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 nowadays the main cause of CHF in most countries.52 In recent years, most research effort about CHF 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 recognised and corrected if possible. For instance, CHF is now seen also as a metabolic problem, with endocrine and immunological disturbances potentially contributing to the progression of the disease.53,54 In particular, the role of the tumour necrosis factor (TNF) is discussed below. Recently it has also been recognised that increased oxidative stress may contribute to the pathogenesis of CHF.55 The intimate link between diet and oxidative stress is obvious, since the major antioxidant defences of our body are derived from essential nutrients.56 See below the section about the antioxidant nutrients.
While it is generally considered that a high sodium diet is detrimental (and may result in acute decompensation of heart failure through a volume overload mechanism), little is known about other aspects of diet in CHF in terms of both general nutrition and micronutrients such as vitamins and minerals. In these patients, it is important not only to take care of the diagnosis and treatment of the CHF syndrome itself, and for the identification and aggressive management of traditional risk factors of CHD such as high blood pressure and cholesterol
(because they can aggravate the syndrome), but also for the recognition and correction of malnutrition and of deficiencies in specific micronutrients.
The vital importance of micronutrients for health and the fact that several micronutrients have antioxidant properties are now fully recognised. These may be as direct antioxidants, such as vitamins C and E, or as components of antioxidant enzymes: superoxide dismutase or glutathione peroxidase.56 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 formation57 and reduced antioxidant defences58 and that vitamin C may improve endothelial function in patients with CHF.59 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.18,60 Taken altogether, these data suggest (but do not demonstrate) that antioxidant nutrients may help prevent CHF in post-infarction patients.
Other nutrients, however, may be also involved in certain cases ofCHF. While deficiency in certain micronutrients, whatever the reason, can 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 such as nausea, loss of appetite and early feeling 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 they can contribute to the development and severity of CHF, they should be recognised and corrected as early as possible.
Finally, it has been shown that up to 50 per cent of patients suffering from CHF are malnourished to some degree,61 and CHF is often associated with weight loss. There may be multiple aetiologies to the weight loss,62 in particular lack of activity resulting in loss of muscle bulk and increased resting metabolic rate. There is also a shift towards catabolism with insulin resistance and increased catabolic relative to anabolic steroids.63 TNF, sometimes called cachectin (see above), is higher in many patients with CHF,53,63 which may explain weight loss in these patients. Interestingly, there is a positive correlation between TNF and markers of oxidative stress in the failing heart64 suggesting a link between TNF and antioxidant defences in CHF (the potential importance of TNF in CHF is discussed below in the section on dietary fatty acids and CHF). Finally, cardiac cachexia is a well-recognised complication of CHF, its prevalence increases as symptoms worsen65 and it is an independent predictor of mortality in CHF patients. However, the pathophysiological alteration leading to cachexia remains unclear and, at present, there is no specific treatment apart from the treatment of the basic illness and correction of the associated biological abnormalities.
As mentioned above, an important practical point is that deficiencies in specific micronutrients can both aggravate and cause CHF. The prevalence of these deficiencies among patients with CHF (and post-infarction patients) is unknown. Whether we should systematically search for them also remains unclear. In particular, we do not know whether the association of several borderline deficiencies that do not individually result in CHF may result in CHF, especially in the elderly. For certain authors, however, there is sufficient evidence to support a large-scale trial of dietary micronutrient supplementation in CHF.66
There is not room here to fully explore the present knowledge in this field. Nevertheless, if we restrict our comments to human data, the situation can be summarised as follows. Cases of hypocalcaemia-induced cardiomyopathy (usually in children with a congenital cause for hypocalcaemia) that can respond dramatically to calcium supplementation have been reported.67 Hypomagnesaemia is often associated with a poor prognosis in CHF,68 and correction of the magnesium levels (in anorexia nervosa for instance) leads to an improvement in cardiac function. Low serum and high urinary zinc levels are found in CHF,69 possibly as a result of diuretic use, but there are no data regarding the clinical effect of zinc supplementation in that context. In a recent study, plasma copper was slightly higher and zinc slightly lower in CHF subjects than in healthy controls.58 As expected, dietary intakes were in the normal range and no significant relationship was found between dietary intakes and blood levels in the two groups. It is not possible to say whether these copper and zinc abnormalities may contribute to the development of CHF or are simple markers for the chronic inflammation known to be associated with CHF.53 63 Further studies are needed to address the point, since the implications for prevention are substantial.
Selenium deficiency has been identified as a major factor in the aetiology of certain nonischaemic CHF syndromes, especially in low-selenium soil areas such as eastern China and Western Africa.70 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.71 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. Whereas 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.58 Actually, in the Keshan area, the selenium status coincides with the 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 the non-endemic areas, the mortality rate declined significantly but clinically latent cases were still found and the echocardiographic prevalence of the disease remained high.70 What we learn from Keshan disease and other studies conducted elsewhere58 is therefore that in patients with a known cause of CHF, even a mild deficiency in selenium may influence the clinical severity of the disease (tolerance to exercise).
These data should serve as a strong incentive 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 an exercise inability disproportionate to their cardiac dysfunction. Finally, low whole blood thiamine (vitamin B1) levels have been documented in patients with CHF on loop diuretics and hospitalised elderly patients, and thiamine supplementation induced a significant improvement in cardiac function and symptoms.72
3.3.2 Dietary fatty acids and sodium intake, 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 also SCD), as well as for cardiovascular and all-cause mortality and morbidity.73'74
The cause of LVH is largely unknown. Whereas male gender, obesity, heredity and insulin resistance may explain some of the variance in LVH, hypertension (High blood pressure, HBP) is generally regarded as the primary culprit.75 Thus, the risks associated with LVH and HBP are intimately linked. Recent data have suggested that low dietary intake of polyunsaturated fatty acids and high intake of saturated fatty acids, as well as HBP and obesity, at age 50 predicted the prevalence of LVH 20 years later.76 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 there was no adjustment for other potential dietary confounders, such as magnesium, potassium, calcium and sodium. Thus this study did not provide conclusive data on the dietary lipid determinants of LVH.76 However, it does suggest that dietary fatty acids may be involved in the development of LVH and that this 'diet-heart connection' may partly explain the harmful effect 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.5363 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.77 Finally, various anti-cytokine and immuno-modulating agents were shown to have beneficial effects on heart function and clinical functional class in patients with advanced CHF78 suggesting a causal relationship between high cytokine production and CHF. This also suggests that there is a potential for therapies altering cytokine production in CHF. In that regard, it has been shown that dietary supplementation with n-3 fatty acids (either fish oil or vegetable oil rich in n-3 fatty acid) reduces cytokine production at least in healthy volunteers.79,80 An inverse exponential relationship between leucocyte n-3 fatty acid content and cytokine production by these cells was found, most of the reduction in cytokine production being seen with eicosapentanoic acid in cell membrane lower than 1 per cent, a level obtained with rather moderate n-3 fatty acid supplementation.80 However, further studies are warranted to test whether (and at which dosage) dietary n-3 fatty acids may influence the clinical course of CHF through an anti-cytokine effect.
Sodium intake is the environmental factor that is currently most suspected of influencing blood pressure and the prevalence of HBP. However, the full damaging potential of high sodium intake for the heart (and also the kidney) seems to be largely independent of the blood pressure effect of sodium. Animal experiments and clinical studies have consistently shown that high sodium intake is a powerful and independent determinant of LVH and that such an effect of salt that is not related to arterial pressure is not confined to the heart.81,82 Whereas the long-term effect of a reduced sodium intake after a recent AMI is unknown, in particular on LVH, experts claim that even a 50 mmol reduction in the daily sodium intake would reduce the average systolic blood pressure by at least 5 mmHg (in patients aged over 50 years) and CHD mortality by about 16 per cent. Thus, as regards the damaging effect of high sodium intake on the heart, and despite the lack of strong data showing the beneficial effect of reducing sodium intake in that specific group of patients, we believe that cardiologists should extend their dietary counselling about sodium not only to the patients with HBP or CHF but also to all post-infarction patients.
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