Clin Nutr. 2005 Jun;24(3):331-8.
Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy.
Bhagavan HN, Chopra RK.
Nutrition Science Department, Tishcon Corporation, 30 New York Avenue, P.O. Box 331, Westbury, NY 11590, USA.
Pediatric cardiomyopathy (PCM) represents a group of rare and heterogeneous disorders that often results in death. While there is a large body of literature on adult cardiomyopathy, all of the information is not necessarily relevant to children with PCM. About 40% of children who present with symptomatic cardiomyopathy are reported to receive a heart transplant or die within the first two years of life. In spite of some of the advances in the management of PCM, the data shows that the time to transplantat ion or death has not improved during the past 35 years. Coenzyme Q10 is a vitamin-like nutrient that has a fundamental role in mitochondrial function, especially as it relates to the production of energy (ATP) and also as an antioxidant. Based upon the bi ochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Addi tional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted.
Atherosclerosis. 2005 Mar;179(1):201-6. Epub 2004 Dec 29.
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
Strey CH, Young JM, Molyneux SL, George PM, Florkowski CM, Scott RS, Frampton CM.
Lipid and Diabetes Research Group, Christchurch Hospital, Christchurch, New Zealand.
Although not currently indicated for chronic heart failure (CHF), statins have been associated with improved outcome in retrospective analysis. However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states. We hypothesized that atorvastatin treatment improves endothelial function in patients with chronic heart failure independent of LDL-cholesterol alterations. Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function. Twenty-four patients with stable, symptomatic heart failure (New York Heart Association Class II or III) and a left ventricular ejection fraction <40% were randomised to 40 mg atorvastatin or placebo for 6 weeks and crossed over to the other treatment arm for a further 6 weeks, after a 2-week wash out. Forearm resistance vessel function was assessed by venous occlusion plethysmography during infusion of acetylcholine (ACh), sodium nitroprusside (SNP), and N(G)-mo nomethyl-L-arginine (L-NMMA) into the brachial artery. Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015). Endothe lium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084). Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelia l function after adjusting for LDL-cholesterol levels (p=0.041). In conclusion, short-term atorvastatin therapy improved endothelial function in chronic heart failure patients. Further studies are required to determine whether coenzyme Q(10) reductions ar e limiting the maximum favourable effects of statin therapy on the microcirculation.
Pediatr Cardiol. 2005 Jan 27; [Epub ahead of print]
The Effect of Coenzyme Q10 on Idiopathic Chronic Dilated Cardiomyopathy in Children.
Soongswang J, Sangtawesin C, Durongpisitkul K, Laohaprasitiporn D, Nana A, Punlee K, Kangkagate C.
Division of Cardiology, Department of Pediatrics, Faculty of Medicine, Siriraj Hospital, Mahidol University, 10700, Bangkok, Thailand.
The objective of this study was to assess the effect of coenzyme Q10 (CoQ10) as supplementation to conventional antifailure drugs on quality of life and cardiac function in children with chronic heart failure due to dilated cardiomyopathy (DCM). The study was an open-label prospective study performed in two of the largest pediatric centers in Thailand from August 2000 to June 2003. A total of 15 patients with idiopathic chronic DCM were included, with the median age of 4.4 years (range, 0.6-16.3). Present ing symptoms were congestive heart failure in 12 cases (80%), cardiogenic shock in 2 cases (13.3%), and cardiac arrhythmia in 1 case (6.7%). Sixty-one percent of patients were in the New York Heart Association functional class 2 (NYHA 2), 31% in NYHA 3, a nd 8% in NYHA 4. Cardiothoracic ratio from chest x-ray, left ventricular ejection fraction, and left ventricular end diastolic dimension in echocardiogram were 0.62 (range, 0.55-0.78), 30% (range, 20-40), and 5.2 cm (range, 3.8-6.5), respectively. CoQ10 w as given at a dosage of 3.1 ? 0.6 mg/kg/day for 9 months as a supplementation to a fixed amount of conventional antifailure drugs throughout the study. At follow-up periods of 1, 3, 6, and 9 months, NYHA functional class was significantly improved, as was CT ratio and QRS duration at 3 and 9 months follow-up with CoQ10 when compared to the baseline and post-discontinuation of CoQ10 at 9 months (range, 4.8-10.8). However, when multiple comparisons were taken into consideration, there was no statistical sig nificant improvement. In addition to the conventional antifailure drugs, CoQ10 may improve NYHA class and CT ratio and shorten ventricular depolarization in children with chronic idiopathic DCM.
Georgian Med News. 2005 Jan;(1):20-5.
Prevention of coronary atherosclerosis by the use of combination therapy with antioxidant coenzyme Q10 and statins.
Chapidze G, Kapanadze S, Dolidze N, Bachutashvili Z, Latsabidze N.
The goal of the present research was to assess the efficacy of combination treatment with antioxidant coenzyme Q10 and simvastatin as well as coenzyme Q10 without statin therapy in order to prevent coronary atherosclerosis. 42 outpatients were divided int o 2 groups: receiving coenzyme Q10 (Hasco-Lek, Poland) 60mg daily and its combination with simvastatin (zocor, vasilip) 10mg daily for an 8-week period. The treatment with coenzyme Q10 demonstrated its potential independent role in positive modification o f oxidative stress, antiatherogenic fraction of lipid profile, atherogenic ratio, platelet aggregability. Taking into consideration the obtained results the study supports the use of coenzyme Q10 in combination with statins. Suggested attractive approach may result in complete correction of dislipidemia, reverse of endothelial dysfunction, reduce degree of oxidative stress and platelet aggregability. Consequently such a combination may be beneficial in preventing of further development of atherosclerosis in native coronary arteries as well as in bypass grafts in all coronary heart disease patients with or without myocardial revascularization.
Integr Cancer Ther. 2005 Jun;4(2):110-30.
Coenzyme q10 for prevention of anthracycline-induced cardiotoxicity.
Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles. email@example.com.
Preclinical and clinical studies suggest that anthracycline-induced cardiotoxicity can be prevented by administering coenzyme Q10 during cancer chemotherapy that includes drugs such as doxorubicin and daunorubicin. Studies further suggest that coenzyme Q1 0 does not interfere with the antineoplastic action of anthracyclines and might even enhance their anticancer effects. Preventing cardiotoxicity might allow for escalation of the anthracycline dose, which would further enhance the anticancer effects. Base d on clinical investigation, although limited, a cumulative dose of doxorubicin of up to 900 mg/m(2), and possibly higher, can be administered safely during chemotherapy as long as coenzyme Q10 is administered concurrently. The etiology of the dose-limiti ng cardiomyopathy that is induced by anthracyclines can be explained by irreversible damage to heart cell mitochondria, which differ from mitochondria of other cells in that they possess a unique enzyme on the inner mitochondrial membrane. This enzyme red uces anthracyclines to their semiquinones, resulting in severe oxidative stress, disruption of mitochondrial energetics, and irreversible damage to mitochondrial DNA. Damage to mitochondrial DNA blocks the regenerative capability of the organelle and ulti mately leads to apoptosis or necrosis of myocytes. Coenzyme Q10, an essential component of the electron transport system and a potent intracellular antioxidant, appears to prevent damage to the mitochondria of the heart, thus preventing the development of anthracycline-induced cardiomyopathy.
Semin Cardiothorac Vasc Anesth. 2005 Jun;9(2):167-71.
Myocardial Metabolism and Improved OutcomesAfter High Risk Heart Surgery.
Keith M, Errett L.
Division of Cardiovascular and Thoracic Surgery, Terrence Donnelly Heart Centre, St. Michael's Hospital and The Department of Surgery, University of Toronto.
The healthy heart relies primarily upon the oxidation of fatty acids for energy, with the remaining coming from the oxidation of glucose and lactate. Changes in energy requirements are met by altering the balance of fuels depending upon the hormonal milie u as well as upon the availability of oxygen and substrates. The use of carbohydrates for fuel is metabolically more efficient and may improve the coupling between glycolysis and pyruvate oxidation. Therefore, promoting a shift in metabolic fuel substrate use during times of reduced oxygen availability may represent a cardioprotective strategy. Subsequently, there has been interest in pharmacologic strategies such insulin or drugs like ranolazine and dichloroacetate that stimulate carbohydrate oxidation e ither by enhancing oxidation at the pyruvate dehydrogenase complex or by limiting fatty acid oxidation. There is evidence that nutrients may also be able to stimulate carbohydrate oxidation. Previous studies by our group suggest that a combination of nutr ients (carnitine, coenzyme Q10, and taurine) may work together, resulting in pleiotropic cardioprotective effects. Our current studies are investigating the potential of nutrients as both a preventative and adjunctive treatment before and after an ischemi c event. These investigations will determine the role of nutritional supplementation in the care of patients with ischemic injury.
Cardiol Rev. 2004 Mar-Apr;12(2):73-84.
Vitamins, supplements, herbal medicines, and arrhythmias.
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA. firstname.lastname@example.org
Nutritional and herbal supplements may have harmful or beneficial effects on arrhythmias. Potential supplements that may have antiarrhythmic activity include omega-3 polyunsaturated fatty acids (N-3 PUFA), coenzyme Q10, and carnitine. Clinical studies sho w that N-3 PUFA or fish oil supplementation appears to reduce mortality and sudden death. Coenzyme Q10, used in treatment of heart failure, and carnitine and its derivatives may have beneficial effects on arrhythmias, although clinical studies have been l imited. Antioxidant supplements may be beneficial, but large studies with vitamin E have been disappointing in that it does not reduce mortality. Correction of electrolyte disturbances has been long advised and magnesium supplementation has been beneficia l in the treatment of torsades de pointes and in some studies after cardiac surgery. However, routine electrolyte supplementation with empiric potassium or magnesium in non-deficient patients has not been convincingly beneficial. Several herbal supplement s have also been promoted to have antiarrhythmic activity. However, clinical studies are lacking to support routine use of these herbal medications. In addition, some herbal supplements may cause serious proarrhythmia, and many supplements significantly i nteract with warfarin and digoxin.
Clin. Cardiol. 27, 295–299 (2004)
Coenzyme Q10 in Patients with End-Stage Heart Failure Awaiting Cardiac Transplantation: A Randomized, Placebo-Controlled Study
MARIUSBERMAN, M.D., ARIEERMAN, PH.D.,* TUVIABEN-GAL, M.D., DANDVIR, M.D., GEORGIOS P. GEORGHIOU, M.D., ALON STAMLER, M.D., YAFFAVERED, PH.D., BERNARDO A. VIDNE, M.D., DANARAVOT, M.D. Department of Cardiothoracic Surgery, Heart-Lung Transplant Unit; *Institute of Nephrology and Hypertension; †Department of Cardiology, Echocardiographic Unit, Rabin Medical Center, Beilinson Campus, Potah Tikva; ‡Clinical Biochemistry Laboratory Tel-Aviv Souraski Medical Center, Tel Aviv; both affiliated with the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Background: The number of patients awaiting heart transplantation is increasing in proportion to the waiting period for a donor. Studies have shown that coenzyme Q10 (CoQ10) has a beneficial effect on patients with heart failure. Hypothesis: The purpose of the present double-blind, placebo-controlled, randomized study was to assess the effect of CoQ10 on patients with end-stage heart failure and to determine if CoQ10 can improve the pharmacological bridge to heart transplantation. Methods: A prospective double-blind design was used. Thirty-two patients with end-stage heart failure awaiting heart transplantation were randomly allocated to receive either 60 mg U/day of Ultrasome CoQ10 (special preparation to increase intestinal absorption) or placebo for 3 months. All patients continued their regular medication regimen. Assessments included anamnesis with an extended questionnaire based partially on the Minnesota Living with Heart Failure Questionnaire, 6-min walk test, blood tests for atrial natriuretic factor (ANF) and tumor necrosis factor (TNF), and echocardiography. Results:Twenty-seven patients completed the study. The study group showed significant improvement in the 6-min walk test and a decrease in dyspnea, New York Heart Association (NYHA) classification, nocturia, and fatigue. No significant changes were noted after 3 months of treatment in echocardiography parameters (dimensions and contractility of cardiac chambers) or ANF and TNF blood levels.
Conclusion: The administration of CoQ10 to heart transplant candidates led to a significant improvement in functional status, clinical symptoms, and quality of life. However, there were no objective changes in echo measurements or ANF and TNF blood levels. Coenzyme Q10 may serve as an optional addition to the pharmacologic armamentarium of patients with end-stage heart failure. The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation.
Coenzyme Q10 Combined With Mild Hypothermia After Cardiac Arrest A Preliminary Study Maxwell Simon Damian, MD, PhD; Diana Ellenberg, MD; Ramona Gildemeister, MD; Jörg Lauermann, MD; Gregor Simonis, MD; Wolfgang Sauter, MD; Christian Georgi, MD From the Department of Neurology, University Hospitals of Leicester, Leicester, United Kingdom (M.S.D.); and the Departments of Neurology (D.E., R.G., W.S.), Internal Medicine/Cardiology (J.L., G.S.), and Cardiothoracic Surgery (C.G.), University of Techn ology, Dresden, Germany.
Correspondence to Maxwell Damian, MD, PhD, Leicester Royal Infirmary, Infirmary Square, Leicester LE15WW, Leicester, UK. E-mail email@example.com
Received February 7, 2004; de novo received June 7, 2004; accepted July 16, 2004.
Background— Therapeutic hypothermia can improve survival after cardiopulmonary resuscitation (CPR). Coenzyme Q10 (CoQ10) has shown a protective effect in neurodegenerative disorders. We investigated whether combining mild hypothermia with CoQ10 after out- of-hospital cardiac arrest provides additional benefit.
Methods and Results— Forty-nine patients were randomly assigned to either hypothermia plus CoQ10 or hypothermia plus placebo after CPR. Hypothermia with a core temperature of 35°C was instituted for 24 hours. Liquid CoQ10 250 mg followed by 150 mg TID for 5 days or placebo was administered through nasogastric tube. Age, sex, premorbidity, cause of arrest, conditions of CPR, and degree of hypoxia were similar in both groups; no side effects of CoQ10 were identified. Three-month survival in the CoQ10 group was 68% (17 of 25) and 29% (7 of 24) in the placebo group (P=0.0413). Nine CoQ10 patients versus 5 placebo patients survived with a Glasgow Outcome Scale of 4 or 5. Mean serum S100 protein 24 hours after CPR was significantly lower in the CoQ10 group (0.4 7 versus 3.5 ng/mL).
Conclusions— Combining CoQ10 with mild hypothermia immediately after CPR appears to improve survival and may improve neurological outcome in survivors.
Clin Cardiol. 2004 May;27(5):295-9.
Comment in: Clin Cardiol. 2004 Oct;27(10):A26; author reply A26, A30.
Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study.
Berman M, Erman A, Ben-Gal T, Dvir D, Georghiou GP, Stamler A, Vered Y, Vidne BA, Aravot D.
Department of Cardiothoracic Surgery, Heart-Lung Transplant Unit, Rabin Medical Center, Beilinson Campus, Potah Tikva, Israel. firstname.lastname@example.org
BACKGROUND: The number of patients awaiting heart transplantation is increasing in proportion to the waiting period for a donor. Studies have shown that coenzyme Q10 (CoQ10) has a beneficial effect on patients with heart failure. HYPOTHESIS: The purpose o f the present double-blind, placebo-controlled, randomized study was to assess the effect of CoQ10 on patients with end-stage heart failure and to determine if CoQ10 can improve the pharmacological bridge to heart transplantation. METHODS: A prospective d ouble-blind design was used. Thirty-two patients with end-stage heart failure awaiting heart transplantation were randomly allocated to receive either 60 mg U/day of Ultrasome--CoQ10 (special preparation to increase intestinal absorption) or placebo for 3 months. All patients continued their regular medication regimen. Assessments included anamnesis with an extended questionnaire based partially on the Minnesota Living with Heart Failure Questionnaire, 6-min walk test, blood tests for atrial natriuretic f actor (ANF) and tumor necrosis factor (TNF), and echocardiography. RESULTS: Twenty-seven patients completed the study. The study group showed significant improvement in the 6-min walk test and a decrease in dyspnea, New York Heart Association (NYHA) class ification, nocturia, and fatigue. No significant changes were noted after 3 months of treatment in echocardiography parameters (dimensions and contractility of cardiac chambers) or ANF and TNF blood levels. CONCLUSIONS: The administration of CoQ10 to hear t transplant candidates led to a significant improvement in functional status, clinical symptoms, and quality of life. However, there were no objective changes in echo measurements or ANF and TNF blood levels. Coenzyme Q10 may serve as an optional additio n to the pharmacologic armamentarium of patients with end-stage heart failure. The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation.
Arch Neurol. 2004 Jun;61(6):889-92.
Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke.
Rundek T, Naini A, Sacco R, Coates K, DiMauro S.
Department of Neurology, Columbia University College of Physicians & Surgeons, New York, NY 10032, USA.
BACKGROUND: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are widely used for the treatment of hypercholesterolemia and coronary heart disease and for the prevention of stroke. There have been various adverse effects, most commonly affecting muscle and ranging from myalgia to rhabdomyolysis. These adverse effects may be due to a coenzyme Q(10) (CoQ(10)) deficiency because inhibition of cholesterol biosynthesis also inhibits the synthesis of CoQ(10). OBJECTIVE: To measure CoQ(10) lev els in blood from hypercholesterolemic subjects before and after exposure to atorvastatin calcium, 80 mg/d, for 14 and 30 days. DESIGN: Prospective blinded study of the effects of short-term exposure to atorvastatin on blood levels of CoQ(10). SETTING: St roke center at an academic tertiary care hospital.Patients We examined a cohort of 34 subjects eligible for statin treatment according to National Cholesterol Education Program: Adult Treatment Panel III criteria. RESULTS: The mean +/- SD blood concentrat ion of CoQ(10) was 1.26 +/- 0.47 micro g/mL at baseline, and decreased to 0.62 +/- 0.39 micro g/mL after 30 days of atorvastatin therapy (P<.001). A significant decrease was already detectable after 14 days of treatment (P<.001). CONCLUSIONS: Even brief e xposure to atorvastatin causes a marked decrease in blood CoQ(10) concentration. Widespread inhibition of CoQ(10) synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.
Systematic review of effect of coenzyme Q10 in physical exercise, hypertension and heart failure.
Rosenfeldt F, Hilton D, Pepe S, Krum H.
Cardiac Surgical Research Unit, Alfred Hospital and Baker Institute, Melbourne, Victoria, Australia. email@example.com
COENZYME Q10 IN PHYSICAL EXERCISE. We identified eleven studies in which CoQ10 was tested for an effect on exercise capacity, six showed a modest improvement in exercise capacity with CoQ10 supplementation but five showed no effect. CoQ10 IN HYPERTENSION. We identified eight published trials of CoQ10 in hypertension. Altogether in the eight studies the mean decrease in systolic blood pressure was 16 mm Hg and in diastolic blood pressure, 10 mm Hg. Being devoid of significant side effects CoQ10 may have a role as an adjunct or alternative to conventional agents in the treatment of hypertension. CoQ10 IN HEART FAILURE. We performed a randomised double blind placebo-controlled pilot trial of CoQ10 therapy in 35 patients with heart failure. Over 3 months, in the CoQ10 patients but not in the placebo patients there were significant improvements in symptom class and a trend towards improvements in exercise time. META-ANALYSIS OF RANDOMISED TRIALS OF COENZYME Q10 IN HEART FAILURE. In nine randomised trials of Co Q10 in heart failure published up to 2003 there were non-significant trends towards increased ejection fraction and reduced mortality. There were insufficient numbers of patients for meaningful results. To make more definitive conclusions regarding the ef fect of CoQ10 in cardiac failure we recommend a prospective, randomised trial with 200-300 patients per study group. Further trials of CoQ10 in physical exercise and in hypertension are recommended.
Overview on coenzyme Q10 as adjunctive therapy in chronic heart failure. Rationale, design and end-points of "Q-symbio"--a multinational trial.
The Heart Centre, Medical Department B, Copenhagen University Hospital, Denmark. firstname.lastname@example.org
Energy starvation of the myocardium is probably a dominant feature of heart failure and attention has been directed towards agents which may stabilize myocardial metabolism and maintain adequate energy stores. A reduced myocardial tissue content of the es sential redox-component and natural antioxidant Coenzyme Q10 (CoQ10) has been detected in patients with heart failure and the observed level of CoQ10 deficiency was correlated to the severity of heart failure. CoQ10 fulfills various criteria of an obvious adjunct in patients with symptomatic heart failure: it is devoid of significant side effects and it improves symptoms and quality of life. Till this date, several double-blind placebo-controlled trials with CoQ10 supplementation in more than 1000 patient s have been positive and statistically significant with respect to various clinical parameters, e.g. improvement in NYHA Class, exercise capacity and reduced hospitalisation frequency. Also treatment with CoQ10 led to a significant improvement of relevant hemodynamic parameters. In only 3 out of 13 double-blind studies comprising 10% of the total number of patients treated the results were neutral. Thus, based on the available controlled data CoQ10 is a promising, effective and safe approach in chronic he art failure. This is why a double-blind multicenter trial with focus on morbidity and mortality has been planned to start in 2003: Q-SYMBIO. Patients in NYHA classes III to IV (N=550) receiving standard therapy are being randomized to treatment with CoQ10 100 mg t.i.d. or placebo in parallel groups. End-points in a short-term evaluation phase of 3 months include symptoms, functional capacity and biomarker status (BNP). The aim of a subsequent 2-year follow-up study is to test the hypothesis that CoQ10 may reduce cardiovascular morbidity (unplanned cardiovascular hospitalisation due to worsening heart failure) and mortality as a composite endpoint. This trial should help to establish the future role of CoQ10 as part of a maintenance therapy in patients wit h chronic heart failure.
J Cardiol. 2003 Jan;41(1):21-7.
Cardiomyopathy showing progression from diffuse left ventricular hypertrophy to dilated phase associated with mitochondrial DNA point mutation A3243G: A case report
Ohmoto N, Fujiwara Y, Kibira S, Kobayashi M, Saito T, Miura M.
Second Department of Internal Medicine, Akita University School of Medicine, Akita.
A 44-year-old man was admitted to our hospital because of congestive heart failure. He had various symptoms caused by insulin-dependent diabetes mellitus, sensorineural deafness, Wolff-Parkinson-White syndrome and cardiomyopathy associated with mitochondr ial DNA point mutation A3243G. Echocardiography had showed symmetrical hypertrophy of the left ventricular wall and normal cardiac function (ejection fraction 55%) at age 32 years. However, echocardiography showed cardiac transformation, consisting of pos terior wall thinning and significantly reduced cardiac function (ejection fraction 11%), at age 44 years. Electrocardiography showed lowered R-wave in the chest leads and QRS widening. Both lactic acid and pyruvate serum levels were increased. Mitochondri al respiratory enzyme analysis in gastrocnemius muscle tissue indicated a partial deficiency of rotenone-sensitive NADH cytochrome C reductase. He was discharged from our hospital, and medically treated with coenzyme Q10(30 mg/day). He had no progression of cardiomyopathy or congestive heart failure. However, he suddenly died of lactic acidosis at age 47 years.
Mol Cell Biochem. 2003 Apr;246(1-2):75-82.
Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.
Singh RB, Neki NS, Kartikey K, Pella D, Kumar A, Niaz MA, Thakur AS.
Medical Hospital and Research Centre, Moradabad, India. email@example.com
In a randomized, double-blind, controlled trial, the effects of oral treatment with coenzyme Q10 (CoQ10, 120 mg/day), a bioenergetic and antioxidant cytoprotective agent, were compared for 1 year, on the risk factors of atherosclerosis, in 73 (CoQ, group A) and 71 (B vitamin group B) patients after acute myocardial infarction (AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02) including non-fatal infarction (13.7 vs. 25.3%, p < 0.05) and cardiac deaths were significantly lower in the inte rvention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma level of vitamin E (32.4 +/- 4.3 vs. 22.1 +/- 3.6 umol/L) and high density lipoprotein cholesterol (1.26 +/- 0.43 vs. 1.12 +/- 0.32 mmol/L) showed significant (p < 0.05) increase whereas thiobarbituric acid reac tive substances, malondialdehyde (1.9 + 0.31 vs. 3.1 + 0.32 pmol/L) and diene conjugates showed significant reduction respectively in the CoQ group compared to control group. Approximately half of the patients in each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and both groups had a significant reduction in total and low density lipoprotein cholesterol compared to baseline levels. It is possible that treatment with CoQ10 in patients with recent MI may be beneficial in patients with high ri sk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of 1 year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ group.
Am Heart J. 2001 Aug;142(2):E2.
The effect of pravastatin and atorvastatin on coenzyme Q10.
Bleske BE, Willis RA, Anthony M, Casselberry N, Datwani M, Uhley VE, Secontine SG, Shea MJ.
College of Pharmacy, the General Clinical Research Center, the Division of Cardiology, Department of Medicine, and the University of Michigan Health Systems, University of Michigan, Ann Arbor, MI 48109-1065, USA. firstname.lastname@example.org
BACKGROUND: Coenzyme Q10 (CoQ10) is an antioxidant and plays an important role in the synthesis of adenosine triphosphate. Studies suggest that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors reduce CoQ10 levels; however, no studies h ave directly compared HMG-CoA reductase inhibitors in a randomized crossover fashion. METHODS: Twelve healthy volunteers received either 20 mg pravastatin (P) or 10 mg atorvastatin (A) for 4 weeks in a randomized crossover fashion. There was a 4- to 8-wee k washout period between the 2 phases. CoQ10 levels and a lipid profile were obtained. RESULTS: There was no difference in CoQ10 levels from baseline to post-drug therapy for either P or A (0.61 +/- 0.14 vs 0.62 +/- 0.2 microg/mL and 0.65 +/- 0.22 vs 0.6 +/- 0.12 microg/mL, respectively; P >.05). There was a significant difference in low-density lipoprotein (LDL) levels from baseline to post-drug therapy for both P and A (97 +/- 21 vs 66 +/- 19 mg/dL and 102 +/- 21 vs 52 +/- 14 mg/dL, respectively; P <.01 ). There was no significant correlation between LDL and CoQ10. CONCLUSIONS: P and A did not decrease CoQ10 despite a significant decrease in LDL levels. These findings suggest that HMG-CoA reductase inhibitors do not significantly decrease the synthesis o f circulating CoQ10 in healthy subjects. Routine supplementation of CoQ10 may not be necessary when HMG-CoA reductase inhibitor therapy is administered.
Annals of Internal Medicine
18 April 2000 | Volume 132 Issue 8 | Pages 636-640
The Effect of Coenzyme Q10 in Patients with Congestive Heart Failure
Meenakshi Khatta, MS, CRNP; Barbara S. Alexander, MD, PhD; Cathy M. Krichten, MS, CRNP; Michael L. Fisher, MD; Ronald Freudenberger, MD; Shawn W. Robinson, MD; and Stephen S. Gottlieb, MD
Background: Coenzyme Q10 is commonly used to treat congestive heart failure on the basis of data from several unblinded, subjective studies. Few randomized, blinded, controlled studies have evaluated objective measures of cardiac performance.
Objective: To determine the effect of coenzyme Q10 on peak oxygen consumption, exercise duration, and ejection fraction.
Design: Randomized, double-blind, controlled trial.
Setting: University and Veterans Affairs hospitals.
Patients: 55 patients who had congestive heart failure with New York Heart Association class III and IV symptoms, ejection fraction less than 40%, and peak oxygen consumption less than 17.0 mL/kg per minute (or <50% of predicted) during standard therapy w ere randomly assigned. Forty-six patients completed the study.
Intervention: Coenzyme Q10, 200 mg/d, or placebo.
Measurements: Left ventricular ejection fraction (measured by radionuclide ventriculography) and peak oxygen consumption and exercise duration (measured by a graded exercise evaluation using the Naughton protocol) with continuous metabolic monitoring.
Results: Although the mean (±SD) serum concentration of coenzyme Q10 increased from 0.95 ± 0.62 µg/mL to 2.2 ± 1.2 µg/mL in patients who received active treatment, ejection fraction, peak oxygen consumption, and exercise duration remained unchanged in bot h the coenzyme Q10 and placebo groups.
Conclusion: Coenzyme Q10 does not affect ejection fraction, peak oxygen consumption, or exercise duration in patients with congestive heart failure receiving standard medical therapy.
Ann Intern Med. 2000 Apr 18;132(8):636-40.
Comment in: Ann Intern Med. 2000 Nov 7;133(9):745-6.
The effect of coenzyme Q10 in patients with congestive heart failure.
Khatta M, Alexander BS, Krichten CM, Fisher ML, Freudenberger R, Robinson SW, Gottlieb SS.
University of Maryland School of Medicine and Veterans Affairs Medical Center, Baltimore 21201, USA.
BACKGROUND: Coenzyme Q10 is commonly used to treat congestive heart failure on the basis of data from several unblinded, subjective studies. Few randomized, blinded, controlled studies have evaluated objective measures of cardiac performance. OBJECTIVE: T o determine the effect of coenzyme Q10 on peak oxygen consumption, exercise duration, and ejection fraction. DESIGN: Randomized, double-blind, controlled trial. SETTING: University and Veterans Affairs hospitals. PATIENTS: 55 patients who had congestive h eart failure with New York Heart Association class III and IV symptoms, ejection fraction less than 40%, and peak oxygen consumption less than 17.0 mL/kg per minute (or <50% of predicted) during standard therapy were randomly assigned. Forty-six patients completed the study. INTERVENTION: Coenzyme Q10, 200 mg/d, or placebo. MEASUREMENTS: Left ventricular ejection fraction (measured by radionuclide ventriculography) and peak oxygen consumption and exercise duration (measured by a graded exercise evaluation using the Naughton protocol) with continuous metabolic monitoring. RESULTS: Although the mean (+/-SD) serum concentration of coenzyme Q10 increased from 0.95+/-0.62 microg/mL to 2.2+/-1.2 microg/mL in patients who received active treatment, ejection frac tion, peak oxygen consumption, and exercise duration remained unchanged in both the coenzyme Q10 and placebo groups. CONCLUSION: Coenzyme Q10 does not affect ejection fraction, peak oxygen consumption, or exercise duration in patients with congestive hear t failure receiving standard medical therapy.
Ann Thorac Surg. 1996 Mar;61(3):829-33.
Comment in: Ann Thorac Surg. 1996 Oct;62(4):1243-4.
Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations.
Taggart DP, Jenkins M, Hooper J, Hadjinikolas L, Kemp M, Hue D, Bennett G.
Department of Cardiothoracic Surgery, Royal Brompton Hospital, London, England.
BACKGROUND: Coenzyme Q10 (CoQ10) is a naturally occurring vitamin-like substance that may have a beneficial role in ischemia-reperfusion injury. Coenzyme Q10 administered either as an additive to cardioplegia or as long-term preoperative oral supplementat ion has been reported to ameliorate myocardial injury after cardiac operations. METHODS: To determine whether short-term supplementation with large doses of CoQ10 (600 mg in divided doses 12 hours before operation) was effective in myocardial protection, 20 patients with well-preserved left ventricular function (ejection fraction greater than 0.50) undergoing elective coronary revascularization were enrolled in a prospective, double-blind, placebo-controlled randomized trial. Serial concentrations of CoQ1 0, myoglobin, creatine kinase MD fraction, and cardiac troponin T were measured preoperatively and 1, 6, 24, 72, and 120 hours postoperatively. Efficacy of myocardial protection was also assessed by clinical outcome and serial changes in electrocardiograp hic indices. RESULTS: The patient groups were similar with respect to preoperative and intraoperative characteristics. There was no significant difference in the preoperative plasma levels of CoQ10. These levels fell significantly in both groups after ope ration, although the magnitude of the decrease was less in the CoQ10-supplemented group (43% versus 60%). In both groups, there were significant postoperative increases in myoglobin, creatine kinase MB fraction, and cardiac troponin T. The magnitude of in creases in cardiac troponin T was greater in the CoQ10-supplemented group, reaching marginal overall statistical significance (p = 0.06). CONCLUSIONS: Short-term supplementation with large doses of CoQ10 does not lead to improved myocardial protection in patients undergoing coronary revascularization with well-preserved ventricular function and relatively short ischemic times.
J Cardiovasc Surg (Torino). 1996 Jun;37(3):229-35.
Protection by coenzyme Q10 of tissue reperfusion injury during abdominal aortic cross-clamping.
Chello M, Mastroroberto P, Romano R, Castaldo P, Bevacqua E, Marchese AR.
Medical School of Catanzaro, Italy.
PURPOSE: To evaluate the effect of coenzyme Q10 in reducing the skeletal muscle reperfusion injury following clamping and declamping the abdominal aorta. METHODS: 30 patients undergoing elective vascular surgery for abdominal aortic aneurysm or obstructiv e aorto-iliac disease were randomly divided into two groups: patients in group I were treated with coenzyme Q10 (150 mg/day) for seven days before operation, and those in group II received a placebo. We studied the hemodynamic profile in each patient duri ng clamping and declamping of the abdominal aorta. The plasma concentrations of thiobarbituric acid reactive substances (malondialdhehyde), conjugated dienes, creatine kinase and lactate dehydrogenase were measured in samples from both arterial and inferi or vena cava sites. Serial sampling was performed after induction of anesthesia, 5 and 30 minutes after abdominal aortic cross clamping, 5 and 30 minutes after aortic cross-clamp removal. RESULTS: The concentrations of malondialdehyde, conjugated dienes, creatine kinase and lactate dehydrogenase in patients who received CoQ10 were significantly lower than in the placebo group. Decrease of plasma malondialdehyde concentrations correlated positively (p < 0.01) with decrease of both creatine kinase and lacta te dehydrogenase release in samples from the inferior vena cava. The hemodynamic profile during clamping and declamping the abdominal aorta was similar in both groups. CONCLUSIONS: Our findings suggest that pre-treatment with coenzyme Q10 may play a prote ctive role during routine vascular procedures requiring abdominal aortic cross clamping by attenuating the degree of peroxidative damage.
J Card Fail. 1995 Mar;1(2):101-7.
Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group.
Hofman-Bang C, Rehnqvist N, Swedberg K, Wiklund I, Astrom H.
Department of Cardiology, Karolinska Hospital, Stockholm, Sweden.
Seventy-nine patients with stable chronic congestive heart failure were randomized into a double-blind, crossover placebo controlled study with 3-month treatment periods, where either 100 mg coenzyme Q10 (CoQ10) or placebo was added to conventional therap y. Mean patient age was 61 +/- 10 years, ejection fraction at rest was 22% +/- 10%, and maximal exercise tolerance was 91 +/- 30 W. The follow-up examinations included ejection fraction (primary objective), exercise test, and quality of life questions. Ej ection fraction at rest, during a slight volume load, and during a submaximal supine exercise increased slightly compared with placebo: 24% +/- 12% versus 23% +/- 12% (NS), 25% +/- 13% versus 23% +/- 12% (P < .05), and 23% +/- 11% versus 22% +/- 11% (NS). Maximal exercise capacity increased from 94 +/- 31 W during the placebo period to 100 +/- 34 W during the CoQ10 period (P < .05). Total score for the quality of life assessment increased significantly from 107 +/- 23 during the placebo period to 113 +/- 22 during the CoQ10 period (P < .05). The results indicate that oral long-term treatment with 100 mg CoQ10 in patients with congestive heart failure only slightly improves maximal exercise capacity and the quality of life and that the clinical importance of this needs to be further evaluated.
Ann Thorac Surg. 1994 Nov;58(5):1427-32.
Protection by coenzyme Q10 from myocardial reperfusion injury during coronary artery bypass grafting.
Chello M, Mastroroberto P, Romano R, Bevacqua E, Pantaleo D, Ascione R, Marchese AR, Spampinato N.
Department of Cardiac Surgery, Medical School of Catanzaro, Italy.
To evaluate the effect of coenzyme Q10 in reducing postoperative cardiac complications after ischemia and reperfusion, we randomly divided 40 patients undergoing elective coronary artery bypass into two groups: patients in group 1 received coenzyme Q10 (1 50 mg/day) for 7 days before operation, and those in group 2 were the control group. Concentrations of thiobarbituric acid-reactive substances (malondialdehyde), conjugated dienes, and cardiac isoenzymes of creatine kinase were measured in samples from bo th arterial and coronary sinus sites. Serial sampling was performed 5 minutes after heparin administration, at 10 and 30 minutes during cardiopulmonary bypass, 15 and 30 minutes after aortic cross-clamp removal, and 5 minutes after protamine administratio n. The concentrations of malondialdehyde, conjugated dienes, and creatine kinase in group 1 were significantly lower than those in group 2. The decrease in plasma malondialdehyde concentrations correlated positively with the decrease in creatine kinase le vels in the coronary sinus. The treatment group showed a significantly lower incidence of ventricular arrhythmias during the recovery period than did the control group (p < 0.05). Although the percentage of patients requiring inotropic agents was not sign ificantly different between the two groups, the mean dosage of dopamine required to maintain stable hemodynamics was significantly lower in patients of group 1 than in those of group 2 (p < 0.01). Our findings suggest that pretreatment with coenzyme Q10 m ay play a protective role during routine bypass grafting by attenuating the degree of peroxidative damage.
Mol Aspects Med. 1994;15 Suppl:s287-94.
Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators.
Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G.
Department of Internal Medicine, V. Buzzi Hospital, Reggio Emilia.
Digitalis, diuretics and vasodilators are considered the standard therapy for patients with congestive heart failure, for which treatment is tailored according to the severity of the syndrome and the patient profile. Apart from the clinical seriousness, h eart failure is always characterized by an energy depletion status, as indicated by low intramyocardial ATP and coenzyme Q10 levels. We investigated safety and clinical efficacy of Coenzyme Q10 (CoQ10) adjunctive treatment in congestive heart failure whic h had been diagnosed at least 6 months previously and treated with standard therapy. A total of 2664 patients in NYHA classes II and III were enrolled in this open noncomparative 3-month postmarketing study in 173 Italian centers. The daily dosage of CoQ1 0 was 50-150 mg orally, with the majority of patients (78%) receiving 100 mg/day. Clinical and laboratory parameters were evaluated at the entry into the study and on day 90; the assessment of clinical signs and symptoms was made using from two-to seven-p oint scales. The results show a low incidence of side effects: 38 adverse effects were reported in 36 patients (1.5%) of which 22 events were considered as correlated to the test treatment. After three months of test treatment the proportions of patients with improvement in clinical signs and symptoms were as follows: cyanosis 78.1%, oedema 78.6%, pulmonary rales 77.8%, enlargement of liver area 49.3%, jugular reflux 71.81%, dyspnoea 52.7%, palpitations 75.4%, sweating 79.8%, subjective arrhytmia 63.4%, i nsomnia 662.8%, vertigo 73.1% and nocturia 53.6%. Moreover we observed a contemporary improvement of at least three symptoms in 54% of patients; this could be interpreted as an index of improved quality of life.
Mol Aspects Med. 1994;15 Suppl:s149-54.
Recovery of load-induced left ventricular diastolic dysfunction by coenzyme Q10: echocardiographic study.
Department of Pediatrics, Fukuoka University, Japan.
Load-induced cardiac dysfunction (LCD), in which a supernormal left ventricular (LV) systolic performance at rest decreases due to an afterload challenge, usually occurs among children with mitral valve prolapse (MVP). However, diastolic performance is al so important because relaxation, like contraction, is based on a process that requires energy. The aim of this study was to examine LV diastolic response patterns to stress in patients with LCD before and after coenzyme Q10 (CoQ) therapy and in controls. The D-E slope, E-F slope and maximal diastolic endocardial velocity were used as echographic diastolic indices. Thirty subjects, aged 9-16 years, were divided into four groups: group 1, 10 normals; group 2, 10 patients with LCD; group 3, the same 10 as in group 2, who recovered with CoQ, 3.0-3.4 mg/kg/day for 7 days; group 4, 10 asymptomatic children with MVP. The heart rate, both at rest and during handgrip (HG), showed little intergroup difference. Only in group 2, were the ejection fraction and all the diastolic indices greater than in the other groups, but these became subnormal with HG. In the other groups, these indices increased with HG to a similar extent, although resting values were smaller than in group 2. In conclusion: (1) in normal hearts an d in hearts with LCD, diastolic performance mimicked systolic performance both in resting and loading conditions; (2) CoQ improved not only the load-induced systolic but also the diastolic dysfunctions in a similar time-course, and (3) mechanical stiffnes s of the cardiac tissue may not be a cause of load-induced diastolic dysfunction, because the dysfunction was quickly resolved with CoQ therapy. CoQ may be a key substance which affects a common bioenergetic process in contraction and relaxation, to keep these functions normal.
Clin Investig. 1993;71(8 Suppl):S134-6.
Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study.
Morisco C, Trimarco B, Condorelli M.
Facolta di Medicina e Chiruriga, Universita degli Studi di Napoli Federico II.
The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q1 0 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we st udied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assig ned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalizat ion for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 vers us 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious com plications in patients with chronic congestive heart failure.
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