Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure11Coenzyme Q and matching placebo tablets were supplied by Health World Limited, Brisbane, Australia.

Watson, Paul S.; Scalia, G.; Galbraith, Andrew; Burstow, Darryl J.; Bett, Nicholas; Aroney, Constantine N.

doi:10.1016/s0735-1097(99)00064-9

Cited by 130 publications

(7 citation statements)

References 11 publications

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“…The incremental benefit of ubiquinone over and above these agents would have produced the most interesting data. However three studies reported no benefit of ubiquinone on existing treatment of heart failure in subjects with low ejection fraction [ 35 , 36 , 37 ]. In one study atrial fibrillation was present and in two studies, the plasma levels of ubiquinone did not reach a desired level and both patients were suffering cardiomyopathy without AMI.…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 Modulates Remodeling Possibly by Decreasing Angiotensin-Converting Enzyme in Patients with Acute Coronary Syndrome

et al. 2018

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The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. In a double blind, randomized, placebo-controlled, parallel group study (a retrospective analysis of an earlier trial) in 55 patients with left ventricular ejection fraction <50% after AMI, the effects of coenzyme Q10 (120 mg/day) or placebo were studied for 24 weeks. Two-dimensional echocardiography was performed at discharge, (approximately 5–10 days after admission) and at 6 months after AMI. The results revealed that wall thickness opposite the site of infarction decreased from (mean ± standard deviation (SD)) 12.2 ± 2.0 mm to 10.0 ± 1.8 mm with coenzyme Q10 compared with 12.8 ± 2.2 mm to 13.3 ± 2.3 mm with placebo (p < 0.01). Left ventricular mass changed from 236 ± 72 g to 213 ± 61 g with coenzyme Q10 compared with 230 ± 77 g to 255 ± 86 g with placebo (p < 0.01). Treatment with coenzyme Q10 also prevented alteration of sphericity index which is a ratio of the long and short axis of the left ventricle (which changed from 1.61 ± 0.28 to 1.63 ± 0.30 with coenzyme Q10 compared with 1.61 ± 0.32 to 1.41 ± 0.31 with placebo (p < 0.05)). Coenzyme Q10 also prevented alteration of the wall thickening abnormality at the infarct site, which changed from 9.4 ± 3.0 cm2 to 9.1 ± 2.8 cm2 compared with 10.1 ± 3.1 to 13.7 ± 4.2 cm2 with placebo (p < 0.05). End diastolic and systolic volumes also showed significant reduction with coenzyme Q10 compared to placebo. The serum level of ACE showed significant decline in the coenzyme Q10 group compared to the control group. Treatment with coenzyme Q10 early after AMI causes attenuation of left ventricular remodeling and decreases the serum ACE level in patients with left ventricular dysfunction.

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Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 Modulates Remodeling Possibly by Decreasing Angiotensin-Converting Enzyme in Patients with Acute Coronary Syndrome

et al. 2018

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“…However, the relationship between coenzyme Q10 and the prevention of the risk of CAD are controversial. Some studies reported the plasma coenzyme Q10 concentration was not related to the risk of coronary atherosclerosis, and there was no beneficial effect of coenzyme Q10 in patients with CAD [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

The Relationship between Coenzyme Q10, Oxidative Stress, and Antioxidant Enzymes Activities and Coronary Artery Disease

Lee

Lin

Huang

et al. 2012

The Scientific World Journal

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A higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the relationship between coenzyme Q10 concentration and lipid peroxidation, antioxidant enzymes activities and the risk of CAD. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery were assigned to the case group (n = 51). The control group (n = 102) comprised healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, malondialdehyde (MDA) and antioxidant enzymes activities (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) were measured. Subjects with CAD had significant lower plasma coenzyme Q10, CAT and GPx activities and higher MDA and SOD levels compared to those of the control group. The plasma coenzyme Q10 was positively correlated with CAT and GPx activities and negatively correlated with MDA and SOD. However, the correlations were not significant after adjusting for the potential confounders of CAD with the exception of SOD. A higher level of plasma coenzyme Q10 (≥0.52 μmol/L) was significantly associated with reducing the risk of CAD. Our results support the potential cardioprotective impact of coenzyme Q10.

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“…Figure 1 illustrates the distribution of size, design and follow-up length of the analyzed clinical studies [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 ].…”

Section: Resultsmentioning

confidence: 99%

Insights from Second-Line Treatments for Idiopathic Dilated Cardiomyopathy

Luciani¹,

Monte

2017

JCDD

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Background: Dilated cardiomyopathy (DCM) is an independent nosographic entity characterized by left ventricular dilatation and contractile dysfunction leading to heart failure (HF). The idiopathic form of DCM (iDCM) occurs in the absence of coronaropathy or other known causes of DCM. Despite being different from other forms of HF for demographic, clinical, and prognostic features, its current pharmacological treatment does not significantly diverge. Methods: In this study we performed a Pubmed library search for placebo-controlled clinical investigations and a post-hoc analysis recruiting iDCM from 1985 to 2016. We searched for second-line pharmacologic treatments to reconsider drugs for iDCM management and pinpoint pathological mechanisms. Results: We found 33 clinical studies recruiting a total of 3392 patients of various durations and sizes, as well as studies that tested different drug classes (statins, pentoxifylline, inotropes). A metanalysis was unfeasible, although a statistical significance for changes upon treatment for molecular results, morphofunctional parameters, and clinical endpoints was reported. Statins appeared to be beneficial in light of their pleiotropic effects; inotropes might be tolerated more for longer times in iDCM compared to ischemic patients. General anti-inflammatory therapies do not significantly improve outcomes. Metabolic and growth modulation remain appealing fields to be investigated. Conclusions: The evaluation of drug effectiveness based on direct clinical benefit is an inductive method providing evidence-based insights. This backward approach sheds light on putative and underestimated pathologic mechanisms and thus therapeutic targets for iDCM management.

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Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure11Coenzyme Q and matching placebo tablets were supplied by Health World Limited, Brisbane, Australia.

Abstract: In patients with left ventricular dysfunction, treatment for three months with oral coenzyme Q failed to improve resting left ventricular systolic function or quality of life despite an increase in plasma levels of coenzyme Q to more than twice basal values.

Cited by 130 publications

References 11 publications

Coenzyme Q10 Modulates Remodeling Possibly by Decreasing Angiotensin-Converting Enzyme in Patients with Acute Coronary Syndrome

Coenzyme Q10 Modulates Remodeling Possibly by Decreasing Angiotensin-Converting Enzyme in Patients with Acute Coronary Syndrome

The Relationship between Coenzyme Q10, Oxidative Stress, and Antioxidant Enzymes Activities and Coronary Artery Disease

Insights from Second-Line Treatments for Idiopathic Dilated Cardiomyopathy

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