The incidence of chronic heart failure (CHF), the common end-result of most cardiac diseases, is increasing steadily in many countries despite (and probably because of) considerable improvements in the acute and chronic treatment of CHD, which is currently the main cause of CHF in most countries.36 In recent years, most CHF research effort has focused on drug treatment, and little attention has been paid to nonpharmacological management. Some unidentified factors may indeed contribute to the rise in the prevalence of CHF and should be recognized and corrected if possible. For instance, CHF is now seen also as a metabolic problem with endocrine and immunological disturbances potentially contributing to its progression.3738 Only recently has it been also recognized that increased oxidative stress may contribute to the pathogenesis of CHF.39 The intimate link between diet and oxidative stress is obvious: the major antioxidant defenses of the body are derived from essential nutrients.40
The vital importance of micronutrients for health and the fact that several micro-nutrients have antioxidant properties are now fully recognized. Micronutrients may function as direct antioxidants such as vitamins C and E or as components of anti-oxidant enzymes such as superoxide dismutase or glutathione peroxidase.40 It is now widely believed (but still not causally demonstrated) that diet-derived antioxidants may play a role in the development (and thus in the prevention) of CHF. For instance, clinical and experimental studies have suggested that CHF may be associated with increased free radical formation41 and reduced antioxidant defences42 and that vitamin C may improve endothelial functions in patients with CHF.43 In the secondary prevention of CHD, in dietary trials in which the tested diet included high intakes of natural antioxidants, the incidence of new episodes of CHF was reduced in the experimental groups.1844 Taken together, these data suggest (but do not demonstrate) that antioxidant nutrients may help prevent CHF in postinfarction patients.
Other nutrients, however, may be also involved in certain cases of CHF. While deficiency in certain micronutrients, whatever the reason, can actually cause CHF and should be corrected (see below), it is important to understand that patients suffering from CHF also have symptoms that can affect their food intake and result in deficiencies, for instance tiredness when strained, breathing difficulties, and gastrointestinal symptoms like nausea, loss of appetite, and early feelings of satiety. Drug therapy can lead to loss of appetite and excess urinary losses in case of diuretic use. All of these are mainly consequences, not causative factors, of CHF. Thus, the basic treatment of CHF should, in theory, improve these nutritional anomalies. However, since the anomalies can contribute to the development and severity of CHF, they should be recognized and corrected as early as possible.
Finally, it has been shown that up to 50% of patients suffering from CHF are malnourished to some degree45 and CHF is often associated with weight loss. The weight loss may be associated with multiple etiologies,46 in particular, the lack of activity resulting in loss of muscle bulk and increased resting metabolic rate. Another factor is a shift toward catabolism with insulin resistance and increased catabolic activity relative to anabolic steroids.47 Tumor necrosis factor (TNF), sometimes called cachectin, is higher in many patients with CHF and may explain their weight losses. Interestingly, there is a positive correlation between TNF and markers of oxidative stress in a failing heart,48 suggesting a link between TNF and antioxidant defenses in CHF (the potential importance of TNF in CHF is discussed in Section 4.3.2). Finally, cardiac cachexia is a well-recognized complication of CHF. Its prevalence increases as symptoms worsen49 and it is an independent predictor of mortality in CHF patients. However, the pathophysiological alteration leading to cachexia remains unclear and, at present, it has no specific treatment apart from treatment of the basic illness and correction of the associated biological abnormalities.
Selenium deficiency has been identified as a major factor in the etiology of certain nonischemic CHF syndromes, especially in low-selenium soil areas such as eastern China and West Africa.50 In Western countries, cases of congestive cardiomyopathy associated with low antioxidant nutrients (vitamins and trace elements) have been reported in malnourished HIV-infected patients and in subjects on chronic parenteral nutrition.51 Selenium deficiency is also a risk factor for peripartum cardiomyopathy.
In China, an endemic cardiomyopathy called Keshan disease seems to be a direct consequence of selenium deficiency. While the question of the mechanism by which selenium deficiency results in CHF remains open, recent data suggest that selenium may be involved in skeletal and cardiac muscle deconditioning (and in CHF symptoms such as fatigue and low exercise tolerance) rather than in left ventricular dysfunction.42 Actually, in the Keshan area of China, the selenium status coincided with clinical severity rather than with the degree of left ventricular dysfunction as assessed by echocardiographic studies. When the selenium levels of residents were raised to the typical levels in nonendemic areas, the mortality rate declined significantly but clinically latent cases were still found and the echocardiographic prevalence of the disease remained high.50 What we learn from Keshan disease and studies conducted elsewhere42 is that even a mild deficiency of selenium may influence the clinical severity of CHF (tolerance to exercise) in patients with known causes of the disease. These data should serve as a strong incentives for the initiation of studies testing the effects of natural antioxidants on the clinical severity of CHF. In the meantime, however, physicians would be well advised to measure selenium in patients with exercise inabilities disproportionate to their cardiac dysfunctions.
Finally, low whole blood thiamine (vitamin B1) levels have been documented in CHF patients on loop diuretics and hospitalized elderly patients, and thiamine supplementation induced significant improvements in cardiac function and symptoms.52
4.3.2 Dietary Fatty Acids, Cytokines, LVH, and CHF
Beyond the well-known effect of high sodium intake in the clinical course of CHF (and the occurrence of acute episodes of decompensation), another important issue is the role of diet in the development of left ventricular hypertrophy (LVH), a major risk factor for CHF and SCD as well as for cardiovascular and all-cause mortality and morbidity.5354
The cause of LVH is largely unknown. While gender, obesity, heredity, and insulin resistance may explain some of the variance in LVH, hypertension (HBP) is generally regarded as the primary culprit.55 Thus, the risks associated with LVH and HBP are intimately linked. Recent data also suggest that low dietary intake of polyunsaturated fatty acids and high intake of saturated fatty acids along with HBP and obesity at age 50 predicted the prevalence of LVH 20 years later.56 Although the source of saturated fatty acids is usually animal fat, the source of unsaturated fatty acids in that specific Scandinavian population and at that time was less clear and no adjustment was made for other potential dietary confounders such as magnesium, potassium, calcium, and sodium. Thus, this study did not provide conclusive data about the dietary lipid determinants of LVH.56 However, it does suggest that dietary fatty acids may be involved in the development of LVH and that this dietheart connection may partly explain the harmful effects of animal saturated fatty acids on the heart.
Another diet-heart connection in the context of advanced CHF relates to the recent theory that CHF also is a low-grade chronic inflammatory disease with elevated circulating levels of cytokines and cytokine receptors that are otherwise independent predictors of mortality.3747 High-dose angiotensin-converting enzyme (ACE) inhibition with enalapril, a treatment that reduces mechanical overload and shear stress (two stimuli for cytokine production in patients with CHF), was recently shown to decrease both cytokine bioactivity and left ventricular wall thickness.57 Finally, various anticytokine and immunomodulating agents were shown to have beneficial effects on heart function and clinical functional class in patients with advanced CHF,58 suggesting a causal relationship between high cytokine production and CHF. This also suggests a potential for CHF therapies that alter cytokine production. In that regard, dietary supplementation with n-3 fatty acids (fish oil or vegetable oil rich in n-3 fatty acid) reduced cytokine production at least in healthy volunteers.5960 An inverse exponential relationship between leukocyte n-3 fatty acid content and cytokine production by these cells was found; most of the reduction in cytokine production was seen with eicosapentanoic acid lower than 1% in cell membranes—a level obtained with rather moderate n-3 fatty acid supplementation.60 Further studies are warranted to test whether (and at what dosage) dietary n-3 fatty acids may influence the clinical course of CHF through an anticytokine effect.
Was this article helpful?