Cardiovascular Diseases

In 1972 Folkers and Littaru from Italy documented a deficiency of coenzyme Q10 in human heart disease (Ernster & Dallner 1995).

Since those early reports, a steady stream of research articles have been published and clinical experience in its use as an adjunct to conventional treatment in various forms of heart disease has accumulated. Data from laboratory studies have also accumulated and generally provide a supportive basis for its use.

A review by Langsjoen and Langsjoen of over 34 controlled studies and additional open studies concluded that CoQ10 supplementation goes beyond the correction of a simple deficiency state with strong evidence to show it has the potential to reduce the risk of cardiovascular disease by the maintenance of optimal cellular and mitochondrial function in cardiomyocytes.

Although investigation into specific cardiovascular diseases has been undertaken, the results of an open study of 424 patients suggested that CoQ10 may have widespread benefits. The study found that CoQ10 supplementation produced clinically significant improvements in cardiac function and reduced medication requirements in patients with a range of cardiovascular disorders, including ischaemic cardiomyopathy, dilated cardiomyopathy, primary diastolic dysfunction, hypertension, mitral valve prolapse and valvular heart disease (Langsjoen et al 1994).

A recent review by Langsjoen and Langsjoen (1999) of more than 34 controlled studies and additional open studies concluded that CoQ10 supplementation goes beyond the correction of a simple deficiency state, with strong evidence to show it has the potential to reduce the risk of cardiovascular disease by the maintenance of optimal cellular and mitochondrial function in cardiomyocytes. Congestive heart failure CoQ10 has been reported to improve symptoms of congestive heart failure (CHF) and QOL, and to reduce hospitalisation, and is used as standard therapy for CHF in some parts of Europe, Russia and Japan.

At the cellular level, oxidative stress, mitochondrial dysfunction and energy starvation are believed to play important roles in the aetiology of CHF (Overvad et al 1999). As such it has been suggested that low CoQ10 levels identified in patients with CHF may play a role in disease development (Jeejeebhoy et al 2002) and that restoring myocyte nutrition with vitamin supplementation, including CoQ10, pro- Coenzyme Q10 300

duces significant improvement (Sole & Jeejeebhoy 2002). Furthermore, an inverse

relationship has been found between the severity of CHF and CoQ10 levels in blood from endocardial biopsies.

Clinical studies Currently, over 1 5 RCTs involving subjects with heart failure have been published in addition to numerous open-trials (Bhagavan & Chopra 2005).

One meta-analyses of 8 RCT found that adjunctive therapy with CoQ10 led to significant improvements in total work capacity, cardiac index, cardiac output and stroke volume (Soja & Mortensen 1997). The subjects had cardiomyopathy and CHF of varying aetiologies (idiopathic, dilated, ischaemia, hypertension, valvular heart disease and congenital heart disease).

In 1994, the results were published of a large multicentre trial of 2664 subjects with New York Heart Association (NYHA) classes II and III that had studied the effects of oral CoQ10 (predominantly 100 mg/day) over 3 months (Baggio et al 1994). The percentages of patients experiencing improvements in clinical signs and symptoms of heart failure were: 78% for cyanosis, 79% for oedema, 72% jugular reflux, 53% dyspnoea, 75% palpitations, 80% sweating, 63% subjective arrhythmia, 63% insomnia, 73% vertigo and 54% nocturia. Improvements in at least three symptoms were reported by 54% of subjects.

Currently, the largest controlled trial in adult cardiomyopathy and CHF was reported in 1993 (Morisco et al) and involved 641 patients with NYHA classes III and IV. The double-blind placebo-controlled study used a dose of 2 mg CoQ10 per kg daily over 1 year and found that active treatment significantly improved arrhythmias and episodes of pulmonary oedema, as well as reducing the number of hospitalisations and overall mortality rate. The same researchers conducted a smaller doubleblind crossover study that again produced positive results. Oral CoQ10 (1 50 mg/day) taken for 4 weeks significantly improved ejection fraction (EF), stroke volume and cardiac output in chronic heart failure patients (Morisco et al 1994). A controlled crossover study of 79 subjects with chronic cardiomyopathy and congestive heart failure showed that 3 months treatment with CoQ10 (100 mg/day) significantly improved volume load EF, arteriovenous oxygen difference and QOL assessment (Hofman-Bang et al 1995). Another randomised, double-blind study of 22 heart failure patients (NYHA classes II and III) found treatment for 12 weeks with 200 mg coenzyme Q10 daily improved left ventricular EF (Munkholm et al 1999).

More recently, a double blind, placebo-controlled study involving 39 patients with a NYHA class II or III heart failure due to ischaemic or dilated cardiomyopathy found that despite the small sample size, 1 50 mg oral CoQ10 taken for 3 months resulted in significant improvement of 0.5 class compared with placebo (Keogh et al 2003). Coenzyme Q10 301

Other parameters that showed significant improvements were Specific Activities Scale

class and the 6-mlnute walk-test distance, and there was a significant correlation between the increase in exercise time and the increase in serum CoQ10 level. Of note, patients were also receiving maximal non-beta-blocker therapy.

Although CoQ10 is generally studied in heart failure patients (NYHA class II and III), a double-blind, placebo-controlled, randomised study published in 2004 (Berman et al) describes its effects in end-stage heart failure among patients awaiting heart transplantation. The study of 32 subjects compared Ultrasome CoQ10 (60 mg/day) to placebo over 3 months as an adjunct to conventional therapy. Significant improvements in functional status, clinical symptoms and QOL were reported for CoQ10; however, no significant changes in the echocardiography parameters (dimensions and contractility of cardiac chambers) or ANF and TNF blood levels were observed.

These results are clearly encouraging; however, three controlled studies in CHF have failed to demonstrate an additional improvement with CoQ10 above that achieved for pharmaceutical therapy (Khatta 2000, Permanetter et al 1989, Watson et al 1999). One theory proposes that the most profound effects on myocardial function occur when supplementation is given shortly after the diagnosis of CHF and before the development of irreversible myocyte loss and fibrosis. Some commentators have suggested that the sample sizes, severity and duration of disease, treatment dose and duration of treatment may have contributed to the neutral effects observed (Langsjoen 2000). An important issue that often fails to be considered is the measurement of plasma and myocyte CoQ10 concentrations and whether supplementation has achieved levels that are within the range likely to produce clinical results.

The review by Langsjoen and Langsjoen in 1999 suggests that maximal effects on the mitochondrial bioenergetics of the heart muscle appear to require above normal plasma levels.

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