coenzyme-q10 and Cardiac-Output--Low

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Oxidative stress appears to play a pivotal role in atherosclerosis. Coenzyme Q10 (CoQ10), one of the most important antioxidants, is synthesized de novo by every cell in the body. Its biosynthesis decreases with age and its deficit in tissues is associated with degenerative changes of aging, thus implicating a possible therapeutic role of CoQl0 in human diseases. There is evidence to support the therapeutic value of CoQ10 as an adjunct to standard medical therapy in congestive heart failure. However, much further research is required, especially in the use of state-of-the-art techniques to assess functional outcomes in patients with congestive heart failure.

Topics: Aging; Antioxidants; Cardiac Output, Low; Coenzymes; Drug Interactions; Heart Failure; Humans; Oxidative Stress; Ubiquinone; Vitamins

Coenzyme Q10 (CoQ10) is an endogenous cofactor in the mitochondrial energy production. CoQ10 has been touted to improve heart failure, but its effect on systolic function is controversial. Several small, randomized controlled trials evaluating CoQ10 showed variable results and were largely underpowered. We conducted a meta-analysis of these trials to evaluate the impact of CoQ10 therapy on ejection fraction and cardiac output.. A systematic literature search was conducted to identify randomized, controlled trials of CoQ10 in heart failure between 1966 and June 2005. Subgroup analysis was conducted to assess clinical heterogeneity between trials. Of the 11 trials identified, 10 evaluated ejection fraction (n = 277) and 2 evaluated cardiac output (n = 42). Doses ranged from 60 to 200 mg/day with treatment periods ranging from 1 to 6 months. There was a 3.7% net improvement in ejection fraction (95% CI 1.59-5.77; P < .00001 for statistical heterogeneity). A more profound effect among patients not receiving angiotensin-converting enzyme inhibitors was observed (6.74% [95% CI 2.63-10.86]). Cardiac output increased an average of 0.28 L/minute (95% CI 0.03-0.53; P = .96 for statistical heterogeneity).. CoQ10 enhances systolic function in chronic heart failure, but its effectiveness may be reduced with concomitant use of current standard therapies.

Topics: Cardiac Output; Cardiac Output, Low; Chronic Disease; Coenzymes; Heart; Humans; Randomized Controlled Trials as Topic; Stroke Volume; Systole; Ubiquinone

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 essential 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 patients 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 heart 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 with chronic heart failure.

Topics: Cardiac Output, Low; Coenzymes; Controlled Clinical Trials as Topic; Double-Blind Method; Humans; Placebos; Randomized Controlled Trials as Topic; Treatment Outcome; Ubiquinone

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 CoQ10 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 effect 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.

Topics: Cardiac Output, Low; Coenzymes; Exercise; Humans; Hypertension; MEDLINE; Meta-Analysis as Topic; Muscle, Skeletal; Oxygen Consumption; Randomized Controlled Trials as Topic; Ubiquinone

There is evidence that plasma CoQ(10) levels decrease in patients with advanced chronic heart failure (CHF).. To investigate whether oral CoQ(10) supplementation could improve cardiocirculatory efficiency in patients with CHF.. We studied 21 patients in NYHA class II and III (18M, 3W, mean age 59 +/- 9 years) with stable CHF secondary to ischemic heart disease (ejection fraction 37 +/- 7%), using a double-blind, placebo-controlled cross-over design. Patients were assigned to oral CoQ(10) (100 mg tid) and to placebo for 4 weeks, respectively.. CoQ(10) supplementation resulted in a threefold increase in plasma CoQ(10) level (P < 0.0001 vs placebo). Systolic wall thickening score index (SWTI) was improved both at rest and peak dobutamine stress echo after CoQ(10) supplementation (+12.1 and 15.6%, respectively, P < 0.05 vs placebo). Left ventricular ejection fraction improved significantly also at peak dobutamine (15% from study entry P < 0.0001) in relation to a decrease in LV end-systolic volume index (from 57 +/- 7 mL/m(2) to 45 mL/m(2), P < 0.001). Improvement in the contractile response was more evident among initially akinetic (+33%) and hypokinetic (+25%) segments than dyskinetic ones (+6%). Improvement in SWTI was correlated with changes in plasma CoQ(10) levels (r = -0.52, P < 0.005). Peak VO(2) was also improved after CoQ(10) as compared with placebo (+13%, <0.005). No side effects were reported with CoQ(10).. Oral CoQ(10) improves LV contractility in CHF without any side effects. This improvement is associated with an enhanced functional capacity.

Topics: Aged; Cardiac Output, Low; Chronic Disease; Coenzymes; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Contraction; Ubiquinone; Ventricular Function, Left

A randomized, prospective study of the effectiveness of preoperative administration of coenzyme Q10 on the prophylaxis of postoperative low cardiac output state was performed in 50 patients with acquired valvular diseases necessitating valve replacement. There were 25 patients in the treatment group and 25 in the control group. Patients in the treatment group received 30 to 60 mg of coenzyme Q10 orally for six days before operation. Preoperative clinical variables, operative procedures, total cardiopulmonary bypass time, and aortic cross-clamping time were similar for the two groups. Postoperatively, mild to severe low cardiac output state developed in 28 of 50 patients (56%) and necessitated the administration of considerable amounts of inotropic agent. The treatment group showed a significantly lower incidence of low cardiac output state during the recovery period than the control group (p less than 0.05). These results suggest that preoperative administration of coenzyme Q10 will increase the tolerance of human hearts to ischemia during aortic cross-clamping.

Topics: Adult; Cardiac Output, Low; Clinical Trials as Topic; Coenzymes; Female; Heart Arrest, Induced; Heart Valve Diseases; Humans; Male; Middle Aged; Premedication; Prospective Studies; Random Allocation; Time Factors; Ubiquinone

The effects of long-term treatment with coenzyme Q10 (CoQ10) on myocardial energy metabolism of rats with chronic heart failure (CHF) were examined. Left coronary artery ligation resulted in decreases in blood pressure, left ventricular developed pressure, the first derivative of left ventricular developed pressure, cardiac output and stroke volume indices and caused an increase in left ventricular end-diastolic pressure 12 weeks after the operation. Significant decreases in adenosine-5'-triphosphate, creatine phosphate, creatine and inorganic phosphate contents and the mitochondrial oxygen consumption rate of the viable left and right ventricles were detected in the CHF rat. Oral administration of 5 mg/kg/day CoQ10 for 12 weeks attenuated the changes in the first derivative of left ventricular developed pressure, cardiac output and stroke volume indices of the CHF rat but did not significantly improve the survival of CHF animals. The developed infarct area was approximately 40% of the whole left ventricle, irrespective of treatment with or without CoQ10. There was no reversal in the decreased myocardial CoQ9 and CoQ10 contents of the CHF rat after treatment with exogenous CoQ10. In the right ventricle of CoQ10-treated animals, a significant recovery of creatine, inorganic phosphate and mitochondrial oxygen consumption rate, and a small restoration of creatine phosphate but not of adenosine-5'-triphosphate, were observed, which suggests an appreciable recovery of energy-producing ability in the right ventricle. In contrast, a significant restoration of tissue creatine and inorganic phosphate, but not of other variables, was detected in the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Cardiac Output, Low; Chronic Disease; Coenzymes; Energy Metabolism; Heart; Heart Ventricles; Hemodynamics; Male; Mitochondria, Heart; Myocardial Infarction; Myocardium; Organ Size; Oxygen Consumption; Rats; Rats, Wistar; Time Factors; Ubiquinone

Topics: Cardiac Output, Low; Coenzymes; Humans; Ubiquinone

Topics: Adult; Aged; Aprotinin; Assisted Circulation; Cardiac Output, Low; Cardiac Surgical Procedures; Coenzymes; Female; Humans; Intra-Aortic Balloon Pumping; Lidocaine; Middle Aged; Postoperative Complications; Ubiquinone

Stress echocardiography (stress echo) by means of isometric handgrip has been proven to be useful for detection of latent cardiac dysfunction in patients with mitral valve prolapse (MVP). In MVP with symptoms (symptomatic MVP), handgrip (HG) stress usually induced an abnormal response, i.e. a decrease in the ejection fraction (EF) in accordance with other echo indices. If an effective treatment with coenzyme Q10 (CoQ) is performed, the response becomes normal (increase in EF) and symptoms disappear. Four hundred consecutive symptomatic MVP were divided into 6 groups according to the dose of CoQ, i.e., 0.6-0.9, 1.0-1.4, 1.5-1.9, 2.0-2.4, 2.5-2.9 and 3.0-3.4 mg/kg/day and followed up with repeated HG. There was a strong relationship between the dose and the time needed for normalization. In the 3.0-to-3.4 mg group, the majority of patients acquired a normal response within 1 week. When a single blind test between CoQ (N = 8) and ATP (adenosine triphosphate, N = 8) groups was conducted, the number of patients normalized within 8 weeks was 7 in the former and 0 in the latter. After reduction of the dose, 41 patients had relapses (re-abnormalizations) within 15 weeks (mean = 6.6). Continuous normalization for 4 months or longer after termination of CoQ occurred 7 to 43 months (mean = 18.5) after onset of symptoms, probably reflecting the self-limited natural course. Some patients (5.8% of patients followed up) showed polycyclic long courses like those of congestive cardiomyopathy and needed long-term CoQ treatment. CoQ was definitely effective for symptomatic MVP and improved stress-induced cardiac dysfunction if the appropriate dose was given. No side-effect was seen.

Topics: Adenosine Triphosphate; Adolescent; Cardiac Catheterization; Cardiac Output, Low; Child; Coenzymes; Echocardiography; Female; Humans; Isometric Contraction; Male; Mitral Valve Prolapse; Recurrence; Stroke Volume; Syncope; Ubiquinone

The effect of combined treatment of coenzyme Q10 (CoQ10) and aprotinin with intra-aortic balloon pumping (IABP) was evaluated in patients who underwent aorto-coronary bypass surgery. Forty-one patients were divided into two groups. Group A (27) were treated by IABP only and Group B (14) were treated by the concomitant use of CoQ10 and aprotinin with IABP. Both groups were subdivided into two groups with regard to the ability to be weaned from IABP (Group A-I, Group B-I) or the inability (Group A-II, Group B-II). CoQ10 was administrated intravenously at doses of 5-10 mg/kg/day and aprotinin was infused at doses 5,000-10,000 KU/kg/day. The percentile incidence of ability to be weaned from IABP was 93 per cent (13/14) in Group B was higher than that of 74 per cent (20/27) in Group A. There were no significant differences among Group A-I, Group A-II, and Group B-I with regard to preoperative and intraoperative factors. Serum GOT and CPK levels on the first postoperative day were significantly higher in Group A-II and Group B-I than those in Group A-I but there was no significant difference between GOT or CPK levels in Group A-II and Group B-I. These results suggest that concomitant treatment of CoQ10 and aprotinin with IABP leads to an improvement in postoperative low cardiac output syndrome.

Topics: Aprotinin; Aspartate Aminotransferases; Assisted Circulation; Cardiac Output, Low; Coenzymes; Coronary Artery Bypass; Creatine Kinase; Drug Therapy, Combination; Humans; Infusions, Parenteral; Injections, Intravenous; Intra-Aortic Balloon Pumping; Isoenzymes; Middle Aged; Postoperative Care; Postoperative Complications; Ubiquinone