Effects of combined administration of low dose atorvastatin and vitamin E on inflammatory markers and endothelial function in patients with heart failure

Tousoulis, Dimitris; Antoniades, Charalambos; Vassiliadou, Carmen; Toutouza, Marina; Pitsavos, Christos; Tentolouris, Costas; Trikas, Athanasios; Stefanadis, Christodoulos

doi:10.1016/j.ejheart.2005.03.007

Cited by 98 publications

(66 citation statements)

References 51 publications

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“…Sola et al [175] found that administration of atorvastatin improved left ventricular ejection fraction and attenuated adverse left ventricular remodeling in patients with nonischemic heart failure. Atorvastatin also dampened the inflammatory process in patients with heart failure [176] . In a rat model of post-myocardial infarction- [177] .…”

Section: Endoplasmic Reticulum Stress Is Involved In the Development mentioning

confidence: 94%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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Endoplasmic reticulum is a principal organelle responsible for folding, post-translational modifications and transport of secretory, luminal and membrane proteins, thus palys an important rale in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) is a condition that is accelerated by accumulation of unfolded/misfolded proteins after endoplasmic reticulum environment disturbance, triggered by a variety of physiological and pathological factors, such as nutrient deprivation, altered glycosylation, calcium depletion, oxidative stress, DNA damage and energy disturbance, etc. ERS may initiate the unfolded protein response (UPR) to restore cellular homeostasis or lead to apoptosis. Numerous studies have clarified the link between ERS and cardiovascular diseases. This review focuses on ERS-associated molecular mechanisms that participate in physiological and pathophysiological processes of heart and blood vessels. In addition, a number of drugs that regulate ERS was introduced, which may be used to treat cardiovascular diseases. This review may open new avenues for studying the pathogenesis of cardiovascular diseases and discovering novel drugs targeting ERS.

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Section: Endoplasmic Reticulum Stress Is Involved In the Development mentioning

confidence: 94%

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

2016

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“…Patients treated with simvastatin, niacin and a combination of different antioxidants (400 IU bis in die (BID; twice a day) vitamin E, 500 mg BID vitamin C, 12.5 mg BID β-carotene and 50 mg BID selenium) profited less than the simvastatin and niacin groups as the protective increase in HDL2 with simvastatin plus niacin was attenuated by concurrent therapy with antioxidants [243,244] . Tousoulis et al [245] treated patients suffering from ischemic heart failure with low dose atorvastatin (10 mg/d) alone or in combination with 400 IU/d vitamin E and found that vitamin E impairs the positive effects of atorvastatin, on, for example, endothelial function or inflammatory response. Many studies focusing on the effects of statins on human lipid levels also analyzed other plasma parameters, such as vitamin E status.…”

Section: Interactions With Pharmaceuticsmentioning

confidence: 99%

Complexity of vitamin E metabolism

Schmölz¹,

Birringer²,

Lorkowski³

et al. 2016

WJBC

183

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Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e. , when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their sidechain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a REVIEW

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“…In patients with ischemic cardiomyopathy (40% with diabetes), atorvastatin (10mg/day) significantly improved post-ischemic FABF, but this effect was blunted by the co-administration of vitamin E (400 IU/day) [231]. Given the potential for statins to inhibit the cellular synthesis of plasma CoQ 10 , a by-product of isoprenoid metabolism, their full benefit on improving endothelial function may be blunted [232,233].…”

Section: Combination Therapiesmentioning

confidence: 99%

Endothelial Dysfunction in Diabetes: Pathogenesis, Significance, and Treatment

2013

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■ AbstractType 2 diabetes (T2D) markedly increases the risk of cardiovascular disease. Endothelial dysfunction (ED), an early indicator of diabetic vascular disease, is common in T2D and independently predicts cardiovascular risk. Although the precise pathogenic mechanisms for ED in T2D remain unclear, at inception they probably involve uncoupling of both endothelial nitric oxide synthase activity and mitochondrial oxidative phosphorylation, as well as the activation of vascular nicotinamide adenine dinucleotide phosphate oxidase. The major contributing factors include dyslipoproteinemia, oxidative stress, and inflammation. Therapeutic interventions are designed to target these pathophysiological factors that underlie ED. Therapeutic interventions, including lifestyle changes, antiglycemic agents and lipid-regulating therapies, aim to correct hyperglycemia and atherogenic dyslipidemia and to improve ED. However, high residual cardiovascular risk is seen in both research and clinical practice settings. Well-designed studies of endothelial function in appropriately selected volunteers afford a good opportunity to test new therapeutic interventions, paving the way for clinical trials and utilization in the care of the diabetic patient. However, based on the results from a recent clinical trial, niacin should not be added to a statin in individuals with low high-density lipoprotein cholesterol and very well controlled low-density lipoprotein cholesterol.

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Effects of combined administration of low dose atorvastatin and vitamin E on inflammatory markers and endothelial function in patients with heart failure

Cited by 98 publications

References 51 publications

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

Complexity of vitamin E metabolism

Endothelial Dysfunction in Diabetes: Pathogenesis, Significance, and Treatment

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