ubiquinone 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

Topics: Drug Evaluation; Heart Diseases; Humans; Hypertension; Ubiquinone

Periprocedural myocardial injury (PMI) following elective percutaneous coronary intervention (PCI) is an important therapeutic concern with remaining some mortality and morbidity. To the best of our knowledge, there is no published study that investigates the potential benefit of CoQ10 in preventing PMI following elective PCI.. In a randomized, clinical trial, 100 patients who scheduled for elective PCI were allocated in to the intervention (n=50) and control group (n=50). The intervention received a 300 mg loading dose CoQ10 12 hours before procedure. The level of CK-MB and troponin-I was measured before procedure, and 8 and 24 hours after. Furthermore, hs-CRP was measured at baseline and 24 hours after. All patients were assessed for the incidence of major adverse cardiac effects (MACEs) after 1 month.. The CK-MB elevation (above the upper limit normal) was occurred in 22% (n=11) of CoQ10 and 20% (n=10) of control (P=.806). The elevation of troponin-I was documented in 8% (n=4) of both groups. No significant change in the level of cardiac biomarkers was noted. However, the significant reduction in hs-CRP level was occurred in CoQ10 group (P=.032).. The results showed that pretreatment with 300 mg CoQ10 12 hours before procedure could not reduce PMI following elective PCI, however, significantly decreased hs-CRP.

Topics: Aged; Angioplasty, Balloon, Coronary; Anti-Inflammatory Agents; Biomarkers; C-Reactive Protein; Creatine Kinase, MB Form; Female; Heart Diseases; Humans; Iran; Male; Middle Aged; Pilot Projects; Prospective Studies; Single-Blind Method; Stents; Time Factors; Treatment Outcome; Troponin I; Ubiquinone

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

The goal of this study was to assess mitochondrial function and ROS production in an experimental model of cocaine-induced cardiac dysfunction. We hypothesized that cocaine abuse may lead to altered mitochondrial function that in turn may cause left ventricular dysfunction. Seven days of cocaine administration to rats led to an increased oxygen consumption detected in cardiac fibers, specifically through complex I and complex III. ROS levels were increased, specifically in interfibrillar mitochondria. In parallel there was a decrease in ATP synthesis, whereas no difference was observed in subsarcolemmal mitochondria. This uncoupling effect on oxidative phosphorylation was not detectable after short-term exposure to cocaine, suggesting that these mitochondrial abnormalities were a late rather than a primary event in the pathological response to cocaine. MitoQ, a mitochondrial-targeted antioxidant, was shown to completely prevent these mitochondrial abnormalities as well as cardiac dysfunction characterized here by a diastolic dysfunction studied with a conductance catheter to obtain pressure-volume data. Taken together, these results extend previous studies and demonstrate that cocaine-induced cardiac dysfunction may be due to a mitochondrial defect.

Topics: Animals; Antioxidants; Cocaine; Cocaine-Related Disorders; Disease Susceptibility; Drug Evaluation, Preclinical; Heart Diseases; Male; Mitochondria, Heart; Mitochondrial Diseases; Molecular Targeted Therapy; Organophosphorus Compounds; Oxygen Consumption; Rats; Rats, Wistar; Reactive Oxygen Species; Ubiquinone

Sepsis elicits severe alterations in cardiac function, impairing cardiac mitochondrial and pressure-generating capacity. Currently, there are no therapies to prevent sepsis-induced cardiac dysfunction. We tested the hypothesis that administration of a mitochondrially targeted antioxidant, 10-(6'-ubiquinonyl)-decyltriphenylphosphonium (MitoQ), would prevent endotoxin-induced reductions in cardiac mitochondrial and contractile function. Studies were performed on adult rodents (n = 52) given either saline, endotoxin (8 mg x kg(-1) x day(-1)), saline + MitoQ (500 microM), or both endotoxin and MitoQ. At 48 h animals were killed and hearts were removed for determination of either cardiac mitochondrial function (using polarography) or cardiac pressure generation (using the Langendorf technique). We found that endotoxin induced reductions in mitochondrial state 3 respiration rates, the respiratory control ratio, and ATP generation. Moreover, MitoQ administration prevented each of these endotoxin-induced abnormalities, P < 0.001. We also found that endotoxin produced reductions in cardiac pressure-generating capacity, reducing the systolic pressure-diastolic relationship. MitoQ also prevented endotoxin-induced reductions in cardiac pressure generation, P < 0.01. One potential link between mitochondrial and contractile dysfunction is caspase activation; we found that endotoxin increased cardiac levels of active caspases 9 and 3 (P < 0.001), while MitoQ prevented this increase (P < 0.01). These data demonstrate that MitoQ is a potent inhibitor of endotoxin-induced mitochondrial and cardiac abnormalities. We speculate that this agent may prove a novel therapy for sepsis-induced cardiac dysfunction.

Topics: Adenosine Triphosphate; Animals; Antioxidants; Caspase 3; Caspase 9; Cell Respiration; Disease Models, Animal; Drug Administration Schedule; Endotoxemia; Enzyme Activation; Heart Diseases; Mice; Mitochondria, Heart; Myocardial Contraction; Myocardium; Organophosphorus Compounds; Protein Carbonylation; Rats; Tumor Necrosis Factor-alpha; Ubiquinone; Ventricular Function, Left; Ventricular Pressure

Antioxidant therapy is a new therapeutical approach for patients with Friedreich ataxia.. To assess the effectiveness of long-term idebenone treatment in Friedreich ataxia patients.. An open-labelled prospective study. Ten paediatric patients (age range 8-18 years) and 14 adults (age range 18-46 years) with genetic diagnosis of Friedreich ataxia were treated with idebenone (5-20mg/kg/day) for 3-5 years. Neurological evolution was evaluated using the International Cooperative Ataxia Rating Scale (ICARS), and cardiological outcomes using echocardiography.. In paediatric patients, no significant differences were observed in ICARS scores and echocardiographic measurements when comparing baseline status and after 5 years of follow-up. Concerning adult cases, ICARS scores showed a significant increase in neurological dysfunctions during 3 years of therapy (Wilcoxon test, p=0.005), while echocardiographic measurements remained unchanged.. Our results indicate that longer-term idebenone treatment prevented progression of cardiomyopathy in both paediatric and adult patients, whereas its stabilizing effect on neurological dysfunction was present only in the paediatric population, mainly before puberty. This suggests that the age at which idebenone treatment is initiated may be an important factor in the effectiveness of the therapy.

Topics: Adolescent; Adult; Antioxidants; Child; Echocardiography; Female; Follow-Up Studies; Friedreich Ataxia; Heart Diseases; Heart Function Tests; Humans; Male; Neurologic Examination; Neuropsychological Tests; Treatment Outcome; Ubiquinone; Young Adult

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 duration of lag-phase of copper-induced free-radical oxidation of atherogenic LDL isolated from the plasma of coronary patients without hypercholesterolemia virtually does not differ from that of normal human LDL. On the other hand, lag-phase of plasma LDL oxidation was minimal in coronary patients with primary hypercholesterolemia without familial history and especially in patients with familial hypercholesterolemia. This can be attributed to sharply decreased content of natural lipid antioxidants in LDL of patients with familial hypercholesterolemia. However, therapy with natural antioxidant vitamin E did not modulate oxidizability of these LDL. By contrast, therapy with beta-hydroxy-beta-methylglutaryl-coenzyme A reductase inhibitor suppressing biosynthesis of ubiphenol Q induced sharp accumulation of lipoperoxides in LDL in vivo. These data suggest that reduced form of ubiquinone Q is the main antioxidant protecting LDL from free-radical oxidation.

Topics: Adult; Antioxidants; Cholesterol; Female; Free Radicals; Heart Diseases; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Kinetics; Lipid Peroxides; Lipoproteins, LDL; Male; Middle Aged; Models, Chemical; Oxygen; Time Factors; 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: Dose-Response Relationship, Drug; Heart Diseases; Humans; Lovastatin; Risk Factors; 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

Recent work suggests that adriamycin (ADM) cardiotoxicity results from the depletion of coenzyme 10 (CoQ10) activity in myocardial mitochondria. CoQ10 is indispensable in the bioenergetics of coupled respiration of oxidative phosphorylation. It exists naturally in mitochondria, especially in the myocardium. Bertazzoli et al have reported a decrease in ADM-induced cardiotoxicity by CoQ10 both in vivo and in the in vitro isolated rabbit heart. The systolic time interval (ATI) (pre-ejection period/left ventricular ejection time ratio) has been shown to increase (indicating cardiac dysfunction) with increasing doses of ADM. We have noted a gradual increase in the STI in eight of ten patients receiving 200-500 mg/m2 of ADM. Two of these eight patients had congestive heart failure (CHF) at doses of 200 and 350 mg/m2. The continued daily oral administration of 50 mg of CoQ10 beginning with the first dose of ADM resulted in a decreased incidence of cardiac dysfunction, and a gradual increase in STI occurred in only two of eight patients receiving 200-400 mg/m2 of ADM. CHF was observed inone patient at a dose of 350 mg/m2. It is suggested that CoQ10 was nontoxic and did not affect the antitumor activity or modify the ADM-induced bone marrow toxicity. A prospective randomized study comparing ADM with and without CoQ10 is in progress.

Topics: Aged; Cyclophosphamide; Doxorubicin; Drug Therapy, Combination; Female; Heart Diseases; Heart Rate; Humans; Male; Middle Aged; Ubiquinone; Vincristine

Topics: Deficiency Diseases; Electron Transport; Heart Diseases; Heart Septal Defects; Heart Valve Diseases; Humans; Mitochondria, Muscle; Myocardium; Respiration; Succinate Dehydrogenase; Tetralogy of Fallot; Ubiquinone

Topics: Adolescent; Adult; Aged; Aspartate Aminotransferases; Atrial Function; Blood Pressure; Cardiovascular Diseases; Child; Child, Preschool; Deficiency Diseases; Electrocardiography; Electron Transport; Female; Heart Diseases; Humans; L-Lactate Dehydrogenase; Male; Middle Aged; Oxidative Phosphorylation; Ubiquinone

Topics: Aortic Aneurysm; Heart Diseases; Heart Septal Defects, Ventricular; Humans; Metabolism, Inborn Errors; Mitochondria, Muscle; Myocardium; Oxidoreductases; Spectrophotometry; Succinate Dehydrogenase; Ubiquinone

Topics: Accidents; Adolescent; Adult; Aged; Aging; Animals; Child; Child, Preschool; Coronary Disease; Female; Heart Diseases; Humans; Infant; Infant, Newborn; Liver; Male; Middle Aged; Neoplasms; Rats; Refrigeration; Ubiquinone; Vitamin A