coenzyme-q10 and Heart-Diseases

Mitochondrial disorders are a heterogeneous group of disorders resulting from primary dysfunction of the respiratory chain. Muscle tissue is highly metabolically active, and therefore myopathy is a common element of the clinical presentation of these disorders, although this may be overshadowed by central neurological features. This review is aimed at a general medical and neurologist readership and provides a clinical approach to the recognition, investigation, and treatment of mitochondrial myopathies. Emphasis is placed on practical management considerations while including some recent updates in the field.

Topics: Biopsy; Cytochrome-c Oxidase Deficiency; Deglutition Disorders; Dietary Supplements; Endocrine System Diseases; Exercise Test; Exercise Therapy; Hearing Disorders; Heart Diseases; Humans; Mitochondrial Myopathies; Muscle, Skeletal; Ubiquinone; Vision Disorders; Vitamins

Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. In addition it has an antioxidant, a free radical scavenging and a vasodilator effect which may be helpful in these conditions. It inhibits LDL oxidation and thus the progression of atherosclerosis. It decreases proinflammatory cytokines and decreases blood viscosity which is helpful in patients of heart failure and coronary artery disease. It also improves ischemia and reperfusion injury of coronary revascularisation. Significant improvement has been observed in clinical and hemodynamic parameters and in exercise tolerance in patients given adjunctive CoQ10 in doses from 60 to 200 mg daily in the various trials conducted in patients of heart failure, hypertension, ischemic heart disease and other cardiac illnesses. Recently it has been found to be an independent predictor of mortality in congestive heart failure. It has also been found to be helpful in vertigo and Meniere-like syndrome by improving the immune system. Further research is going on to establish firmly its role in the therapy of cardiovascular diseases.

Topics: Animals; Cardiotonic Agents; Clinical Trials as Topic; Heart Diseases; Humans; Hypertension; Meniere Disease; Ubiquinone; Vitamins

Anthracycline-induced cardiotoxicity after treatment for childhood cancer is a considerable and serious problem. In this review, important insight into the current state of the evidence on the use of different cardioprotective agents, different anthracycline analogues, and different anthracycline infusion durations to reduce or prevent cardiotoxicity in children treated with anthracyclines is provided. It has become clear that, at the present time, there is not enough reliable evidence for many aspects of the prevention of anthracycline-induced cardiotoxicity in children. More high quality research is necessary. Suggestions for future research have been presented. As the results of these new studies become available, it will hopefully be possible to develop evidence-based recommendations for preventing anthracycline-induced cardiotoxicity in children. Until then, we can only advise care providers to carefully monitor the cardiac function of children treated with anthracyclines. With regard to the use of the cardioprotectant dexrazoxane, it might be justified to use dexrazoxane in children if the risk of cardiac damage is expected to be high. However, for each individual patient, care providers should weigh the cardioprotective effect of dexrazoxane against the possible risk of adverse effects including a lower response rate. We recommend its use in the context of well-designed studies.

Topics: Anthracyclines; Antineoplastic Agents; Cardiotonic Agents; Child; Coenzymes; Heart Diseases; Humans; Randomized Controlled Trials as Topic; Razoxane; Risk Factors; Ubiquinone

Statins are drugs of known and undisputed efficacy in the treatment of hypercholesterolemia, usually well tolerated by most patients. In some cases treatment with statins produces skeletal muscle complaints, and/or mild serum CK elevation; the incidence of rhabdomyolysis is very low. As a result of the common biosynthetic pathway Coenzyme Q (ubiquinone) and dolichol levels are also affected, to a certain degree, by the treatment with these HMG-CoA reductase inhibitors. Plasma levels of CoQ10 are lowered in the course of statin treatment. This could be related to the fact that statins lower plasma LDL levels, and CoQ10 is mainly transported by LDL, but a decrease is also found in platelets and in lymphocytes of statin treated patients, therefore it could truly depend on inhibition of CoQ10 synthesis. There are also some indications that statin treatment affects muscle ubiquinone levels, although it is not yet clear to which extent this depends on some effect on mitochondrial biogenesis. Some papers indicate that CoQ10 depletion during statin therapy might be associated with subclinical cardiomyopathy and this situation is reversed upon CoQ10 treatment. We can reasonably hypothesize that in some conditions where other CoQ10 depleting situations exist treatment with statins may seriously impair plasma and possible tissue levels of coenzyme Q10. While waiting for a large scale clinical trial where patients treated with statins are also monitored for their CoQ10 status, with a group also being given CoQ10, physicians should be aware of this drug-nutrient interaction and be vigilant to the possibility that statin drugs may, in some cases, impair skeletal muscle and myocardial bioenergetics.

Topics: Animals; Biochemistry; Biosynthetic Pathways; Clinical Trials as Topic; Coenzymes; Cricetinae; Dogs; Heart Diseases; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hyperlipidemias; Models, Biological; Rats; Ubiquinone; Vitamins

Animals with cardiac disease can have a variety of nutritional alterations for which interventional nutrition can be beneficial. Deviation from optimal body weight, both obesity and cachexia, is a common problem in cardiac patients and adversely affects the animal. Methods for maintaining optimal weight are important for good quality of life in dogs and cats with cardiac disease. Providing proper diets to prevent excess intake of sodium and chloride also is important, but severe salt restriction may not be necessary until later stages of disease. Certain nutrient deficiencies may play a role in the pathogenesis or complications of cardiac disease, but nutrients also may have effects on cardiac disease which are above and beyond their nutritional effects (nutritional pharmacology). Supplementation of nutrients such as taurine, carnitine, coenzyme Q10, and omega-3 polyunsaturated fatty acids may have benefits in dogs or cats with cardiac disease through a number of different mechanisms. By addressing each of these areas maintaining optimal weight, avoiding nutritional deficiencies and excesses, and providing the benefits of nutritional pharmacology, optimal patient management can be achieved.

Topics: Animals; Antioxidants; Cachexia; Cat Diseases; Cats; Coenzymes; Dietary Supplements; Dog Diseases; Dogs; Fatty Acids, Omega-3; Heart Diseases; Magnesium Deficiency; Potassium Deficiency; Taurine; Ubiquinone; Vitamins

To investigate whether the effect of 48-month usage of coenzyme Q10 and selenium on cardiac function was different for participants with different levels of cardiac wall tension as measured by plasma levels of N-terminal natriuretic peptide (NT-proBNP) at baseline.. A 48-month randomized double-blind controlled trial in a cohort of community-dwelling elderly (mean age 78 years) was carried out. A total of 443 participants were given coenzyme Q10 combined with selenium, or a placebo. NT-proBNP measured at baseline and 48 months was used to evaluate the cardiac wall tension.. After 48 months, supplementation of coenzyme Q10 and selenium had varying impacts depending on the severity of impairment of cardiac function. Analyses of the responses in the different quintiles of baseline NT-proBNP showed that those with active supplementation, and a plasma level of NT-proBNP in the second to fourth quintiles demonstrated significantly reduced NT-proBNP levels (p = 0.022) as well as cardiovascular mortality after 48 months (p = 0.006).. Long-term supplementation of coenzyme Q10/selenium reduces NT-proBNP levels and cardiovascular mortality in those with baseline NT-proBNP in the second to fourth quintiles indicating those who gain from supplementation are patients with mild to moderate impaired cardiac function.

Topics: Aged; Aged, 80 and over; Antioxidants; Biomarkers; Double-Blind Method; Female; Heart Diseases; Humans; Male; Natriuretic Peptide, Brain; Peptide Fragments; Selenium; Sweden; Ubiquinone; Vitamins

Doxorubicin (DOX) is used as an anticancer drug despite its several side effects, especially its irreversible impacts on cardiotoxicity. Coenzyme Q10 (Q10) as a powerful antioxidant and lisinopril (LIS) as an angiotensin-converting enzyme inhibitor seem to provide protection against DOX-induced cardiotoxicity. Therefore, this study aimed to assess the cardioprotective effects of Q10 and LIS against DOX-induced cardiotoxicity in rats. Adult male Sprague-Dawley rats were randomly assigned into the control, LIS, Q10, DOX, DOX + LIS, and DOX + Q10 groups. On day 21, ECG was recorded and the right ventricle was dissected for evaluation of catalase activity and malondialdehyde (MDA) concentration. Additionally, the left ventricle and the sinoatrial (SA) node were dissected to assess the stereological parameters. The results of ECG indicated bradycardia and increase in QRS duration and QT interval in the DOX group compared to the control group. Meanwhile, the total volumes of the left ventricle, myocytes, and microvessels and the number of cardiomyocyte nuclei decreased, whereas the total volume of the connective tissue and the mean volume of cardiomyocytes increased in the DOX group. On the other hand, the SA node and the connective tissue were enlarged, while the volume of the SA node nuclei was reduced in the DOX group. Besides, catalase activity was lower and MDA concentration was higher in the DOX-treated group. Q10 could recover most stereological parameters, catalase activity, and MDA concentration. LIS also prevented some stereological parameters and ECG changes and improved catalase activity and MDA concentration in the DOX group. The findings suggested that Q10 and LIS exerted cardioprotective effects against DOX-induced cardiac toxicity.

Topics: Animals; Antibiotics, Antineoplastic; Cardiotoxicity; Catalase; Disease Models, Animal; Doxorubicin; Electrocardiography; Heart Conduction System; Heart Diseases; Heart Rate; Lisinopril; Male; Malondialdehyde; Myocytes, Cardiac; Rats, Sprague-Dawley; Ubiquinone

Doxorubicin (DOX) is a chemotherapeutic agent used for treatment of different cancers and its clinical usage is hindered by the oxidative injury-related cardiotoxicity. This work aims to declare if the harmful effects of DOX on heart can be alleviated with the use of Coenzyme Q10 (CoQ10) or L-carnitine. The study was performed on seventy two female Wistar albino rats divided into six groups, 12 animals each: Control group; DOX group (10mg/kg); CoQ10 group (200mg/kg); L-carnitine group (100mg/kg); DOX+CoQ10 group; DOX+L-carnitine group. CoQ10 and L-carnitine treatment orally started 5days before a single dose of 10mg/kg DOX that injected intraperitoneally (IP) then the treatment continued for 10days. At the end of the study, serum biochemical parameters of cardiac damage, oxidative stress indices, and histopathological changes were investigated. CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 β), tumor necrosis factor alpha (TNF-α), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels. Both corrected the cardiac alterations histologically and ultrastructurally. With a visible improvements in α-SMA, vimentin and eNOS immunohistochemical markers. CoQ10 or L-carnitine supplementation improves the functional and structural integrity of the myocardium.

Topics: Animals; Cardiotoxicity; Carnitine; Doxorubicin; Female; Heart Diseases; Myocardium; Oxidative Stress; Rats; Rats, Wistar; Ubiquinone

The aim of this study was to examine the effects of ubiquinone (CoQ10) on heart tissue and erythrocytes in acute organophosphate poisoning (AOP). A total of 20 rabbits were divided into three groups: sham (n = 8), pralidoxime (PAM) + atropine (n = 6), and CoQ10 + PAM + atropine (n = 6). Blood samples were taken from each test subject to measure the values of acetylcholinesterase (AChE), nitric oxide (NO), and malondialdehyde (MDA) in the plasma and erythrocyte before administration of 50 mg/kg dichlorvos by orogastric tube. Blood samples were then taken at 1, 12, and 24 h post-dichlorvos to determine plasma and erythrocyte levels of AChE, NO, and MDA. Sham group received no treatment. PAM + atropine group received 0.05 mg/kg atropine with repeated doses and PAM: first a 30-mg/kg intravenous (IV) bolus, then a 15-mg/kg IV bolus every 4 h. CoQ10 + PAM + atropine group received same dose PAM and atropine and a 50-mg bolus of IV CoQ10. Thoracotomy was performed in all the animals 24 h after poisoning and then heart tissue samples were obtained. At 12 and 24 h, erythrocyte AChE levels in the CoQ10 animals were considerably higher than those in PAM + atropine animals (p = 0.023 and 0.017, respectively). At 12 and 24 h, erythrocyte MDA and NO levels in CoQ10 animals were significantly lower than those in PAM + atropine animals (p < 0.05). Heart tissue AChE levels in CoQ10 animals were considerably higher than those of the sham and PAM + atropine animals (p = 0.001). Heart tissue MDA and NO levels of CoQ10 animals were significantly lower than those of the sham and PAM + atropine animals (p < 0.01). Treatment of AOP with CoQ10 + PAM + atropine in this animal model had a beneficial effect on both erythrocyte and heart tissue lipid peroxidation and AChE activity.

Topics: Acetylcholinesterase; Animals; Antioxidants; Atropine; Cholinesterase Reactivators; Drug Therapy, Combination; Erythrocytes; Female; Heart Diseases; Lipid Peroxidation; Male; Malondialdehyde; Myocardium; Nitric Oxide; Organophosphate Poisoning; Pralidoxime Compounds; Rabbits; Ubiquinone

Cardiac surgery represents major metabolic, physical and mental stresses associated with an increased production of reactive oxygen species. These stresses may hamper post-operative recovery, increasing hospitalisation times and operative mortality. We conducted a quality assurance and feasibility study to evaluate and monitor the safety and efficacy of a new program of combined pre-operative metabolic (enhanced antioxidant), physical and mental therapy to counter these stresses prior to cardiac surgery.. Sixteen cardiac surgery patients received metabolic therapy consisting of the antioxidants coenzyme Q(10) (CoQ(10)) (300 mg) and alpha-lipoic acid (300 mg), combined with magnesium orotate (1200 mg), and omega-3 fatty acids (3g) given daily for a mean 36+/-7 days up until the day of operation. Patients also received a regimen of physical therapy incorporating non-exhaustive, light exercise and stretching techniques. Mental therapy in the form of stress reduction, relaxation and music was also provided. Blood levels of CoQ(10) and malondialdehyde (MDA) were measured and a quality of life (QoL) questionnaire (SF-36) was administered before, after the program and 1 month after surgery. A patient satisfaction survey was conducted at six weeks post-operatively.. During the pre-operative period, treated patients (n=16) showed significant improvements in QoL composite scores, physical (33.5+/-4.1 to 41.0+/-4.5, p=0.005) and mental (44.3+/-4.5 to 54.1+/-5.3, p=0.006). CoQ(10) levels increased from 725.6+/-96.1 nmol/l to 3019.9+/-546.4 nmol/l (p=0.006), MDA levels decreased from 2.2+/-0.9 microM to 1.4+/-0.7 microM (p=0.013) and systolic blood pressure decreased from 140+/-4.0 mmHg to 132+/-3.0 mmHg (p=0.002). One month after surgery the treated group (n=14) demonstrated significant improvements from pre-operative baseline in QoL composite scores, physical (38.9+/-4.0 to 57.9+/-5.4, p=0.01) and mental (50.3+/-5.6 to 69.3+/-4.8, p=0.03) compared to a previously reported similar group of cardiac surgery patients (n=74) whose physical and mental scores decreased from 43.0 to 42.8 (p=0.05) and 53.8 to 49.8, respectively (p=0.05).. These preliminary results suggest that a program of combined metabolic, physical and mental preparation before cardiac surgery is safe, feasible and may improve quality of life, lower systolic blood pressure, reduce levels of oxidative stress and thus has the potential to enhance post-operative recovery.

Topics: Aged; Antioxidants; Cardiac Surgical Procedures; Coenzymes; Elective Surgical Procedures; Female; Heart Diseases; Humans; Male; Malondialdehyde; Oxidative Stress; Preoperative Care; Psychotherapy; Quality of Life; Stress, Psychological; Ubiquinone

Topics: Coenzymes; Drug Therapy, Combination; Heart Diseases; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Muscular Diseases; Ubiquinone

The objective of this study was to test the hypothesis that doxorubicin treatment for cancer in childhood and adolescence causes a dose-related decrease in the concentration of plasma coenzyme Q(10). The concentration of plasma coenzyme Q(10) was measured before and after administration of doxorubicin in six patients, and before and after chemotherapy in six patients undergoing treatments that did not include doxorubicin. There was a significant increase in the concentration of plasma coenzyme Q(10) in post-treatment samples compared to pre-treatment samples in patients treated with doxorubicin (P=0.008; n=32), whereas there were no significant changes in plasma coenzyme Q(10) concentrations in patients treated with chemotherapy that did not include doxorubicin. (P=0.770; n=30). We hypothesise that the increase in plasma coenzyme Q(10) that was observed in patients undergoing doxorubicin treatment is due to release of coenzyme Q(10) from apoptotic or necrotic cardiac tissue. We conclude that the cardiotoxicity due to doxorubicin therapy does not involve acute myocardial depletion of coenzyme Q(10).

Topics: Adolescent; Adult; Antineoplastic Agents; Antioxidants; Child; Child, Preschool; Cholesterol; Coenzymes; Cytoprotection; Doxorubicin; Female; Heart Diseases; Humans; Male; Neoplasms; Ubiquinone

Topics: Coenzymes; Heart Diseases; Humans; Ubiquinone

Topics: Adult; Coenzymes; Drug Evaluation; Echocardiography; Electrocardiography; Exercise Test; Female; Heart Diseases; Humans; Lactates; Lactic Acid; Male; Middle Aged; Myocardial Contraction; Time Factors; Ubiquinone

A series of 38 patients with solid tumours (N=29) and haematological malignancies (N=9) and with suspicion of cardiotoxicity (CTX) due to antineoplastic drugs was studied. The series comprised 22 females and 16 males (mean age 52 years). The patients were examined clinically by ECG, chest X-ray and echocardiography. Seventeen patients were classified as having moderate or severe chronic CTX; 16 patients developed either arrhythmias shortly after the administration of chemotherapy (acute CTX) or arrhythmias and/or signs of myocardial dysfunction (without overt congestive heart failure) at a later date, after chemotherapy had been suspended (latent CTX). In 5 cases the suspicion of CTX could not be confirmed. Weak and non-specific symptoms such as unexplained tachycardia or coughing at night should alert the clinician and result in ECG control and further non-invasive cardiological investigations (including radionuclide angiocardiography) before additional anthracycline is administered. Chest X-ray is a very insensitive method with respect to early diagnosis of chronic CTX; in cases of doubt heart catheterization with endomyocardial biopsy should be carried out to obtain a reliable estimate of the extent of morphological damage. As anthracycline CTX may present without prominent clinical symptoms or as latent disease, one should be aware of potential precipitating factors such as volume load (during i.v. chemotherapy), surgical trauma and general anaesthesia and alcohol abuse. Further effects to lessen CTX should be made, using supposed cardio-protective substances in randomized clinical trials. Promising research on coenzyme Q10 and carnitine may usher in a new era in the prevention of anthracycline cardiotoxicity.

Topics: Adolescent; Adult; Aged; Antibiotics, Antineoplastic; Antineoplastic Combined Chemotherapy Protocols; Arrhythmias, Cardiac; Biopsy; Cardiac Catheterization; Carnitine; Coenzymes; Electrocardiography; Endocardium; Female; Follow-Up Studies; Heart; Heart Diseases; Humans; Male; Middle Aged; Myocardium; Naphthacenes; Risk; Ubiquinone

Topics: Aged; Chronic Disease; Coenzymes; Female; Heart Diseases; Humans; Liver Diseases; Male; Middle Aged; Ubiquinone

Topics: Aged; Angina Pectoris; Coenzymes; Coronary Disease; Female; Heart Diseases; Humans; Male; Middle Aged; Ubiquinone; Urologic Diseases

Topics: Adult; Aged; Coenzymes; Female; Heart Diseases; Humans; Intensive Care Units; Male; Middle Aged; Pain; Pain Management; Ubiquinone

Topics: Adult; Aged; Coenzymes; Female; Heart Diseases; Humans; Male; Middle Aged; Ubiquinone

Topics: Aged; Coenzymes; Coronary Disease; Female; Heart Diseases; Humans; Male; Middle Aged; Ubiquinone

Topics: Adolescent; Adult; Aged; Antineoplastic Agents; Coenzymes; Daunorubicin; Female; Heart Diseases; Humans; Male; Middle Aged; Ubiquinone

Topics: Aged; Bronchial Diseases; Coenzymes; Female; Heart Diseases; Humans; Male; Middle Aged; Pneumonia; Ubiquinone

Topics: Aged; Antineoplastic Agents; Coenzymes; Female; Heart Diseases; Humans; Male; Middle Aged; Ubiquinone

Coenzyme Q10 (CoQ10) is a redox component in the respiratory chain. CoQ10 is necessary for human life to exist; and a deficiency can be contributory to ill health and disease. A deficiency of CoQ10 in myocardial disease has been found and controlled therapeutic trials have established CoQ10 as a major advance in the therapy of resistant myocardial failure. The cardiotoxicity of adriamycin, used in treatment modalities of cancer, is significantly reduced by CoQ10, apparently because the side-effects of adriamycin include inhibition of mitochondrial CoQ10 enzymes. Models of the immune system including phagocytic rate, circulating antibody level, neoplasia, viral and parasitic infections were used to demonstrate that CoQ10 is an immunomodulating agent. It was concluded that CoQ10, at the mitochondrial level, is essential for the optimal function of the immune system.

Topics: Aged; Aging; Cardiac Output; Coenzymes; Double-Blind Method; Doxorubicin; Female; Heart Diseases; Heart Failure; Humans; Immunity; Male; Middle Aged; Myocardial Infarction; Stroke Volume; Ubiquinone