Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome.

Co-enzyme Q10 (ubiquinone) is a naturally occurring substance which has properties potentially beneficial for preventing cellular damage during myocardial ischemia and reperfusion. It plays a role in oxidative phosphorylation and has membrane stabilizing activity. The substance has been used in oral form to treat various cardiovascular disorders including angina pectoris, hypertension, and congestive heart failure. Its clinical importance is now being established in clinical trials worldwide.

Co-Enzyme Q10: A New Drug for Cardiovascular Disease

The clinical experience in cardiology with CoQ10 includes studies on congestive heart failure, ischemic heart disease, hypertensive heart disease, diastolic dysfunction of the left ventricle, and reperfusion injury as it relates to coronary artery bypass graft surgery. The CoQ10-lowering effect of HMG-CoA reductase inhibitors and the potential adverse consequences are of growing concern. Supplemental CoQ10 alters the natural history of cardiovascular illnesses and has the potential for prevention of cardiovascular disease through the inhibition of LDL cholesterol oxidation and by the maintenance of optimal cellular and mitochondrial function throughout the ravages of time and internal and external stresses. The attainment of higher blood levels of CoQ10 (> 3.5 micrograms/ml) with the use of higher doses of CoQ10 appears to enhance both the magnitude and rate of clinical improvement. In this communication, 34 controlled trials and several open-label and long-term studies on the clinical effects of CoQ10 in cardiovascular diseases are reviewed.

Overview of the use of CoQ10 in cardiovascular disease.

Background Increasing numbers of the adult population are using alternative or complementary health resources in the treatment of chronic medical conditions. Systemic hypertension affects more than 50 million adults and is one of the most common risk factors for cardiovascular morbidity and mortality. This study evaluates the antihypertensive effectiveness of oral coenzyme Q10 (CoQ), an over-the-counter nutritional supplement, in a cohort of 46 men and 37 women with isolated systolic hypertension. Methods We conducted a 12-week randomized, double-blind, placebo-controlled trial with twice daily administration of 60 mg of oral CoQ and determination of plasma CoQ levels before and after the 12 weeks of treatment. Results The mean reduction in systolic blood pressure of the CoQ-treated group was 17.8 +/- 7.3 mm Hg (mean +/- SEM). None of the patients exhibited orthostatic blood pressure changes. Conclusions Our results suggest CoQ may be safely offered to hypertensive patients as an alternative treatment option.

Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension

OBJECTIVES This study evaluated the effects of oral therapy with coenzyme Q on echocardiographic and hemodynamic indexes of left ventricular function and on quality of life in patients with chronic left ventricular dysfunction. BACKGROUND Coenzyme Q a coenzyme for oxidative phosphorylation and an antioxidant and free radical scavenger. It has been claimed to improve symptoms, quality of life, left ventricular ejection fraction and prognosis in patients with cardiac failure. METHODS Thirty patients with ischemic or idiopathic dilated cardiomyopathy and chronic left ventricular dysfunction (ejection fraction 26 +/- 6%) were randomized to a double-blind crossover trial of oral coenzyme Q versus placebo each for 3 months. Right heart pressures, cardiac output and echocardiographic left ventricular volumes were measured at baseline and after each treatment phase, and quality of life was assessed using the Minnesota Living With Heart Failure questionnaire. It was calculated that to demonstrate an increase in left ventricular ejection fraction from 25% to 30% with a standard deviation of 5% using 95% confidence intervals with a power of 80% we would require 17 patients. RESULTS Twenty-seven completed both treatment phases. There was no significant difference in left ventricular ejection fraction, cardiac volumes or hemodynamic and quality of life indices after treatment with coenzyme Q placebo, although plasma coenzyme Q levels increased from 903 +/- 345 nmol/l(-1) to 2,029 +/- 856 nmol/l(-1). CONCLUSIONS Inpatients with left ventricular dysfunction, treatment for three months with oral coenzyme Q failed to improve resting left ventricular systolic function or quality of life despite an increase in plasma levels of coenzyme Q to more than twice basal values. (C) 1999 by the American College of Cardiology.

Lack of Effect of Coenzyme Q on Left Ventricular Function in Patients with Congestive Heart Failure

The vectorcardiogram with the FRANK system in patients with hypertension, aortic in-sufficiency, mitral stenosis, pulmonary emphy-serna and atrial septal defect are collected and the criteria of left and right ventricular hypertrophy are presented. The criteria of left ventricular hypertrophy are as follows: 1) The magnitude of the main QRS vector in horizontal plane over 2.00 mV, and/or 2) The angle of the maximal T vector in horizontal plane over + 70°. The criteria of right ventricular hypertrophy are as follows: 1) Sx/Rx over 0.4, 2) The clockwise inscription or figure of eight of the horizontal T loop, and 3) The angle of the maximal T vector in horizontal plane less than O°. The specific criterion of atrial septal defect is the anterior convexity of the afferent limb of the left sagittal QRS loop.

Vectorcardiographic criteria of left and right ventricular hypertrophy with the Frank system.

Clinical Use of Coenzyme-Q for Treatment of Cardiovascular Diseases

Vectorcardiogram in right bundle branch block with frank's system.

The prognosis of cardiac hypertrophy.

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Vectorcardiographic criteria of left and right ventricular hypertrophy with the Frank system.

Clinical Use of Coenzyme-Q for Treatment of Cardiovascular Diseases

Vectorcardiogram in right bundle branch block with frank's system.

The prognosis of cardiac hypertrophy.