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In a randomized, double-blind, controlled trial, the effects of oral treatment with coenzyme Q10 (CoQ10, 120 mg/day), a bioenergetic and antioxidant cytoprotective agent, were compared for 1 year, on the risk factors of atherosclerosis, in 73 (CoQ, group A) and 71 (B vitamin group B) patients after acute myocardial infarction (AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02) including non-fatal infarction (13.7 vs. 25.3%, p < 0.05) and cardiac deaths were significantly lower in the intervention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma level of vitamin E (32.4 ± 4.3 vs. 22.1 ± 3.6 umol/L) and high density lipoprotein cholesterol (1.26 ± 0.43 vs. 1.12 ± 0.32 mmol/L) showed significant (p < 0.05) increase whereas thiobarbituric acid reactive substances, malondialdehyde (1.9 + 0.31 vs. 3.1 + 0.32 pmol/L) and diene conjugates showed significant reduction respectively in the CoQ group compared to control group. Approximately half of the patients in each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and both groups had a significant reduction in total and low density lipoprotein cholesterol compared to baseline levels. It is possible that treatment with CoQ 10 in patients with recent MI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of I year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ group. (Mol Cell Biochem246 : 75-82, 2003)

Coronary risk factors such as hypertension, tobacco consumption, hypercholesterolemia and diabetes as well as coronary artery disease (CAD) have become a major health problem in developing and newly industrialized countries despite a moderate increase in fat intake and low rates of obesity. It is a paradox that in some of these countries the increased risk of people to diabetes and CAD, especially at a younger age, is difficult to explain by conventional risk factors. It is possible that the presence of new risk factors especially higher lipoprotein (a) (Lp(a)), hyperhomocysteinemia, insulin resistance, low high density lipoprotein cholesterol and poor nutrition during fetal life, infancy and childhood may explain at least in part, the cause of this paradox. The prevalence of obesity, central obesity, smoking, physical inactivity and stress are rapidly increasing in developing and newly industrialized countries due to economic development and affluence. Many countries in Eastern Europe (such as Slovakia, Poland, and Hungary) and Hong Kong, Singapore and Taiwan that are more affluent have greater prevalence of these adverse effects in comparison to less developed countries such as Philippines, China, Thailand, and Brazil. Hypertension, diabetes and CAD are very low in the rural population of India, China, and in the African sub-continent which has less economic development. However, in urban and immigrant populations of India and Chinese origin, the prevalence of hypertension (> 169/95, 12–20%), diabetes (6–18%) and CAD (7–14%) are significantly higher than they are in some of the developed countries. Mean serum cholesterol (180–200 mg/dl), obesity (5–8%) and dietary fat intake (25–30% en/day) are paradoxically not very high and do not explain the cause of increased susceptibility to CAD and diabetes in some South Asian countries. The force of lipid-related risk factors appear to be greater in these populations due to the presence of the above factors and results into CVD at a younger age in these countries. Available studies support the consensus that people of poor economic origin on rapid nutritional transition may develop CVD at a younger age. They should therefore have lower desirable limits of serum cholesterol, body mass index, dietary fat intake and should also decrease the new risk factors for prevention of CAD. These findings may require modification of the existing guidelines of the International Task Force for Prevention of CAD.

CoQ10 (CoQ10) deficiency has been reported in apparently healthy subjects as well as in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse, diabetes mellitus and after coronary revascularization. Since CoQ10 bolsters the synthesis of ATP and inhibits free radical damage, its administration may be useful in cellular energy production as well as preventing cellular damage during ischaemia-reperfusion injury. Clinical benefits of CoQ10 are mainly due to its ability to improve energy production, antioxidant activity, and membrane stabilizing properties. Several small scale studies indicate that CoQ10 could be useful in patients with congestive heart failure, angina pectoris, cardiomyopathy, coronary artery disease, acute myocardial infarction, diabetes, and in the preservation of myocardium. It may also decrease plasma lipoproteins, insulin and angiotensin converting enzyme. CoQ10 is normally present in the low density lipoprotein cholesterol fraction and inhibits its oxidation, indicating that it can inhibit atherosclerosis. CoQ10 also regenerates vitamin E. These actions of CoQ10 indicate that it can inhibit the development of atherosclerosis and prevent the instability and disruption of plaques. The adverse effects of CoQ10 are minor gastrointestinal discomfort and elevation in SGOT and LDH.

The various mechanisms that may explain the association between brain-heart connection and nutrition, leading to abnormal heart rate variability (HRV) and blood pressure variability (BPV) resulting into increased morbidity and mortality due to cardiovascular diseases (CVD), are reviewed. Medline search til December, 2001 and articles published in various national and international journals were reviewed. Experts working in the field were also consulted. There is compelling evidence that saturated and total fat and sedentary behaviour can enhance sympathetic activity and increase the secretion of catecholamine and serotonin, whereas omega-3 fatty acid supplementation may enhance parasympathetic activity and increase the secretion of acetylecholine in the hippocampus. While increased sympathetic activity has adverse effects on HRV and BPV, increased parasympathetic activity has beneficial effects and can directly inhibit sympathetic tone. A large body of evidence is available demonstrating that abnormal HRV measured over a 24 hour period, or for 7 days, provides information on the risk of subsequent death in subjects with and without heart disease. There is a need to study 7-day record by Holter cardiac monitoring to further elucidate the role of HRV in the pathogenesis of CVD. Meditation, beta blockers, ACE inhibitors, n-3 fatty acids, trimetazidine and oestrogen may have a beneficial influence on HRV. However, no definite and specific therapy is currently available to improve the prognosis for patients with abnormal HRV and blood pressure variability (BPV). Low HRV has been most commonly associated with a risk of arrhythmias and arrhythmic death, unstable angina, myocardial infarction, progression of heart failure and atherosclerosis. There is a need to develop a consensus on the measure of HRV for clinical purposes and whether 7-day record is necessary and practical. New analysis methods based on nonlinear dynamics may be more useful in risk stratification. More precise insight into the patho-physiological link between HRV and nutrition may be applied to clinical practice and used to direct therapy for prevention of disease risk.