Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coenzyme Q10 (CoQ10) has already been favorably evaluated in the clinical treatment of heart disease. In the otolaryngological field, it has been reported that CoQ10 is effective in promoting recovery from acute sudden deafness. However, the pharmakinetics of CoQ10 in the inner ear is not yet clarified. The present study focuses upon the pharmacokinetics of CoQ10 using guinea pigs with acute sensorineural hearing loss artificially induced by hypoxia conditions. The respiration of the animals was controlled in an artificial respirator while the ABR, ECG and blood pressure were monitored. Repeated hypoxia caused a gradual disappearance of the ABR. After the experiments, the animals were sacrificed and brain and inner ear were examined by histological and histochemical methods as well as by SEM and TEM. The results indicated that CoQ10 is effective in promoting recovery from damage in auditory hairs as well as preventing respiratory metabolic impairment of hair cell due to hypoxia.
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PMID:Pharmacokinetics of coenzyme Q10 in recovery of acute sensorineural hearing loss due to hypoxia. 324 40

An investigation was undertaken to evaluate the antiarrhythmic effect of CoQ10 on VPBs using the Holter ECG, in 27 patients with no clinical findings of organic cardiopathies. As a result, the effect of CoQ10 on VPBs was considered beneficial in 6 (22%) of 27 cases, consisting of 1 patient with hypertension and 5 patients with DM. Even in the remaining 2 patients with DM, the frequency of VPBs was reduced by 50% or more during treatment with CoQ10. The mean reduction of VPBs frequency in the 5 responders plus these 2 patients with DM was 85.7%. These findings suggest that CoQ10 exhibits an effective antiarrhythmic action not merely on organic heart disease but also on VPBs supervening on DM.
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PMID:Clinical study of cardiac arrhythmias using a 24-hour continuous electrocardiographic recorder (5th report)--antiarrhythmic action of coenzyme Q10 in diabetics. 668 May 22

Serum coenzyme Q10 (CoQ10: 2-(3,7,11,15,19,23,27,31,35,39-decamethyl-2,6,10,14,18,22,26,30,34 ,38 -tetracontadecaenyl)-5,6-dimethoxy-3-methyl-1,4-benzoquinone, CAS 303-98-0) and cholesterol levels were measured to assess the effect of cholesterol-lowering therapy in patients with non-insulin-dependent diabetes mellitus (NIDDM). Twenty healthy volunteers, 97 NIDDM patients and 2 patients with familial hypercholesterolemia were studied. None had overt heart failure or any other heart disease. Mean serum CoQ10 concentrations were significantly (p < 0.01) lower in diabetic patients with normal serum cholesterol concentrations, either with or without administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (HMG-CoA RIs) including simvastatin (normal: 0.91 +/- 0.26 (mean +/- SD) mumol 1(-1); diabetic with HMG-CoA RI: 0.63 +/- 0.19; diabetic without HMG-CoA RI: 0.66 +/- 0.21). CoQ10 concentrations were higher (1.37 +/- 0.48, p < 0.001) in diabetic patients with hypercholesterolemia. Simvastatin or low density lipoprotein apheresis decreased serum CoQ10 concentrations along with decreasing serum cholesterol. Oral CoQ10 supplementation in diabetic patients receiving HMG-CoA RI significantly (p < 0.001) increased serum CoQ10 from 0.81 +/- 0.24 to 1.47 +/- 0.44 mumol 1(-1), without affecting cholesterol levels. It significantly (p < 0.03) decreased cardiothoracic ratios from 51.4 +/- 5.1 to 49.2 +/- 4.7%. In conclusion, serum CoQ10 levels in NIDDM patients are decreased and may be associated with subclinical diabetic cardiomyopathy reversible by CoQ10 supplementation.
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PMID:Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. 1033 51

Ubiquinones (coenzyme Qs (CoQ)) are essential for oxidative phosphorylation in yeasts and humans, although the isomers present in each are different. The human coenzyme Q, CoQ10, is administered orally for the treatment of heart disease and other disorders. Some patients, however, require much higher doses than others to attain a therapeutic CoQ10 blood level. We propose that one possible explanation for this variability is Candida colonization of the GI tract. Many common medical treatments including antibiotics and anti-hyperchlorhydric agents increase the risk of GI tract Candida colonization. Subsequent uptake and utilization of supplemental CoQ10 by the yeast could diminish availability for the human subject. Data from one patient and an in vitro pilot study using two pathogenic strains of C. albicans support this hypothesis. If C. albicans in the GI tract can hinder availability and interfere with therapeutic effects of CoQ10, it could be of clinical significance for large numbers of patients.
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PMID:Does gastrointestinal Candida albicans prevent ubiquinone absorption? 1173 12

Coenzyme Q10 (CoQ10) is synthesized by the human body and found in certain foods. Daily supplementation of CoQ10 could protect against heart disease but the bioavailability of CoQ10 supplements depends on the formulation taken. We compared the bioavailability and antioxidant properties of two commercial CoQ10 formulations, a commercial grade CoQ10 powder (commercial grade CoQ) and a new BT-CoQ10 BIO-TRANSFORMED (BT-CoQ10) obtained by fermentation of a soy-based, CoQ10-rich media with baker's yeast. Eleven healthy individuals participated in a randomized two-way crossover trial, with a 3-week washout period. Capsules containing 300 mg of either BT-CoQ10 or commercial grade CoQ10 were given daily for 1 week and multiple blood samples were taken for CoQ10, glutathione and glutathione peroxidase (GPx) determination. In 3 subjects, baseline plasma CoQ10 levels were lower prior to BT than prior to commercial grade CoQ treatment. In the remaining participants, ingestion of BT vs. commercial grade CoQ significantly increased maximum plasma CoQ10 concentration (+126%, p = 0.04) and tended to increase CoQ10 area under the curve from 0 to 24 h (+160%, p = 0.07). One week of treatment with each formulation increased plasma CoQ10 but did not alter plasma glutathione or GPx activity. The enhanced bioavailability of the BT product might be due to its predominantly reduced, hydrophilic membrane-complex form.
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PMID:Relative bioavailability and antioxidant potential of two coenzyme q10 preparations. 1262 83

Epidemiological data show a rise in the mean age of patients affected by heart disease undergoing cardiac surgery. Senescent myocardium reduces the tolerance to ischemic stress and there are indications about age-associated deficit in post-operative cardiac performance. Coenzyme Q10 (CoQ10), and more specifically its reduced form ubiquinol (QH), improve several conditions related to bioenergetic deficit or increased exposure to oxidative stress. This trial (Eudra-CT 2009-015826-13) evaluated the clinical and biochemical effects of ubiquinol in 50 elderly patients affected by severe aortic stenosis undergoing aortic valve replacement and randomized to either placebo or 400 mg/day ubiquinol from 7 days before to 5 days after surgery. Plasma and cardiac tissue CoQ10 levels and oxidative status, circulating troponin I, CK-MB (primary endpoints), IL-6 and S100B were assessed. Moreover, main cardiac adverse effects, NYHA class, contractility and myocardial hypertrophy (secondary endpoints) were evaluated during a 6-month follow-up visit. Ubiquinol treatment counteracted the post-operative plasma CoQ10 decline (p<0.0001) and oxidation (p=0.038) and curbed the post-operative increase in troponin I (QH, 1.90 [1.47-2.48] ng/dL; placebo, 4.03 [2.45-6.63] ng/dL; p=0.007) related to cardiac surgery. Moreover, ubiquinol prevented the adverse outcomes that might have been associated with defective left ventricular ejection fraction recovery in elderly patients.
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PMID:Ubiquinol supplementation in elderly patients undergoing aortic valve replacement: biochemical and clinical aspects. 3274 73

Comorbidities, dietary supplement use, and prescription drug use may negatively (or positively) affect mental health in cardiovascular patients. Although the significance of mental illnesses, such as depression, anxiety, and schizophrenia, on cardiovascular disease is well documented, mental illnesses resulting from heart disease are not well studied. In this paper, we introduce the risk factors of mental illnesses as an exploratory study and develop a prediction framework for mental illness that uses comorbidities, dietary supplements, and drug usage in heart disease patients. Particularly, the data used in this study consist of the records of 68,647 patients with heart disease, including the patient's mental illness information and the patient's intake of dietary supplements, antibiotics, and comorbidities. Patients in age groups <61, gender differences, and drug intakes, such as Azithromycin, Clarithromycin, Vitamin B6, and Coenzyme Q10, were associated with mental illness. For predictive modeling, we consider applying various state-of-the-art machine learning techniques with tuned parameters and finally obtain the following: Depression: 78.01% accuracy, 79.13% sensitivity, 72.65% specificity, and 86.26% Area Under the Curve (AUC). Anxiety: 82.93% accuracy, 82.86% sensitivity, 83.35% specificity, and 88.45% AUC. Schizophrenia: 87.59% accuracy, 87.70% sensitivity, 85.14% specificity, and 92.73% AUC. Disease: 86.63% accuracy, 95.50% sensitivity, 77.76% specificity, and 91.59% AUC. From the results, we conclude that using heart disease information, comorbidities, dietary supplement use, and antibiotics enables us to accurately predict the mental health outcome.
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PMID:Prediction of Mental Illness in Heart Disease Patients: Association of Comorbidities, Dietary Supplements, and Antibiotics as Risk Factors. 3318 35