The aim of dietary guidelines is to maintain body weight and follow basic rules to facilitate digestion and avoid certain food-associated reflex stimuli.
Consume the foods listed in Table III daily. This weight-preserving diet is suitable for stable heart failure patients outside the specialist setting (ie, not under the care of a nutritionist and cardiologist), with normal digestion and no malabsorption, and whether of normal weight or obese. Its purpose is twofold:
To maintain body weight in the normal-weight patient.
To control weight loss in the overweight patient. Patients must have a sedentary lifestyle.
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Those following a personalized physical activity program require a specific diet.
Fractionate food intake into >5 meals daily (to avoid overloading the cardiovascular and digestive systems).
Avoiding very hot or very cold foods (vagal reflex risk).
Avoiding stimulants (coffee, tea, cola) that increase myocardial energy consumption.
Carnitine and its derivatives are essential for maintaining cell metabolism, notably oxidative lipid metabolism. Although carnitine may help in severe exercise intolerance, there is no firm evidence favoring propi-onyl-L-carnitine supplementation in heart failure.
Phosphocreatine supplies phosphate to maintain high intracellular ATP levels: creatinine supplementation increases phosphocreatinine synthesis. Although creatinine has been used to increase skeletal muscle strength in heart failure, the results are inconsistent, being positive, if at all, only in muscles with demonstrated creatinine deficiency.
Amino acids in humans are stored predominantly in skeletal muscle. Muscle atrophy is often present in catabolic syndromes such as heart failure. Preliminary data suggest that treatment with specific amino acids alleviates muscle atrophy and/or improves exercise capacity.
Table IV. Diagnosis of malnourishment.
Omega-3 fatty acids omega-3 docosahexaenoic acid (DHA), docosapentaenoic acid (DPA) and eicosapen-taenoic (EPA) acid (fish oils) have numerous biologic effects, including anti-arrhythmic and lipid-lowering actions, and marked antiaggregant activity: EPA competes with arachidonic acid for the conversion of thromboxane and leukotriene, generating homologous products with less proaggregant, anti-inflamma-tory, and vasoconstrictor activity. In the GISSI secondary prevention study, supplementation with EPA+DHA 1 g daily decreased reinfarction by 15% and sudden death by 40%, indirectly confirming the experimental antiarrhythmic activity documented in vitro and in vivo. However, omega-3 fatty acids are very susceptible to oxidative stress due to their high number of double bonds. Mercury salts, occurring in fish, have a direct prooxidant activity, and can be particularly dangerous in the presence of high doses of omega-3 fatty acids. Mercury also binds selenium, thereby inhibiting the selenium-containing antioxidant enzymes. It is therefore important to realize that the mercury in fish may attenuate the protective effect of the omega-3 fatty acids.
Table TV is a guide to the diagnosis of malnourishment in stable sedentary patients with predictable daily life activity. Malnourishment is understood as an imbalance towards a high-calorie state (mainly calories in the table) or high-protein state (mainly protein).
Dietary therapy for cardiac cachexia.
Patients who are clinically unstable or losing weight despite an apparently appropriate diet must be referred to a dietician for personalized therapy. The aim of dietary therapy is to preserve skeletal muscle mass and functional capacity. A high-calorie diet is ineffective for this purpose (protein breakdown in cachexia exceeds.
The potential increase in protein synthesis induced by a high calorie diet). Appetite stimulants increase fat rather than lean mass. Anabolic therapies (eg, growth hormone) have proved ineffective, perhaps due to acquired resistance to the hormone. Studies of anticytokine and anti-inflammatory therapy are ongoing. Meanwhile, physical training and regular exercise have positive nutritional effects even in heart failure.
Anker SD, Rauchhaus M. Insights into the pathogenesis of chronic heart failure: immune activation and cachexia. Curr Opin Cardiol. 1999,14: 211 -216. Anker SD, Volterrani M, Pflaum CD, et al. Acquired growth hormone resistance in patients with chronic heart failure: implications for therapy with growth hormone. J Am Coll Cardiol. 2001;38:443-452.
Kotfer DP. Cachexia. Ann Intern A4ed. 2000;133:622-634.
Witte KK, Clark AL, Cleland JG. Chronic heart failure and micronutrients. J Am Coll Cardiol. 2001 ;37:1765-1774.
Management; therapy; weight loss; cachexia; nutrient deficiency; vitamin; dietary recommendation; nutrition; nutritional supplement.