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. 2024 Jun 6;20(4):221–228. doi: 10.1080/14796678.2024.2352308

Evaluating the efficacy of ubiquinol in heart failure patients: a systematic review and meta-analysis

Shurjeel Uddin Qazi a,*, Muhammad Ahrar Bin Naeem b, Muhammad Umar b, Muhammad Jawad Zahid c, Mah I Kan Changez d, Laraib Iqbal e, Ismail Abdur Rahman Khan Sherwani f, Hassan Mehmood b, Abeera Farooq Abbasi a, Amna Zahid g, Prinka Perswani h, Jishanth Mattumpuram i
PMCID: PMC11285286  PMID: 39049769

Abstract

Aim: We aim to analyze past literature to evaluate the efficacy of coenzyme Q10 (CoQ-10) in the population with heart failure (HF). Methods: A systematic literature search was conducted through MEDLINE (via PubMed) and Cochrane Library. The outcomes analyzed were a reduction in HF-related mortality, an improvement in exercise capacity, and the left ventricular ejection fraction (LVEF). Results: Among 16 studies, CoQ-10 significantly reduced HF-related mortality by 40% and improved exercise capacity in patients with HF, but demonstrated no significant difference in LVEF however, the potential of its efficacy on LVEF could not be ruled out. Conclusion: CoQ-10 significantly enhances exercise capacity and reduces HF-related mortality; however, its impact on patients with reduced LVEF requires further investigation.

Keywords: : cardiovascular disorders, coenzyme Q10, CoQ-10, heart failure, ubiquinol

Plain language summary

Article highlights.

  • This meta-analysis aimed to investigate the efficacy of coenzyme-Q10 in improving outcomes in participants with heart failure.

  • We assessed people with heart failure belonging to NYHA functional class II-IV who were clinically stable for the past 3 months.

  • Studies were excluded if they enrolled people having any prior revascularization procedures done or significant co-morbidities potentially confounding the results.

  • We included a total of 16 randomized trials in which 1087 were randomized to coenzyme-Q10 while 1049 people received placebo.

  • Pooled analysis of 16 studies demonstrated that coenzyme-Q10 leads to a significant reduction in risk of mortality as compared with the placebo groups.

  • Our analysis of the past literature reveals that coenzyme-Q10 leads to improvement in the exercise capacity of patients with heart failure leading to improved functionality outcomes.

  • Our analysis of the previous literature demonstrates no significant improvement in ejection fraction.

  • Further studies are recommended to evaluate its efficacy in patients stratified according to the ejection fraction status.

  • Coenyme-Q10 supplementation may enhance heart failure therapy, improving exercise capacity and mortality outcomes, as indicated by our findings.

1. Background

Heart failure (HF) is a complex and debilitating condition characterized by the heart's inability to pump blood efficiently to the lungs or peripheral parts of the body, leading to symptoms like fatigue, dyspnea and edema [1]. It affects more than 64 million people worldwide, and treatment approaches are being developed to provide relief from the underlying causes and enhance drug therapies for the management of heart failure [2]. It is projected that 8 million people will have HF by 2030 [3].

In the population with HF, a hallmark of the disorder is mitochondrial dysfunction, particularly for the chronic subtype [4]. This leads to a deficit of myocardial adenosine triphosphate (ATP) and deviation of oxygen to form free radicals, overwhelming the scavenging system and causing increasing heart fatigue and pump failure [5]. The current HF therapies aim to modulate the derailed neurohormonal pathways, such as the renin-angiotensin-aldosterone system or the neprilysin pathways. However, these therapeutics are limited by dose titration and electrolyte and hemodynamic adverse effects [6]. Hence, modulating cardiac energetics and increasing the energy production for the heart presents an intriguing concept. In this perspective, coenzyme Q10 (CoQ-10) has emerged as a potential drug for HF.

CoQ-10 works as an antioxidant in the bodywork by stabilizing myocardial calcium-dependent ion channels and preventing the consumption of metabolites essential for ATP synthesis. It decreases the toxic effect of reactive oxygen species produced by heart failure as it has antioxidant activity [7,8]. Considering this, several pre-clinical and clinical studies have been conducted in various regions globally and investigated the impact of CoQ-10 supplementation as a therapeutic drug on HF-related outcomes [6]. Nevertheless, the findings have been heterogeneous, with some studies suggesting beneficial effects, while others report more side effects than better outcomes or mixed results hence, we aim to conduct a comprehensive systematic review and meta-analysis to provide conclusive evidence regarding the efficacy of CoQ-10 in different HF-related outcomes [9].

2. Methods

The current systematic review and meta-analysis were performed according to the Preferred Reporting Items for Systematic Review and Meta-Analysis Statement (PRISMA) guidelines [10,11].

2.1. Data source & search strategy

A systematic literature search of MEDLINE via PubMed and the Cochrane Library databases was performed from inception to October 2023 to identify potentially relevant studies, using the relevant keywords and MeSH terms such as ‘Ubiquinol’, ‘Coenzyme’, ‘CoQ-10’, ‘heart failure’ and ‘HF’. The search was conducted without any language or time restrictions. CoQ-10 was used synonymously for ubiquinol as well as other forms of CoQ-10 such as ubiquinone. We also searched the proceedings of the American College of Cardiology, the European Society of Cardiology and the American Heart Association and hand-searched reference lists for relevant additional studies that were not identified in the database search.

2.2. Study selection

2.2.1. Inclusion criteria

The studies were included if they met the following inclusion criteria: randomized controlled trials (RCTs), administration of a specified dosage to a consistent number of individuals over a similar time frame, adult patients (≥18 years of age) that presented with typical signs and symptoms of stage CHF (NYHA functional class II–IV) as defined by the American College of Cardiology/American Heart Association Joint Committee [12], underwent investigative treatment with CoQ-10, participants were clinically stable for the past 3 months with no hospitalizations for acute heart failure, no need for change in medications and the ability to exercise was maintained.

2.2.2. Exclusion criteria

Studies were excluded if they were letters to editors/commentaries, case reports, cross-sectional studies, observational studies, animal or in vitro studies, guidelines, literature reviews, meta-analyses or systemic reviews. Further exclusion was done based on whether patients had a recent acute coronary syndrome and/or coronary interventions or revascularization (PTCA or CABG), renal insufficiency (serum creatinine >2.5 mg/dl), liver abnormalities, uncontrolled hypertension, habitual use of antioxidants (vitamin C, E, A or CoQ-10), orthopedic or neurological limitations, or other significant comorbidities that would affect the interpretation of the study results. Lastly, studies that had inadequate clinical information pertaining to the outcomes under scrutiny were also excluded.

2.3. Literature search & eligibility assessment

The articles selected from the systematic search were exported to EndNote Reference Library software (Version X9; Clarivate Analytics, PA, USA), and duplicates were removed. Initial screening of the papers was done based on title and abstract; after that, further selection was made after reviewing the full text. Two independent reviewers screened the articles (MABN, MU). Any discrepancies were resolved by a third reviewer (SUQ).

2.4. Data extraction & quality assessment

From the finalized trials, the following data was extracted: publication year, first authors, sample sizes of the study, patient population's baseline demographics and various clinical scores/values used to compare the efficacy of CoQ-10, such as mortality, ejection fraction and exercise capacity test. Quality assessment was conducted using the modified Cochrane Collaboration's risk of bias tool (Rob 2), designed to assess the quality of RCTs [13]. The quality of evidence was assessed with the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) scale [14] (Supplementary Table S1).

2.5. Statistical analysis

Extracted data were combined for meta-analysis using Review Manager (Version 5.4.1, Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2014) and Comprehensive Meta Analyst Version 3.7 (CMA). For all outcomes, the random-effects model was employed to pool data. This assumes that different studies estimated different intervention effects, partly explaining the heterogeneity between studies. We used the DerSimonian and Laird variance estimator for tau. Weightage of dichotomous variables such as mortality was assigned using the inverse variance method, with OR and the corresponding 95% CI being extracted and analyzed from all relevant studies. For continuous baseline characteristics such as exercise capacity test and ejection fraction, we extracted mean differences (MD) with corresponding standard deviations (SD) and used the inverse variance method to allocate weight. The Higgins (I2) statistic was used to evaluate heterogeneity and a value of 25–50% was considered mild, 50–75% as moderate and >75% as severe heterogeneity. The tolerated level of heterogeneity, meriting little further discussion, is set at less than or equal to 40%, a benchmark decided upon by reviewing the Cochrane Handbook [15]. Publication bias was assessed through visual inspection of funnel plots and the Eggers regression test [16]. No unpublished data was sought. A p-value of <0.05 was considered statistically significant in all cases. Outcomes at maximum follow-up times reported in each study were analyzed to provide a more representative picture.

3. Results

3.1. Literature search results

The PRISMA flowchart summarizes our literature search. (Figure 1). Our search strategy yielded a total of 455 results. After removing duplicate records, 441 records were assessed. A total of 23 articles were assessed for eligibility, and reports were excluded due to different comparison groups (n = 3), incorrect study designs (n = 2), and inadequate information about outcomes (n = 2). We proceeded to include 16 RCTs in our meta-analysis [16–31]. The baseline demographic characteristics of the included studies are summarized in Supplementary Table S2.

Figure 1.

Figure 1.

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Prisma flowchart showing the process of data collection.

3.2. Mortality

The mortality analysis revealed that 65 out of 1049 participants in the treatment group and 116 out of 1087 in the control group died. CoQ-10 demonstrated a significant reduction in mortality compared with the placebo (RR = 0.60; 95% CI: 0.45–0.81; p < 0.01), as depicted in Figure 2.

Figure 2.

Figure 2.

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Efficacy of coenzyme-Q10 in reducing mortality in heart failure patients.

95% CI: 95% confidence interval and and I2 statistics; Co-Q: Coenzyme-Q10; RR: Risk ratio.

3.3. Results of the exercise capacity test

Our study analyzed five clinical trials that focused on exercise capacity as an end point. Among the participants, 211 participants received treatment with CoQ-10, while 207 participants were treated with a placebo. Utilizing the random-effects model, we observed a significant improvement in exercise capacity for participants who used CoQ-10 compared with those who received the placebo (SMD = 0.46; 95% CI: [0.08–0.85]; p = 0.02; I2 = 67%) (Figure 3).

Figure 3.

Figure 3.

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Efficacy of coenzyme-Q10 on exercise capacity.

95% CI: 95% Confidence interval and I2 statistics; Co-Q: Coenzyme-Q10; SD: Standard deviation; SMD: Standardized mean difference.

3.4. Change in ejection fraction

The study analyzed the left heart ejection fraction as reported in 13 trials. These trials involved 590 participants in the CoQ-10 treatment group and 612 participants in the placebo treatment group. The comparison of the two groups indicated that there was no significant difference in left heart ejection fraction (SMD = 0.14; 95% CI: [-0.02–0.30]; p = 0.09; I2 = 35%) when a random-effects model was employed, as depicted in Figure 4.

Figure 4.

Figure 4.

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Efficacy of coenzyme-Q10 on the ejection fraction in heart failure patients.

95% CI: 95% Confidence interval and I2 statistics; Co-Q: Coenzyme-Q10; SD: Standard deviation; SMD: Standardized mean difference.

3.5. Publication bias analysis

The publication bias analysis was conducted using Egger's test for both end points (Supplementary Table S3). The results of Egger's regression for all four clinical end points yielded no significant evidence of publication bias. Sensitivity analysis was performed to rule out the potential causes of heterogeneity by the leave-one-out method which revealed no significant change in the results after removal of each study (Supplementary Figures S1–S3).

3.6. Quality assessment

The seven domains of Cochrane's tool were used in our study, which included random sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, incomplete outcome data, selective reporting and other biases. Our review yielded that all of the included studies reported satisfactory randomization of the participants. However, only three studies Mortensen et al., Samuel et al. and Sobirin et al. adequately concealed the allocation of the groups but there was a high risk of performance and detection bias in the study by Sobirin et al. [26,29,32]. The studies by Kocharain et al., Munkholm et al. and Pourmoghaddas et al. did not adequately report the follow-up data of participants leading to the risk of attrition bias [22,27,28] (Supplementary Figures S4 & S5).

4. Discussion

CoQ-10 supplementation has emerged as a new frontier in the study of HF, offering promising applications in improving metabolic processes, repairing damaged cells and boosting the immune system. Acting as a potent antioxidant, CoQ-10 reduces harmful free radicals in the body. Our meta-analysis assessed CoQ-10 interventions across various end points, yielding mixed results. We observed a favorable influence on mortality rates and exercise capacity. However, it is noteworthy that the left ejection fraction remained unaffected. This implies that, although CoQ-10 appears to benefit the overall cardiovascular function, it may not directly affect left ventricular function.

Several studies have highlighted the importance of deficiency CoQ-10 in HF pathophysiology, motivating the conduct of several clinical trials to evaluate the efficacy of CoQ-10 supplementation in the population with HF, with promising results [7,9]. Alehagen et al. reported that CoQ-10 can have direct antioxidant effects by increasing myocardial energy generation via stimulating oxidative phosphorylation of the cells. Patients with HF have reduced CoQ-10 levels, which decline with increasing severity [17].

Alarcon-Vieco et al. in their review of previously published literature concluded CoQ-10 efficacy in improving mortality outcomes, however, they highlighted the doubt of the effectiveness of CoQ-10 in improving exercise capacity of participants with HF across the studies [33]. Our analysis demonstrated a significant improvement in exercise tolerance in the population with heart failure. It echoes the results of the most recent investigation conducted by Lei et al. [34], highlighting its potential significance in promoting the physical well-being of heart failure patients. In addition, our findings go in tandem with the study by Di-Lorenzo et al. where they highlighted majority of the studies observed an improved functional status with CoQ-10 supplementation; namely, a significant reduction in NYHA classification, improvement in echocardiographic parameters and functional capacity [8]. Given the importance of exercise tolerance in the management of heart failure, this is especially encouraging. Since multiple studies were included, the results for the end point of exercise capacity varied. It is worth mentioning that insufficient clinical information on exercise capacity outcomes was included, which may have contributed to the observed heterogeneity in our analysis. Unfortunately, we could not precisely estimate the extent of this heterogeneity due to this constraint.

We observed no significant improvement in LVEF, which contrasts with previous studies that indicated varying improvements in ejection fraction after CoQ-10 supplementation however the possibility of its effect cannot be ruled out [24,26]. Our meta-analysis proves that there is no direct correlation between improving LVEF and CoQ-10 supplementation. One possible explanation is that improvement in EF can be a late feature of CoQ-10 supplementation, arising after 1–2 years of administration. The inclusion of studies lasting 6 months or less could skew the findings toward statistical error [21,27]. As CoQ-10 primarily works by increasing myocardial energy requirement, thereby stabilizing cardiac output to some extent, it may prove to be beneficial for patients with reduced EF. Thus, we recommend future trials with a larger sample size to fully elucidate its effects in the relevant population.

We report a significant reduction in mortality rates in the population with HF with CoQ-10 supplementation. Among the eight studies pooled for this outcome, only one could not conclusively link CoQ-10 administration to a reduction in mortality [10]. However, it is important to note that the study had a relatively small sample size (55 patients) compared with most other studies included in our meta-analysis.

These findings highlight the clinical significance and potential benefits of CoQ-10 supplementation in the therapy of heart failure, prompting a future investigation to determine the best timing and duration of supplementation to maximize its therapeutic potential. However, our meta-analysis does exhibit certain limitations. First, the inconsistency in reporting brain natriuretic peptide (BNP) measures, with some studies using NT-pro BNP and others using serum BNP, led to their elimination as end points. Similarly, the lack of a standardized technique for reporting New York Heart Association (NYHA) classification improvement, which can be reported in various ways, precluded its inclusion as an end point. Our analysis was further constrained by its emphasis on English-language articles, which could introduce language bias and exclude non-English studies. The variance in sample sizes, with most studies having small populations except the Q-SYMBIO trial, may create bias favoring larger studies. Furthermore, discrepancies in CoQ-10 doses supplied to control groups among trials and non-uniform dosing and treatment durations might have affected the reliability of our results. Finally, trial design variability, including differences in patient demographics and therapies, may lead to statistical heterogeneity. Hence, we recommend more rigorous, large-sample, worldwide trials with standardized methodologies are required for confirmation to strengthen the robustness of our conclusion.

5. Conclusion

The use of CoQ-10 in heart failure resulted in a significant improvement in exercise capacity and a reduction in mortality rates compared with those treated with a placebo. However, compared with the placebo, there were no significant differences in the end points of LVEF with CoQ-10. Overall, our findings indicate that CoQ-10 supplementation may be a useful complement to the therapy of heart failure, providing improved exercise capacity and mortality outcomes.

Supplementary Material

Supplementary Figures S1-S5 and Tables S1-S3
IFCA_A_2352308_SM0001.docx (1.2MB, docx)

Acknowledgments

The authors would like to acknowledge Research Council of Pakistan (RCOP) for their support along all aspects of conducting this study.

Supplemental material

Supplementary data for this article can be accessed at https://doi.org/10.1080/14796678.2024.2352308

Author contributions

Study concept and design: SU Qazi; acquisition of data: M Umar, L Iqbal, H Mehmood; analysis and interpretation of data: AF Abbasi, IAR Khan Sherwani, MJ Zahid; drafting of the manuscript: MIK Changez, A Zahid, MA Bin Naeem; critical revision of the manuscript: J Mattumpuram, P Perswani.

Financial disclosure

The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Competing interests disclosure

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The present meta-analysis does not involve direct data collection from human subjects or animals. All data used in this study were obtained from previously published and publicly available sources, adhering to the ethical guidelines of the respective studies. No identifiable patient information is presented in this meta-analysis.

Data availability statement

The data set generated for the manuscript will be made available upon reasonable request from the corresponding author.

References

Papers of special note have been highlighted as: • of interest

  • 1.Mosterd A, Hoes AW. Clinical epidemiology of heart failure. Heart. 2007;93:1137–1146. doi: 10.1136/hrt.2003.025270 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Savarese G, Becher PM, Lund LH, Seferovic P, Rosano GMC, Coats AJS. Global burden of heart failure: a comprehensive and updated review of epidemiology. Cardiovasc Res. 2023;118:3272–3287. doi: 10.1093/cvr/cvac013 [DOI] [PubMed] [Google Scholar]
  • 3.Khan MS, Arshad MS, Greene SJ, et al. Artificial intelligence and heart failure: a state-of-the-art review. Eur J Heart Fail. 2023;25:1507–1525. doi: 10.1002/ejhf.2994 [DOI] [PubMed] [Google Scholar]; • This review article provides a comprehensive overview of the current state-of-the-art in the application of artificial intelligence (AI) to heart failure. Published in 2003, it encompasses recent advancements and insights in this field of cardiology and the potential usage of AI in the field of cardiology.
  • 4.Chaanine AH, Joyce LD, Stulak JM, et al. Mitochondrial morphology, dynamics, and function in human pressure overload or ischemic heart disease with preserved or reduced ejection fraction. Circ Heart Fail. 2019;12:e005131. doi: 10.1161/CIRCHEARTFAILURE.118.005131 [DOI] [PubMed] [Google Scholar]; • Explores mitochondrial aspects, including morphology, dynamics and function, in human hearts under pressure overload or ischemic heart disease conditions with preserved or reduced ejection fraction.
  • 5.Aimo A, Castiglione V, Borrelli C, et al. Oxidative stress and inflammation in the evolution of heart failure: from pathophysiology to therapeutic strategies. Eur J Prev Cardiol. 2020;27:494–510. doi: 10.1177/2047487319870344 [DOI] [PubMed] [Google Scholar]
  • 6.Al Saadi T, Assaf Y, Farwati M, et al. Coenzyme Q10 for heart failure. Group Cochrane Heart editor. Cochrane Database Syst. Rev. 2021. doi: 10.1002/14651858.CD008684.pub3 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Heart Failure - Treatment | NHLBI, NIH [Internet]. 2022. [cited 2023 Dec 2]. Available from: https://www.nhlbi.nih.gov/health/heart-failure/treatment
  • 8.Di Lorenzo A, Iannuzzo G, Parlato A, et al. Clinical evidence for Q10 coenzyme supplementation in heart failure: from energetics to functional improvement. J Clin Med. 2020;9:1266. doi: 10.3390/jcm9051266 [DOI] [PMC free article] [PubMed] [Google Scholar]; • Delves into the clinical evidence supporting the supplementation of coenzyme Q10 in heart failure, exploring its impact from an energetics perspective to functional improvement.
  • 9.Sharma A, Fonarow GC, Butler J, Ezekowitz JA, Felker GM. Coenzyme Q10 and heart failure: a state-of-the-art review. Circ Heart Fail. 2016;9:e002639. doi: 10.1161/CIRCHEARTFAILURE.115.002639 [DOI] [PubMed] [Google Scholar]; • This is a comprehensive review article that provides a state-of-the-art overview of the role of coenzyme Q10 in heart failure.
  • 10.Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. J Clin Epidemiol. 2021;134:178–189. doi: 10.1016/j.jclinepi.2021.03.001 [DOI] [PubMed] [Google Scholar]
  • 11.Higgins JPT, Altman DG, Gotzsche PC, et al. The Cochrane Collaboration's tool for assessing the risk of bias in randomised trials. BMJ. 2011;343:d5928–d5928. doi: 10.1136/bmj.d5928 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145:145. doi: 10.1161/CIR.0000000000001062 [DOI] [PubMed] [Google Scholar]
  • 13.Sterne JAC, Savović J, Page MJ, et al. RoB 2: a revised tool for assessing risk of bias in randomised trials. BMJ. 2019;366:l4898. doi: 10.1136/bmj.l4898 [DOI] [PubMed] [Google Scholar]
  • 14.Guyatt GH, Oxman AD, Vist GE, et al. Rating quality of evidence and strength of recommendations: GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ. 2008;336:924. doi: 10.1136/bmj.39489.470347 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Higgins JPT, Thomas J, Chandler J, et al. Cochrane Handbook for Systematic Reviews of Interventions version 6.4 (updated August 2023). United Kingdom; John Wiley & Sons. [Google Scholar]
  • 16.Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ. 1997;315:629–634. doi: 10.1136/bmj.315.7109.629 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Alehagen U, Aaseth J, Johansson P. Reduced cardiovascular mortality 10 years after supplementation with selenium and coenzyme Q10 for four years: follow-up results of a prospective randomized double-blind placebo-controlled trial in elderly citizens. PLOS ONE. 2015;10:e0141641. doi: 10.1371/journal.pone.0141641 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Belardinelli R, Mucaj A, Lacalaprice F, et al. Coenzyme Q10 and exercise training in chronic heart failure. Eur Heart J. 2006;27:2675–2681. doi: 10.1093/eurheartj/ehl158 [DOI] [PubMed] [Google Scholar]
  • 19.Hofman-Bang C, Rehnqvist N, Swedberg K, Wiklund I, Åström H. Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. J Card Fail. 1995;1:101–107. doi: 10.1016/1071-9164(95)90011-X [DOI] [PubMed] [Google Scholar]
  • 20.Keogh A, Fenton S, Leslie C, et al. Randomised double-blind, placebo-controlled trial of coenzyme Q10 therapy in class II and III systolic heart failure. Heart Lung Circ. 2003;12:135–141. doi: 10.1046/j.1443-9506.2003.00189.x [DOI] [PubMed] [Google Scholar]
  • 21.Khatta M, Alexander BS, Krichten CM, et al. The effect of coenzyme Q10 in patients with congestive heart failure. Ann Intern Med. 2000;132:636. doi: 10.7326/0003-4819-132-8-200004180-00006 [DOI] [PubMed] [Google Scholar]
  • 22.Kocharian A, Shabanian R, Rafiei-Khorgami M, Kiani A, Heidari-Bateni G. Coenzyme Q10 improves diastolic function in children with idiopathic dilated cardiomyopathy. Cardiol Young. 2009;19:501–506. doi: 10.1017/S1047951109990795 [DOI] [PubMed] [Google Scholar]
  • 23.Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. Clin Investig. 1993;71:S134–S136. doi: 10.1007/BF00226854 [DOI] [PubMed] [Google Scholar]
  • 24.Morisco C, Nappi A, Argenziano L, et al. Noninvasive evaluation of cardiac hemodynamics during exercise in patients with chronic heart failure: effects of short-term Coenzyme Q10 treatment. Mol Aspects Med. 1994;15:S155–S163. doi: 10.1016/0098-2997(94)90025-6 [DOI] [PubMed] [Google Scholar]
  • 25.Mortensen SA, Rosenfeldt F, Kumar A, et al. The effect of coenzyme Q 10 on morbidity and mortality in chronic heart failure. JACC Heart Fail. 2014;2:641–649. doi: 10.1016/j.jchf.2014.06.008 [DOI] [PubMed] [Google Scholar]
  • 26.Mortensen AL, Rosenfeldt F, Filipiak KJ. Effect of coenzyme Q10 in Europeans with chronic heart failure: a sub-group analysis of the Q-SYMBIO randomized double-blind trial. Cardiol J. 2019;26:147–156. doi: 10.5603/CJ.a2019.0022 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Munkholm H, Hansen HHT, Rasmussen K. Coenzyme Q10 treatment in serious heart failure. Biofactors. 1999;9:285–289. doi: 10.1002/biof.5520090225 [DOI] [PubMed] [Google Scholar]
  • 28.Pourmoghaddas M, Rabbani M, Shahabi J, Garakyaraghi M, Khanjani R, Hedayat P. Combination of atorvastatin/coenzyme Q10 as adjunctive treatment in congestive heart failure: a double-blind randomized placebo-controlled clinical trial. ARYA Atheroscler. 2014;10:1–5. [PMC free article] [PubMed] [Google Scholar]
  • 29.Samuel TY, Hasin T, Gotsman I, et al. Coenzyme Q10 in the treatment of heart failure with preserved ejection fraction: a prospective, randomized, double-blind, placebo-controlled trial. Drugs RD. 2022;22:25–33. doi: 10.1007/s40268-021-00372-1 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Watson PS, Scalia GM, Galbraith A, Burstow DJ, Bett N, Aroney CN. 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. J Am Coll Cardiol. 1999;33:1549–1552. doi: 10.1016/S0735-1097(99)00064-9 [DOI] [PubMed] [Google Scholar]
  • 31.Zhao Q, Kebbati AH, Zhang Y, Tang Y, Okello E, Huang C. Effect of coenzyme Q10 on the incidence of atrial fibrillation in patients with heart failure. J Investig Med. 2015;63:735–739. doi: 10.1097/JIM.0000000000000202 [DOI] [PubMed] [Google Scholar]
  • 32.Sobirin MA, Herry Y, Sofia SN, Uddin I, Rifqi S, Tsutsui H. Effects of coenzyme Q10 supplementation on diastolic function in patients with heart failure with preserved ejection fraction. Drug Discov Ther. 2019;13:38–46. doi: 10.5582/ddt.2019.01004 [DOI] [PubMed] [Google Scholar]
  • 33.Alarcón-Vieco E, Martínez-García I, Sequí-Domínguez I, Rodríguez-Gutiérrez E, Moreno-Herráiz N, Pascual-Morena C. Effect of coenzyme Q10 on cardiac function and survival in heart failure: an overview of systematic reviews and meta-analyses. Food Funct. 2023;14:6302–6311. doi: 10.1039/d3fo01255g [DOI] [PubMed] [Google Scholar]; • Presents an overview of systematic reviews and meta-analyses, examining the impact of coenzyme Q10 on cardiac function and survival in heart failure.
  • 34.Lei L, Liu Y. Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials. BMC Cardiovasc Disord. 2017;17:196. doi: 10.1186/s12872-017-0628-9 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary Figures S1-S5 and Tables S1-S3
IFCA_A_2352308_SM0001.docx (1.2MB, docx)

Data Availability Statement

The data set generated for the manuscript will be made available upon reasonable request from the corresponding author.

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