I'm still trying myself to gradually increase my vitamins after being on coumdain for a year now.
I've been trying to gradually increase my vitamins while monitoring my INR level. Right now I'm taking 25mg per day of a powdered CoQ10 and will soon switch to a more standardized brand (Solgar) as different manufacturers have different amounts of CoQ10 in their products. I'd like to eventually get up to the 100mg day of the Q-Gel brand but I'd be afraid to take that much without gradually increasing to make sure there was no drastic interation. I've been increasing my CoQ10 about 5mg at a time to slowly monitor for any changes in INR.
It is ironic that some vitmins/supplements like garlic, fish oil, vit E are said by some to possibly increase the INR whereas others like vit C, CoQ10 are said by some to possibly decrease the INR. It makes one wonder if by taking both types if the changes could be somewhat offset?
I guess the bottom line is to go with frequent testing if making any changes so as to adjust for any possible interations with the coumadin. Also using the same brand/type consistently and monitoring frequently if changing brands is probably a good idea.
I wish I knew the "hows" of the vitamin/coumadin issue - I'm just gradually increasing my vitamins and testing frequently - though I wish I were taking a lot more vitamins than I am now.
As to whether there is any evidence for CoQ10 to be helpful with CHF - there are many articles that say it is - here's some of them - not that it is a 'cure' but that it can improve CHF symptoms in many people -
From:
http://www.lef.org/magazine/mag2003/jan2003_abs_01.html
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LE Magazine January 2003
CoQ10
Perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone).
A defective myocardial energy supply-due to lack of substrates and/or essential cofactors and a poor utilization efficiency of oxygen-may be a common final pathway in the progression of myocardial diseases of various etiologies. The vitamin-like essential substance coenzyme Q10, or ubiquinone, is a natural antioxidant and has a key role in oxidative phosphorylation. A biochemical rationale for using coenzyme Q10 as a therapy in heart disease was established years ago by Folkers and associates; however, this has been further strengthened by investigations of viable myocardial tissue from the author's series of 45 patients with various cardiomyopathies. Myocardial tissue levels of coenzyme Q10 determined by high-performance lipid chromatography were found to be significantly lower in patients with more advanced heart failure compared with those in the milder stages of heart failure. Furthermore, the myocardial tissue coenzyme Q10 deficiency might be restored significantly by oral supplementation in selected cases. In the author's open clinical protocol study with coenzyme Q10 therapy (100 mg daily) nearly two-thirds of patients revealed clinical improvement, most pronounced in those with dilated cardiomyopathy.
Double-blind placebo-controlled trials have definitely confirmed that coenzyme Q10 has a place as adjunctive treatment in heart failure with beneficial effects on the clinical outcome, the patients' physical activity, and their quality of life. The positive results have been above and beyond the clinical status obtained from treatment with traditional principles-including angiotensin-converting enzyme inhibitors.
Clin Investig 1993;71(8 Suppl):S116-23
Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment.
Symptoms of fatigue and activity impairment, atypical precordial pain and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15% and 7% showed significant myocardial hypertrophy, and 87%, 30% and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome, respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups.
CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.
Clin Investig 1993;71(8 Suppl):S140-4
Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy.
During 1982 to 1986, 43/137 patients with cardiomyopathy, Classes II, III and IV, had ejection fractions (EF) below 40%, and a mean EF of 25.1 +/- 10.3%. During treatment of these 43 patients with coenzyme Q10 (CoQ10), EF increased to 41.6 +/- 14.3% (p less than 0.001) over a mean period of three months (range, two to four months). At four subsequent periods up to 36 months EF ranged from 43.1 +/- 13.3 to 49.7 +/- 6.4% (each period, p less than 0.001). The mean CoQ10 control blood level was 0.85 +/- 0.26 micrograms/ml, which increased on treatment to 1.7 to 2.3 micrograms/ml for five periods up to 36 months (each period, p less than 0.001). The survival rates for all 137 patients treated with CoQ10 and for the 43 patients with EF below 40% were both about 75%/46 months. These two survival rates were comparable between 24 and 46 months, which is of extraordinary significance and importance when compared to survival of about 25%/36 months for 182 patients with EF below 46% on conventional therapy without CoQ10.
The improved cardiac function and pronounced increase of survival show that therapy with CoQ10 is remarkably beneficial due to correction of CoQ10 deficiency in mechanisms of bioenergetics.
Int J Tissue React 1990;12(3):163-8
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