The highest concentration of coenzyme Q10 in the human body is found in the muscle cells of the heart so, not surprisingly; it has been found to benefit those with heart complaints. Simple oral supplementation with coenzyme Q10 caused an increased vigour in failing cardiac systems with significantly better heart efficiency, cardiac output and stroke volume. In a similar manner, those individuals suffering from Angina Pectoris (arising from a disease of the coronary arteries) found benefit after taking the supplement orally. They noticed that they could tolerate exercise much better whilst on the therapy and the incidence of the stabbing pains that are a feature of the condition decreased dramatically.
The early trials on the use of coenzyme Q10 in heart disease were started in 1985 by Dr Folkers and his co-workers. Over an eight year period (1985-1993) they treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10 to their medical course of treatments. Doses of CoQ10 ranged from 75 to 600 mg/day by mouth (average 242mg).
Treatment was primarily guided by the patient’s response. In many instances, however, CoQ10 levels were used with the aim of producing a whole blood level of greater than or equal to 2.0 pg/ml N=297. Patients were followed for an average period of 17.8 months, with a total accumulation of 632 patient years on CoQ10 therapy. Eleven patients were omitted from this study, ten due to non-compliance and one who experienced nausea after starting treatment. There were 18 deaths during the study, 10 attributable to cardiac causes. These patients were divided into the following six diagnostic categories: ischemic cardiomyopathy (ICM) dilated cardiomyopathy(DMC) primary diastolic dysfunction (PDD) hypertension (HTN) mitral valve prolapsed (MVP) and valvular heart disease(VHD).The setting was a private cardiology practice, and includes and expands upon the study they published in 1992.
For the group as a whole and for each diagnostic category, they evaluated clinical response according to the New York Heart Association (NYHA) functional scale and found significant improvement in every group. Of 424 patients 58% improved by one NYHA class 28% by two classes and 1.2% by three classes. A total of 210 patients had pre-treatment following (treatment echocardiograms available for comparison to echocardiograms made during the study period. A small but statistically significant improvement in myocardial function could be documented using the following (echocardiographic) parameters left ventricular (cavity) wall thickness, mitral valve inflow slope and fractional shortening. As expected, most patients were already taking from one to five other cardiac medications. A significant finding in this study was the fact that each
Overall medication requirements dropped considerably. There were no apparent effects from CoQ10 treatment other than a single case of transient nausea. Perhaps their most interesting finding occurred by accident. They found that the commonly available commercial preparations of CoQ10 (in tablets or powder filled capsules) were not always well absorbed unless taken simultaneously with a fat-containing food, with best results obtained when the CoQ10 was chewed and swallowed with peanut butter. In several patients this technique produced fairly striking clinical responses correlating with a prompt elevation of CoQ10 levels.
They concluded that CoQ10 is a safe and effective treatment for a broad range of cardiovascular diseases. This is consistent with an idea put forward for verification that different diseases of the cardiovascular system (whether ischemic, mechanical, infectious, post-infectious or of unknown origin) ultimately share a common pathway, at the cellular level, in their production of myocardial (heart) failure. Oral supplementation with CoQ10 appears to be both protective and restorative in clinical disease states. Not only did they see positive response in individual patients, but there was a reduction in the medical and financial burden of the administration of numerous drugs.
In Denmark, Dr S A Mortensen and his team were also carrying out controlled double-blind trails with CoQ10 in chronic heart failure and angina pectoris (disease of the coronary arteries).
A biochemical rationale for using CoQ10 as a therapy in heart disease had already been established more than 20 years ago by Folkers and co-workers. In their collaborative study with Folkers the levels of coenzyme Q10 in blood and fresh myocardial (heart) tissue (endomyocardial biopsies were studied in a series of 50 patients with heart failure of varying causes. Their measurements revealed a myocardial deficiency of coenzyme Q10 in failing hearts which is higher with increasing severity of the disease and is reduced by oral therapy.
Open clinical studies with Q10 as adjunctive therapy in heart failure 10 years ago were positive, which is why they dared to use the rather strong words that “CoQ10 was a major advance in therapy” This conclusion was due to the following observations.
- The clinical effectiveness of CoQ10.
- It’s safety
- The fact that it heralded a new biochemical avenue in the classification of patients with heart failure and constituted a rationale for therapy beyond the conventional anti-failure principles.
Six international double-blind trails have been conducted on the therapy with CoQ10 in chronic heart failure. A meta-analysis of these trails was presented with emphasis on the Italian and Scandinavian multicentre trails. All studies confirmed the safety and effectiveness of CoQ10 with respect to improvement in symptoms, functional capacity and quality of life. Interestingly, the clinical effects have been achieved above and beyond the status obtained from the traditional principles, probably via correction of a deficiency state-a restorative effect on the myocardium.
A possible role of CoQ10 as adjunctive in ischaemic heart disease is intriguing, however to a lesser degree after investigating in humans. There are solid experimental data to justify further controlled clinical trials with CoQ10 as an attractive metabolic modifier in ischaemic heart disease, especially in the setting of myocardial ischaemia and reperfusion. Till this date there at least 3 double-blind trails unstable angina pectoris confirming that CoQ10 may have anti-ischaemic properties.
The improved myocardial function in failing hearts and the observed anti-anginal effect of CoQ10 in chronic ischaemia support the explanation that mitochondrial dysfunction and energy starvation are prominent in these conditions and that the exhausted bioenergetics-and the decreased utilization efficiency of oxygen-are corrected by coenzyme Q10 replenishment.
CoQ10 SUPPLEMENTATION AND USE WITH ORTHODOX MEDICINES
Coenzyme Q10 does not replace lifesaving drugs but what it does is to complement their action. Doctors have found that the addition of coenzyme Q10 supplements allowed them to reduce the drug dosages in their patients without losing any of the desirable therapeutic results. A reduction in drug dosage meant that the chances of adverse reaction due to these drugs were decreased and in many cases did not materialize at all.
NO ADVERSE EFFECTS REPORTED
Initial reports on new effective drugs in cardiovascular disease are often presented with passion and enthusiasm which is subsequently cooled down after the appearance of adverse reports or drug failure. This has not been the case with CoQ10. This vitamin-like substance fulfils various criteria of a first-line agent in the treatment of chronic heart failure e.g. it is safe and well-tolerated and it improves symptoms. Possibly it may change the natural history of the disease in some cases via a correction of a molecular dysfunction.
FURTHER CONTROLLED AND OPEN TRAILS ON CoQ10
One trail investigated safety and clinical efficacy of CoQ10 adjunctive treatment (main dosage was 100mg/day p.o) in heart failure which had been diagnosed at least 6 months previously and treated with standard therapy. A total of 2664 patients mean age 68.5 years in NYHA (New York Heart Association ) class11 and 111 were enrolled into this open non comparative 3-month, post-marketing drug-surveillance study in 73 Italian centres. Patients statistically evaluable were 2359 (89.8% of pts enrolled 72.7% in NYHA class 11 and 2.3% in NYHA class 111) 155 patients dropped out from the study (5.8%) and 150 patients did not satisfy inclusion criteria or compliance requirement (5.4%) The mean duration of heart failure was 34.6 months, Digitalis, diuretics and ACE-inhibitors were the most commonly used drugs. The assessment of clinical signs and symptoms was made using 2 to 7 point scales. A low incidence of side effects was recorded; 38 adverse reactions were recorded in 36 (1.4%) pts of which only 22 reactions were probably correlated to the test treatment. All reactions were mild and in only 9 cases required treatment withdrawal.
After three months of test treatment the percentage of patients with improvement in clinical signs and symptoms were as follows;
78.1% for cyanosis (blueness in extremities) 78.1% for oedema (swelling of limbs) 77.9% for pulmonary rates.49.3% for enlargement of liver area, 71.8% for jugular reflex, 52.8% for dyspnoea (difficulty in breathing), 75.5% for palpitations, 79.8% for sweating, 63.4% for subjective perception of arrhythmia (irregular heartbeat) 62.9% for insomnia. 73.1% for vertigo and 53.7% for nocturia (excess passing of urine at night). Moreover, the contemporary improvement of at least 3 symptoms in 53.5% of patients may be interpreted as an index of improved quality of life. The clinical improvement was present for both the two classes of patients enrolled and the end-study computing of the scores seems to allow a down-regrading of NYHA class 111 patients to the lower class.
Six patients with congestive heart failure (NYHA class’s 11-1V) were evaluated in a double-blind cross-over study in their haemodynamic response to exercise before and after treatment with CoQ10. After 3 weeks of pharmacological washout the patients underwent the first haemodynamic evaluation during exercise and started the treatment with placebo(P) or CoQ10(50 mg x 3 daily p.o). After 4 weeks they repeated the haemodynamic evaluation and then treatment was inverted, at the end of further 4 week period they repeated the haemodynamic evaluation. No change in exercise tolerance was found during both treatments while CoQ10 induced a significant increase at rest and at exercise peak in myocardial strength compared to the values obtained in control conditions and during P treatment.
The results demonstrated that, despite the unchanged exercise tolerance, the administration of CoQ10 improves cardiac haemodynamic response to exercise in patients with congestive heart failure.