Obesity-Related High-Output Heart Failure: An Integrative Review.

BACKGROUND: High-output heart failure (HF) is a type of HF characterized by signs and symptoms of HF and a cardiac output of 8 L/min or greater or a cardiac index greater than 3.9 L/min/m 2 . High-output HF occurs secondary to an underlying condition that requires high cardiac output due to an increase in oxygen consumption or decreased systemic vascular resistance. Obesity is a major cause of high-output HF, yet there is limited research on obesity-related high-output HF. Thus, the pathophysiologic mechanisms of this syndrome are not fully understood. OBJECTIVE: The objectives of this integrative review were to describe the current state of the research regarding obesity-related high-output HF and to recommend direction for future research. METHODS: We conducted an integrative review focusing on the peer-reviewed literature on patients with obesity-related high-output HF using Whittemore and Knafl's methodology. MEDLINE, CINAHL, and EMBASE electronic databases were searched for all publications indexed in the databases as of March 9, 2022. A narrative synthesis of definitions and symptoms, obesity as an underlying condition, pathophysiology, and treatments of obesity-related high-output HF was completed. RESULTS: A total of 6 articles were included in the integrative review, with 1 nonexperimental, retrospective study and 5 literature reviews. Understanding of obesity-related high-output HF is very limited because of scant empirical evidence in the existing literature. Possible pathophysiologic mechanisms include increased pressure in the upper airways, adipokine dysregulation, increased metabolic activity, and insulin resistance. CONCLUSION: Additional research is needed on the pathophysiologic mechanisms of obesity-related high-output HF to begin investigations on therapeutic interventions to improve health outcomes.

Effects of Ubiquinol and/or D-ribose in Patients With Heart Failure With Preserved Ejection Fraction.

Patients with heart failure with preserved ejection fraction (HFpEF) have few pharmacologic therapies, and it is not known if supplementing with ubiquinol and/or d-ribose could improve outcomes. The overall objective of this study was to determine if ubiquinol and/or d-ribose would reduce the symptoms and improve cardiac performance in patients with HFpEF. This was a phase 2 randomized, double-blind, placebo-controlled trial of 216 patients with HFpEF who were ≥ 50 years old with a left ventricular ejection fraction (EF) ≥ 50%. A total of 4 study groups received various supplements over 12 weeks: Group 1 received placebo ubiquinol capsules and d-ribose powder, Group 2 received ubiquinol capsules (600 mg/d) and placebo d-ribose powder, Group 3 received placebo ubiquinol capsules with d-ribose powder (15 g/d), and Group 4 received ubiquinol capsules and d-ribose powder. There were 7 outcome measures for this study: Kansas City Cardiomyopathy Questionnaire (KCCQ) clinical summary score, level of vigor using a subscale from the Profile of Mood States, EF, the ratio of mitral peak velocity of early filling to early diastolic mitral annular velocity (septal E/e' ratio), B-type natriuretic peptides, lactate/adenosine triphosphate ratio, and the 6-minute walk test. Treatment with ubiquinol and/or d-ribose significantly improved the KCCQ clinical summary score (17.30 to 25.82 points), vigor score (7.65 to 8.15 points), and EF (7.08% to 8.03%) and reduced B-type natriuretic peptides (-72.02 to -47.51) and lactate/adenosine triphosphate ratio (-4.32 to -3.35 × 10-4). There were no significant increases in the septal E/e' or the 6-minute walk test. In conclusion, ubiquinol and d-ribose reduced the symptoms of HFpEF and increased the EF. These findings support the use of these supplements in addition to standard therapeutic treatments for patients with HFpEF.

Post-COVID-19 Syndrome.

BACKGROUND: Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, many individuals have reported persistent symptoms and/or complications lasting beyond 4 weeks, which is now called post-COVID-19 syndrome. SARS-CoV-2 is a respiratory coronavirus that causes COVID-19, and injury to the lungs is expected; however, there is often damage to numerous other cells and organs, leading to an array of symptoms. These long-term symptoms occur in patients with mild to severe COVID-19; currently, there is limited literature on the potential pathophysiological mechanisms of this syndrome. OBJECTIVES: The purpose of this integrative review is to summarize and evaluate post-COVID-19 syndrome from a biological perspective. METHODS: An integrative review was conducted using Whittemore and Knafl's methodology for literature published through August 30, 2021. The PubMed, CINAHL, and Web of Science databases were searched for articles published as of August 30, 2021, using combinations of the following key words: post-COVID-19 syndrome, post-SARS-CoV-2, long COVID-19, long COVID-19 syndrome, and pathophysiology of post-COVID-19. Data were analyzed using the constant comparison method. RESULTS: The search generated 27,929 articles. After removing duplicates and screening abstracts and full-text reviews, we retained 68 articles and examined 54 specific articles related to the pathophysiology of post-COVID-19 syndrome. The findings from our review indicated that there were four pathophysiological categories involved: virus-specific pathophysiological variations, oxidative stress, immunologic abnormalities, and inflammatory damage. DISCUSSION: Although studies examining the pathophysiology of post-COVID-19 syndrome are still relatively few, there is growing evidence that this is a complex and multifactorial syndrome involving virus-specific pathophysiological variations that affect many mechanisms but specifically oxidative stress, immune function, and inflammation. Further research is needed to elucidate the pathophysiology, pathogenesis, and longer term consequences involved in post-COVID-19 syndrome.

Mitochondrial bioenergetics and D-ribose in HFpEF: a brief narrative review.

OBJECTIVE: In this review article, we briefly describe the status of treatment options for HFpEF and the role of mitochondrial dysfunction in the pathogenesis of HFpEF as an alternative therapeutic target. We also examine the mechanisms of D-ribose in cellular energy production and discuss the potential disadvantages and benefits of supplemental use of D-ribose in patients with HFpEF. BACKGROUND: Heart failure is a major cardiovascular disease that impacts over 6 million Americans and is one of the leading causes for morbidity and mortality. Patients with heart failure often experience shortness of breath and fatigue along with impaired physical capacity, all leading to poor quality of life. As a subtype of heart failure, heart failure with preserved ejection fraction (HFpEF) is characterized with impaired diastolic function. Currently, there are no effective treatments specifically for HFpEF, thus clinicians and researchers are searching for therapies to improve cardiac function. Emerging evidence indicate that mitochondrial dysfunction and impaired cardiac bioenergetics are among the underlying mechanisms for HFpEF. There is increased interest in investigating the use of supplements such as D-ribose to enhance mitochondrial function and improve production of adenosine triphosphate (ATP). METHODS: For this narrative review, more than 100 relevant scientific articles were considered from various databases (e.g., PubMed, Web of Science, CINAHL, and Google Scholar) using the keywords "Heart Failure", "HFpEF", "D-ribose", "ATP", "Mitochondria", Bioenergetics", and "Cellular Respiration". CONCLUSIONS: It is essential to find potential targeted therapeutic treatments for HFpEF. Since there is evidence that the HFpEF is related to impaired myocardial bioenergetics, enhancing mitochondrial function could augment cardiac function. Using a supplement such as D-ribose could improve mitochondrial function by increasing ATP and enhancing cardiac performance for patients with HFpEF. There is a recently completed clinical trial with HFpEF patients that indicates D-ribose increases ATP production and improves cardiac ejection fraction.

Clinical Trial Visits in the Age of COVID-19: Implementation of Research Participant Safety Measures.

The COVID-19 pandemic is having a major impact on how current clinical trials are being conducted in the U.S. Researchers have experienced the effects of COVID-19 through the halting and delaying of clinical trials, the lack of personal protection equipment (PPE), the closing of clinical sites, and a decrease in participant recruitment. Many clinical trials will have more missing data because of a participant's inability to attend in-person visits, discontinuation of trial activities, or interruption of time-sensitive study collection data due to COVID-19. All of these events affect the data quality of trials. Government agencies such as the Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDC), and National Institutes of Health (NIH) have issued recommendations for investigators conducting clinical trials to combat the spread of COVID-19 and to maintain data integrity. Institutions sponsoring clinical trials have also provided guidelines to continue, modify, or pause research studies that are essential to ensure participant and research team safety. Key recommendations include implementing telehealth appointments, wearing a protective mask and face shield, quarantining for 14 days if exposed to COVID-19 or having traveled, and, if possible, maintaining a 6-foot distance. It is also recommended that investigators implement COVID-19 screening questionnaires prior to and during on-site visits. This includes participants and research personnel completing a temperature check and questionnaire screen before in-person data collection. This article will discuss the challenges encountered by researchers conducting clinical trials and provide resources and examples to assist investigators during the COVID-19 pandemic.

Understanding Obesity-Related High Output Heart Failure and Its Implications.

Morbid obesity remains most common cause of high output failure. The prevalence of the obesity is growing when two-thirds of American adults already are overweight or obese. Obesity is the risk factor for heart disease and eventually leads to heart failure. High output heart failure is common in obese patients and is characterized by high cardiac output, decreased systemic vascular resistance, and increased oxygen consumption. It often occurs in patients with chronic severe anemia, hyperthyroidism, pregnancy, arterial-venous fistulas, and liver disease. However, the pathogenesis of obesity-related high output heart failure is not fully understood. The clinical management of obesity-related high output heart failure follows conventional heart failure regimens due to lack of specific clinical recommendations. This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.

Potential use of ubiquinol and d-ribose in patients with heart failure with preserved ejection fraction.

•Manuscript Highlights.•HFpEF is associated with reduced ATP production in the myocardium.•Ubiquinol and d-ribose both contribute to the generation of myocardial ATP.•Both ubiquinol and d-ribose are being studied as supplemental treatments for patients with HFpEF.

Using the NIH symptom science model to understand fatigue and mitochondrial bioenergetics.

The symptom of fatigue is prevalent among patients with chronic diseases and conditions such as congestive heart failure and cancer. It has a significant debilitating impact on patients' physical health, quality of life, and well-being. Early detection and appropriate assessment of fatigue is essential for diagnosing, treating, and monitoring disease progression. However, it is often challenging to manage the symptom of fatigue without first investigating the underlying biological mechanisms. In this narrative review, we conceptualize the symptom of fatigue and its relationship with mitochondrial bioenergetics using the National Institute of Health Symptom Science Model (NIH-SSM). In particular, we discuss mental and physical measures to assess fatigue, the importance of adenosine triphosphate (ATP) in cellular and organ functions, and how impaired ATP production contributes to fatigue. Specific methods to measure ATP are described. Recommendations are provided concerning how to integrate biological mechanisms with the symptom of fatigue for future research and clinical practice to help alleviate symptoms and improve patients' quality of life.

Use of speckle tracking to assess heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) currently represents approximately 50% of heart failure (HF) cases in the USA and is increasingly recognized as a leading cause of morbidity and mortality. Recent data suggest that the prevalence of HFpEF relative to HF with reduced ejection fraction (HFrEF) is increasing at a rate of 1% per year. With an aging population and increasing risk factors such as hypertension, obesity, and diabetes mellitus, HFpEF will soon be the most prevalent HF phenotype. Two-dimensional speckle-tracking echocardiography (STE) has been used to diagnose HFpEF specifically by focusing on the longitudinal systolic function of the left ventricle (LV). Yet there are many patients with HFpEF in whom there are no differences in LV global longitudinal systolic strain, but there are changes in left atrial function and structure. There are several proposed pathophysiological mechanisms for HFpEF such as endothelial dysfunction, interactions among proteins, signaling pathways, and myocardial bioenergetics. Yet only one specific therapy, mineralocorticoid receptor antagonist, spironolactone, is recommended as a treatment for patients with HFpEF. However, spironolactone does not address many of the pathophysiologic changes that occur in HFpEF, thus new novel therapeutic agents are needed. With the limited available therapies, clinicians should use STE to assess for the presence of this syndrome in their patients to provide effective diagnosis and management.

Development of a point-of-contact technique to measure adenosine triphosphate: A quality improvement study.

PURPOSE: Patients with heart failure with preserved ejection fraction (HFpEF) experience fatigue due to impaired myocardial bioenergetics. Cardiomyocyte function depends on the delivery of adenosine triphosphate (ATP), yet there is no convenient bedside method to measure ATP. The purpose of this study was to develop a point-of-contact measurement of ATP that can be used in a clinical setting. METHODS: In a laboratory setting, digital finger punctures were conducted using 5 µl and 10 µl of capillary blood placed into various amounts of water (H2O). After mixing the solution for 10 s, a Hygiena AquaSnapTM Free ATP probe was placed into the solution for 10 s for the detection of ATP. The probe was then placed into the Hygiena luminometer for 15 s, and a value in relative light units (RLU) was obtained. RESULTS: Test samples using 10 µl of blood diluted from 50 to 500 mls of H2O produced ATP readings of 10,000-7569 RLUs. Using 5 µl of blood in 375-900 ml of H2O decreased the ATP values to 6459-4189 RLUs. Dilutional volume sparing experiments were conducted with ATP standards to determine the concentration of ATP per RLUs. CONCLUSION: Patients with HFpEF have increased metabolic demand and impaired myocardial bioenergetics. Thus, identifying a method to measure ATP that is quick and accurate is imperative to accurately assess cellular energy production in this population. Point-of-contact measures, such as ATP, are needed for precision-guided treatment. Data from this study provides the first step toward developing evidence for health policies related to managing fatigue.

Understanding D-Ribose and Mitochondrial Function.

Mitochondria are important organelles referred to as cellular powerhouses for their unique properties of cellular energy production. With many pathologic conditions and aging, mitochondrial function declines, and there is a reduction in the production of adenosine triphosphate. The energy carrying molecule generated by cellular respiration and by pentose phosphate pathway, an alternative pathway of glucose metabolism. D-ribose is a naturally occurring monosaccharide found in the cells and particularly in the mitochondria is essential in energy production. Without sufficient energy, cells cannot maintain integrity and function. Supplemental D-ribose has been shown to improve cellular processes when there is mitochondrial dysfunction. When individuals take supplemental D-ribose, it can bypass part of the pentose pathway to produce D-ribose-5-phosphate for the production of energy. In this article, we review how energy is produced by cellular respiration, the pentose pathway, and the use of supplemental D-ribose.

Study protocol, randomized controlled trial: reducing symptom burden in patients with heart failure with preserved ejection fraction using ubiquinol and/or D-ribose.

BACKGROUND: Heart failure (HF), the leading cause of morbidity and mortality in the US, affects 6.6 million adults with an estimated additional 3 million people by 2030. More than 50% of HF patients have heart failure with preserved left ventricular ejection fraction (HFpEF). These patients have impaired cardiac muscle relaxation and diastolic filling, which investigators have associated with cellular energetic impairment. Patients with HFpEF experience symptoms of: (1) fatigue; (2) shortness of breath; and (3) swelling (edema) of the lower extremities. However, current HF guidelines offer no effective treatment to address these underlying pathophysiologic mechanisms. Thus, we propose a biobehavioral symptom science study using ubiquinol and D-ribose (therapeutic interventions) to target mitochondrial bioenergetics to reduce the complex symptoms experienced by patients with HFpEF. METHODS: Using a randomized, double-blind, placebo-controlled design, the overall objective is to determine if administering ubiquinol and/or D-ribose to HFpEF patients for 12 weeks would decrease the severity of their complex symptoms and improve their cardiac function. The measures used to assess patients' perceptions of their health status and level of vigor (energy) will be the Kansas City Cardiomyopathy Questionnaire (KCCQ) and Vigor subscale of the Profile of Mood States. The 6-min walk test will be used to test exercise tolerance. Left ventricular diastolic function will be assessed using innovative advanced echocardiography software called speckle tracking. We will measure B-type natriuretic peptides (secreted from ventricles in HF) and lactate/ATP ratio (measure of cellular energetics). DISCUSSIONS: Ubiquinol (active form of Coenzyme Q10) and D-ribose are two potential treatments that can positively affect cellular energetic impairment, the major underlying mechanism of HFpEF. Ubiquinol, the reduced form of CoQ10, is more effective in adults over the age of 50. In patients with HFpEF, mitochondrial deficiency of ubiquinol results in decreased adenosine triphosphate (ATP) synthesis and reduced scavenging of reactive oxygen species. D-ribose is a substrate required for ATP synthesis and when administered has been shown to improve impaired myocardial bioenergetics. Therefore, if the biological underpinning of deficient mitochondrial ATP in HFpEF is not addressed, patients will suffer major symptoms including lack of energy, fatigue, exertional dyspnea, and exercise intolerance. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03133793 ; Data of Registration: April 28, 2017.

Ubiquinol treatment for TBI in male rats: Effects on mitochondrial integrity, injury severity, and neurometabolism.

Following traumatic brain injury (TBI), there is significant secondary damage to cerebral tissue from increased free radicals and impaired mitochondrial function. This imbalance between reactive oxygen species (ROS) production and the effectiveness of cellular antioxidant defenses is termed oxidative stress. Often there are insufficient antioxidants to scavenge ROS, leading to alterations in cerebral structure and function. Attenuating oxidative stress following a TBI by administering an antioxidant may decrease secondary brain injury, and currently many drugs and supplements are being investigated. We explored an over-the-counter supplement called ubiquinol (reduced form of coenzyme Q10), a potent antioxidant naturally produced in brain mitochondria. We administered intra-arterial ubiquinol to rats to determine if it would reduce mitochondrial damage, apoptosis, and severity of a contusive TBI. Adult male F344 rats were randomly assigned to one of three groups: (1) Saline-TBI, (2) ubiquinol 30 minutes before TBI (UB-PreTBI), or (3) ubiquinol 30 minutes after TBI (UB-PostTBI). We found when ubiquinol was administered before or after TBI, rats had an acute reduction in brain mitochondrial damage, apoptosis, and two serum biomarkers of TBI severity, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1). However, in vivo neurometabolic assessment with proton magnetic resonance spectroscopy did not show attenuated injury-induced changes. These findings are the first to show that ubiquinol preserves mitochondria and reduces cellular injury severity after TBI, and support further study of ubiquinol as a promising adjunct therapy for TBI.

A pilot study exploring the effects of ubiquinol on brain genomics after traumatic brain injury.

BACKGROUND: Traumatic brain injury is a major cause of morbidity and mortality that affects military service members and veterans. PURPOSE: Explore the effects of ubiquinol before traumatic brain injury on cerebral gene expression to elucidate molecular mechanisms of ubiquinol neuroprotection. METHOD: In this experimental study, Fisher rats in the untreated (n = 2) and ubiquinol-treated (n = 2) groups received respectively either normal saline or ubiquinol 30 min before traumatic brain injury induced by controlled cortical impact. Ribonucleic acid sequencing and ingenuity pathway analysis were conducted to detect cerebral gene and signaling expression profiles. DISCUSSION: In the ubiquinol-treated group, 67 ingenuity pathway analysis transcripts in the ubiquinol-treated group were statistically different from those in the untreated group (p <.0001). CONCLUSIONS: Administering ubiquinol 30 min before traumatic brain injury significantly affected cerebral gene expression profiles that may be involved in the most fundamental molecular mechanisms of bioenergetics and free radical production.

The use of antioxidants in the treatment of traumatic brain injury.

AIMS: The aim of this study was to discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. BACKGROUND: One of the leading causes of death globally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life. Secondary injury occurs when metabolic and physiologic processes alter after initial injury and includes increased release of toxic free radicals that cause damage to adjacent tissues and can eventually lead to neuronal necrosis. Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defence mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species. DESIGN: Discussion paper. DATA SOURCES: Research literature published from 2011-2016 in PubMed, CINAHL and Cochrane. IMPLICATIONS FOR NURSING: Prompt and accurate assessment of patients with traumatic brain injury by nurses is important to ensure optimal recovery and reduced lasting disability. Thus, it is imperative that nurses be knowledgeable about the secondary injury that occurs after a traumatic brain injury and aware of possible antioxidant treatments. CONCLUSION: The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury.

Impaired Myocardial Bioenergetics in HFpEF and the Role of Antioxidants.

Heart failure with preserved ejection fraction (HFpEF) is a significant cardiovascular condition for more than 50% of patients with heart failure. Currently, there is no effective treatment to decrease morbidity and mortality rates associated with HFpEF because of its pathophysiological heterogeneity. Recent evidence shows that deficiency in myocardial bioenergetics is one of the key pathophysiological factors contributing to diastolic dysfunction in HFpEF. Another known mechanism for HFpEF is an overproduction of free radicals, specifically reactive oxygen species. To reduce free radical formation, antioxidants are often used. This article is a summative review of the recent relevant literature that addresses cardiac bioenergetics, deficiency in myocardial bioenergetics, and increased reactive oxygen species associated with HFpEF and the promising potential use of antioxidants in managing this condition.

Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes.

BACKGROUND: Traumatic brain injury (TBI) is an acquired brain injury that occurs when there is sudden trauma that leads to brain damage. This acute complex event can happen when the head is violently or suddenly struck or an object pierces the skull or brain. The current principal treatment of TBI includes various pharmaceutical agents, hyperbaric oxygen, and hypothermia. There is evidence that secondary injury from a TBI is specifically related to oxidative stress. However, the clinical management of TBI often does not include antioxidants to reduce oxidative stress and prevent secondary injury. AIMS: The purpose of this article is to examine current literature regarding the use of antioxidant therapies in treating TBI. This review evaluates the evidence of antioxidant therapy as an adjunctive treatment used to reduce the underlying mechanisms involved in secondary TBI injury. METHODS: A systematic review of the literature published between January 2005 and September 2015 was conducted. Five databases were searched including CINAHL, PubMed, the Cochrane Library, PsycINFO, and Web of Science. FINDINGS: Critical evaluation of the six studies that met inclusion criteria suggests that antioxidant therapies such as amino acids, vitamins C and E, progesterone, N-acetylcysteine, and enzogenol may be safe and effective adjunctive therapies in adult patients with TBI. Although certain limitations were found, the overall trend of using antioxidant therapies to improve the clinical outcomes of TBI was positive. LINKING EVIDENCE TO ACTION: By incorporating antioxidant therapies into practice, clinicians can help attenuate the oxidative posttraumatic brain damage and optimize patients' recovery.

Traumatic brain injury and mitochondrial dysfunction.

Traumatic brain injury (TBI) is a major cause of death and disability in the United States and causes mitochondrial damage leading to impaired brain function. The purpose of this review is to (1) describe TBI processes and manifestations, (2) examine the mitochondrial alterations after TBI, specifically increased reactive oxygen species production, decreased bioenergetics and apoptosis and (3) current TBI treatments. There are various degrees of severity of TBI, yet all affect mitochondrial function. Currently, health care professionals use various methods to assess TBI severity-from brain imaging to serum biomarkers. The major cause of TBI-associated brain damage is secondary injury, which is mainly from mitochondrial injury dysfunction. Mitochondrial injury leads to oxidative stress and subsequent apoptosis and decreased cellular energy production. These brain cellular alterations impair neurologic functions, which are observed in individuals with TBI. The complex mitochondrial dysfunction after TBI requires treatment that specifically addresses the secondary injury. There are numerous therapies being used, including (1) hypothermia, (2) hyperbaric oxygen, (3) exercise and (4) antioxidants. Researchers are exploring novel approaches to prevent, diagnose and treat TBI focusing on maintaining mitochondrial function.

Myocardial energetics and ubiquinol in diastolic heart failure.

Diastolic heart failure, or heart failure with preserved ejection fraction, is a leading cause of morbidity and mortality. There are no current therapies effective in improving outcomes for these patients. The aim of this article is to review the literature and examine the role of coenzyme Q10 in heart failure with preserved ejection fraction related to mitochondrial synthesis of adenosine triphosphate and reactive oxygen species production. The study results reflect that myocardial energetics alters in diastolic heart failure and that there is defective energy metabolism and increased oxidative stress. Studies are emerging to evaluate coenzyme Q10 , particularly ubiquinol, as a supplemental treatment for heart-failure patients. In diastolic heart-failure patients, clinicians are beginning to use supplemental therapies to improve patient outcomes, and one promising complementary treatment to improve left ventricular diastolic function is ubiquinol. Additional studies are needed using large-scale randomized models to confirm if ubiquinol would be beneficial. Since ubiquinol is an antioxidant and is required for adenosine triphosphate production, clinicians and health scientists should be aware of the potential role of this supplement in the treatment of diastolic heart failure.