Lack of Effect of Coenzyme Q on Left Ventricular Function in Patients with Congestive Heart Failure

Watson, Pat; Scalia, G.; Aj, Galbraith; Burstow, Darryl J.; Bett, Nicholas; Aroney, Constantine N.

doi:10.1097/00008483-200001000-00013

Cited by 41 publications

(73 citation statements)

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“…Some studies have suggested a possible effect for coenzyme Q10 in reduced hospitalization rates, dyspnea, and edema in patients with HF, but these benefits have not been seen uniformly. [471][472][473][474] Because of possible adverse effects and drug interactions of nutritional supplements and their widespread use, physicians caring for patients with HF should routinely inquire about their use. Until more data are available, nutritional supplements or hormonal therapies are not recommended for the treatment of HF.…”

Section: 3147mentioning

confidence: 99%

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults

Hunt¹,

Abraham²,

Chin³

et al. 2009

Circulation

1,929

757

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Section: 3147mentioning

confidence: 99%

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults

Hunt¹,

Abraham²,

Chin³

et al. 2009

Circulation

1,929

757

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“…Persson et al demonstrated restored mitochondrial O 2 consumption and an improvement in mitochondrial and renal functions in db/db diabetic mice fed a diet supplemented with the aforementioned coenzyme (236). Since CoQ10 is present at high concentrations in the heart, its potential benefits for cardiac dysfunction have been widely tested in humans with discrepant results (18,345). Similar dicrepances have been reported in animal models; whereas CoQ10 attenuated amyloid b-peptide-induced mitochondrial dysfunction in brain mitochondria isolated from diabetic Goto-Kakizaki rats (207), and its administration was not fully advantageous for heart mitochondrial function in this model (223).…”

Section: Non-targeted Antioxidant Treatmentsmentioning

confidence: 99%

Molecular Strategies for Targeting Antioxidants to Mitochondria: Therapeutic Implications

Apostolova

Víctor

2015

Antioxidants & Redox Signaling

234

147

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Mitochondrial function and specifically its implication in cellular redox/oxidative balance is fundamental in controlling the life and death of cells, and has been implicated in a wide range of human pathologies. In this context, mitochondrial therapeutics, particularly those involving mitochondria-targeted antioxidants, have attracted increasing interest as potentially effective therapies for several human diseases. For the past 10 years, great progress has been made in the development and functional testing of molecules that specifically target mitochondria, and there has been special focus on compounds with antioxidant properties. In this review, we will discuss several such strategies, including molecules conjugated with lipophilic cations (e.g., triphenylphosphonium) or rhodamine, conjugates of plant alkaloids, amino-acid-and peptide-based compounds, and liposomes. This area has several major challenges that need to be confronted. Apart from antioxidants and other redox active molecules, current research aims at developing compounds that are capable of modulating other mitochondria-controlled processes, such as apoptosis and autophagy. Multiple chemically different molecular strategies have been developed as delivery tools that offer broad opportunities for mitochondrial manipulation. Additional studies, and particularly in vivo approaches under physiologically relevant conditions, are necessary to confirm the clinical usefulness of these molecules. Antioxid. Redox Signal. 22, 686-729.

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“…It is therefore conceivable that CoQ10 depletion, which has been found in the myocardium from patients with heart failure, 23) may contribute to the deterioration of functional capacity of failing hearts. Several studies 24,25) showed improvements in symptoms, quality of life, left ventricular function, and the prognosis of patients with heart failure after supplementation with CoQ10, while other studies 26,27) failed to demonstrate an improvement. Unfortunately, we did not evaluate the effect of CoQ10 supplementation on BNP levels in the present study.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin-Induced Changes in Plasma Coenzyme Q10 and Brain Natriuretic Peptide in Patients With Coronary Artery Disease

et al. 2008

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SUMMARYThe beneficial effects of statins in patients with coronary artery disease (CAD) may be balanced by concerns that statins can depress production of ubiquinone (CoQ10), which serves as a component of mitochondrial energy production and an antioxidant. Accordingly, the effects of atorvastatin (ATO)-induced changes in plasma CoQ10 on BNP and oxidative stress were investigated. In 29 patients with CAD, the plasma levels of CoQ10 and BNP and urinary excretion of 8-iso-prostaglandin F2α (8-iso-PGF) were determined before and after 3-month treatment with ATO. Ten patients had received pravastatin and 10 patients fluvastatin, while 9 patients had not received any statin before ATO. There was a linear correlation between ATO-induced changes in total cholesterol and CoQ10 (r = 0.632, P < 0.01), and an inverse correlation between ATO-induced changes in CoQ10 and BNP (r = -0.497, P < 0.01). There was no significant correlation between ATO-induced changes in CoQ10 and 8-iso-PGF. Multivariate analysis revealed that ATO-induced decreases in plasma CoQ10 were significantly associated with increasing BNP levels. In conclusion, long-term treatment with ATO might increase plasma levels of BNP in patients with CAD when it is accompanied by a greater reduction in plasma CoQ10. However, ATO-induced decreases in CoQ10 might not increase oxidative stress. (Int Heart J 2008; 49: 423-433)

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Lack of Effect of Coenzyme Q on Left Ventricular Function in Patients with Congestive Heart Failure

Cited by 41 publications

References 0 publications

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults

Molecular Strategies for Targeting Antioxidants to Mitochondria: Therapeutic Implications

Atorvastatin-Induced Changes in Plasma Coenzyme Q10 and Brain Natriuretic Peptide in Patients With Coronary Artery Disease

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