA2a. The antioxidant activity of vitamin E was sufficient to normalize the levels of FKBP12.6 and SERCA2a and phosphorylation of PKCvarepsilon. Thus by testing with biomarkers FKBP12.6 and SERCA2a, we have shown that the endothelin receptor antagonist CPU0213 and the antioxidant vitamin E may relieve risk of lethal arrhythmias and heart failure by suppressing PKCvarepsilon.
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PMID:Endothelin receptor antagonist CPU0213 and vitamin E reverse downregulation of FKBP12.6 and SERCA2a: a role of hyperphosphorylation of PKCepsilon. 1861 97

The safety of large doses of vitamin E went virtually unquestioned until the early 2000s, when several studies were published showing that consumption of vitamin E from dietary supplements increased mortality, as well as the risk of gastrointestinal cancer and heart failure. These studies prompted numerous letters to the editors of medical journals and widespread coverage in the media. Both the medical community and the general public became confused and concerned about the use of vitamin E supplements. The purpose of this article is to review the medical literature and to explain these unusual findings. First we provide an overview of the earlier literature on vitamin E. Second, we provide a critical assessment of three meta-analyses that were neutral or negative toward vitamin E supplementation. Third, we review the limitations of meta-analyses in general. Fourth, we assess the individual studies that comprised one of the three meta-analyses. Since all three meta-analyses used many of the same studies, the individual critique should further the understanding of the limitations of these meta-analyses, and the meta-analysis approach in general. Lastly, we offer some guidance for healthcare professionals to give to the general, healthy public and those with chronic conditions who are no doubt left puzzled as to what to do regarding vitamin E supplementation.
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PMID:How safe is vitamin E supplementation? 1875 98

1. It has recently been shown that oxidative stress is involved in the pathogenesis of congestive heart failure (CHF) in broiler chickens. Vitamins E and C, common antioxidants, have been advocated for the prevention of heart failure in humans. The present study examines the effects of supplementation of these vitamins on incidence of CHF and prevention of oxidative stress in the myocardium. 2. Commercial male broilers were randomly allocated to three experimental groups and, respectively, offered commercial broiler diet (control), commercial diets fortified with vitamin E (960 IU/kg) or vitamin C (400 mg/kg). The broilers were monitored daily for overt signs of heart failure and clinical data including ECG and blood gas analysis were collected periodically. Lipid peroxidation was measured in cardiac tissues from apparently normal broilers and broilers developing CHF in each group using thiobarbituric acid reactive substances (TBARS) assay. 3. Overall, the incidence of CHF in broilers given diets fortified with vitamin E or vitamin C was not significantly different as compared to the control group. The incidence of overt signs of hypoxaemia was lower in the vitamin C group than in the control group. Lipid peroxidation was highest in broilers that developed CHF as compared to apparently normal broilers fed either vitamin E or C fortified diets. Neither vitamin E nor vitamin C was effective in preventing oxidative damage in broilers that developed CHF. 4. In conclusion, the present study confirmed that oxidative stress is involved in the pathogenesis of heart failure in broilers, but dietary supplementation of antioxidant vitamins did not prevent oxidative damage in broilers that developed CHF. Beneficial effects of vitamin C supplementation were evidenced by lower incidence of hypoxaemia, and the tendency to reduce the susceptibility of broilers to heart failure. However, vitamin E did not have any impact on clinical status or the incidence of CHF.
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PMID:Effects of dietary vitamin E and C supplementation on heart failure in fast growing commercial broiler chickens. 1909 42

The objective of this article is to review the role of vitamin E in cardiovascular disease. We begin by describing the general characteristics and metabolism of vitamin E and the pathogenesis of atherosclerosis as it relates to oxidation. We also discuss key in vitro studies, animal studies, observational studies, and clinical trials regarding the potentially cardioprotective effect of vitamin E. Lastly, we outline the current recommendations regarding vitamin E in the prevention and treatment of cardiovascular disease as stated by the American Heart Association. Vitamin E is a fat-soluble antioxidant vitamin and alpha-tocopherol is its most naturally abundant and active form. Oxidation is a key step in atherogenesis. Oxidized low-density lipoprotein stimulates endothelial cells to produce inflammatory markers, is involved in foam cell formation, has cytotoxic effects on endothelial cells, inhibits the motility of tissue macrophages, and inhibits nitric oxide-induced vasodilatation. Vitamin E has been shown to increase oxidative resistance in vitro and prevent atherosclerotic plaque formation in mouse models. Consumption of foods rich in vitamin E has been associated with lower risk of coronary heart disease in middle-aged to older men and women. Clinical studies at large have not demonstrated a benefit of vitamin E in the primary and secondary prevention of cardiovascular disease. Vitamin E supplementation might be associated with an increase in total mortality, heart failure, and hemorrhagic stroke. The American Heart Association does not support the use of vitamin E supplements to prevent cardiovascular disease, but does recommend the consumption of foods abundant in antioxidant vitamins and other nutrients.
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PMID:Vitamin E and cardiovascular disease. 1945 7

Oxidative stress resulting from imbalance between reactive oxygen species (ROS) generation and antioxidant mechanisms is important in the pathogenesis of cardiovascular diseases such as atherosclerosis, ischemic heart disease, heart failure, stroke, hypertension and diabetes. Paradoxically, antioxidant therapy such as vitamin E has not been shown on large randomized clinical trials to favorably affect clinical outcomes. Since mitochondria are involved not only with bioenergetics but also with oxidative damage through ROS generation and cell signaling leading to apoptosis, antioxidants targeted at the mitochondria are appealing novel agents to attenuate oxidative stress. In particular, antioxidants conjugated with triphenylphosphonium cation such as mitoquinone, mitovitamin E and mitophenyltertbutyline achieve concentrations in the mitochondrial matrix several-fold greater than those achieved in the cytosol because of the high negative membrane potential of the inner mitochondrial membrane. We review preliminary experiments and also some patents on cell and animal models of cardiovascular diseases where mitochondrially targeted antioxidants have been used and were shown to reduce ROS production and the effects of oxidative stress due to ROS, apoptosis and improve cardiac function. Although ongoing human clinical studies involve only non-cardiovascular applications at this time, preclinical studies show promise for eventual human trials for cardiovascular diseases.
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PMID:Mitochondrially targeted antioxidants for the treatment of cardiovascular diseases. 1980 85

In dogs with heart failure, cell oxygenation and cellular metabolism do not work properly, leading to the production of a large amount of free radicals. In the organism, these free radicals are responsible of major cellular damages: this is oxidative stress. However, a suitable food intake plays an important role in limiting this phenomenon: on the one hand, the presence of essential fatty acids in the composition of membranes decreases sensitivity of cells to free radicals and constitutes a first protection against the oxidative stress; on the other hand, coenzyme Q10, vitamin E, and polyphenols are antioxidant molecules which can help cells to neutralize these free radicals.
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PMID:Oxidative stress in dog with heart failure: the role of dietary Fatty acids and antioxidants. 2154 62

Heart failure is a common condition in the Western world, particularly among elderly persons and with an ever-aging population, the incidence is expected to increase. Diet in the setting of heart failure is important--patients with this condition are advised to consume a low-salt diet and monitor their weight closely. Nutritional status of patients with heart failure also is important--those with poor nutritional status tend to have a poor long-term prognosis. A growing body of evidence suggests an association between heart failure and micronutrient status. Reversible heart failure has been described as a consequence of severe thiamine and selenium deficiency. However, contemporary studies suggest that a more subtle relationship may exist between micronutrients and heart failure. This article reviews the existing literature linking heart failure and micronutrients, examining studies that investigated micronutrient intake, micronutrient status, and the effect of micronutrient supplementation in patients with heart failure, and focusing particularly on vitamin A, vitamin C, vitamin E, thiamine, other B vitamins, vitamin D, selenium, zinc, and copper.
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PMID:The role of micronutrients in heart failure. 2270 14

Herbicide poisoning is most common method of suicide in India and it is associated with high morbidity and mortality. Among different herbicidal poisonings the most predominantly found poisonings are paraquat and glyphosate. These compounds are highly toxic and their poisonings require proper management techniques. High fatality is seen in these cases which are mainly due to its inherent toxicity and lack of effective treatment. Common symptoms of these poisonings includes gastrointestinal corrosive effects with mouth and throat, epigastric pain and dysphagia, acid-base imbalance, pulmonary edema, shock and arrhythmia. Long term health effects include pulmonary fibrosis, renal failure, hepatic failure, heart failure, multi-organ failure or death. No proven antidote exists for these poisonings. So the treatment is mainly supportive. Initially gastric lavage or whole-gut irrigation using adsorbents such as Fuller's earth, bentonite or activated charcoal is recommended. In case of renal failure hemodialysis or hemoperfusion may be considered. However novel approaches like treatment with N-acetylcysteine, vitamin C, vitamin E, cyclophosphamide may also be helpful.
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PMID:Demographics, clinical characteristics and management of herbicide poisoning in tertiary care hospital. 2525 33

Mitochondria are one of the major sites for the generation of reactive oxygen species (ROS) as an undesirable side product of oxidative energy metabolism. Damaged mitochondria can augment the generation of ROS. Dysfunction of mitochondria increase the risk for a large number of human diseases, including cardiovascular diseases (CVDs). Heart failure (HF) following ischemic heart disease, infantile cardiomyopathy and cardiac hypertrophy associated with left ventricular dilations are some of the CVDs in which the role of mitochondrial oxidative stress has been reported. Advances in mitochondrial research during the last decade focused on the preservation of its function in the myocardium, which is vital for the cellular energy production. Experimental and clinical trials have been conducted using mitochondria-targeted molecules like: MnSOD mimetics, such as EUK-8, EUK-134 and MitoSOD; choline esters of glutathione and N-acetyl-L-cysteine; triphenylphosphonium ligated vitamin E, lipoic acid, plastoquinone and mitoCoQ10; and Szeto-Schiller (SS)- peptides (SS-02 and SS-31). Although many results are inconclusive, some of the findings, especially on CoQ10, are worthwhile. This review summarizes the role of mitochondria-targeted delivery of agents and their consequences in the control of HF.
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PMID:Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases. 2534 53


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