The Role of Nutritional Status in Elderly Patients with Heart Failure

Abstract

Evidence indicates that malnutrition very frequently co-occurs with chronic heart failure (HF) and leads to a range of negative consequences. Studies show associations between malnutrition and wound healing disorders, an increased rate of postoperative complications, and mortality. In addition, considering the increasing age of patients with HF, a specific approach to their treatment is required. Guidelines proposed by the European Society of Cardiology (ESC) for treating acute and chronic HF refer to the need to monitor and prevent malnutrition in HF patients. However, the guidelines feature no strict nutritional recommendations for HF patients, who are at high nutritional risk as a group, nor do they offer any such recommendations for the poor nutritional status subgroup, for which high morbidity and mortality rates have been observed. In the context of multidisciplinary healthcare, recommended by the ESC and proven by research to offer multifaceted benefits, nutritional status should be systematically assessed in HF patients. Malnutrition has become a challenge within healthcare systems and day-to-day clinical practice, especially in developed countries, where it affects the course of disease and patients' prognosis.

Introduction

Heart failure (HF) typically develops as the final stage in a range of cardiovascular diseases (1). As a chronic, progressive disease, it predisposes the patient to various adverse health outcomes. Nutritional status seems to be one of the important factors contributing to the development of HF (2).

Malnutrition has become a challenge within healthcare systems and day-to-day clinical practice, especially in developed countries, where it affects the course of disease and patients' prognosis (3). Both chronic disease and acute clinical conditions may induce or intensify processes resulting in poor nutritional status (4).

The deterioration of nutritional status is correlated with an increase in brain natriuretic peptide (BNP) levels, demonstrating the link between nutrition and disease progression (2). This is a mechanism of patients with increased filling heart pressures. In elderly individuals, poor nutrition may be related not only to the concurrent chronic disease, but may also result from deteriorated cognitive and physical function, the pharmaceutical treatment administered, social isolation or low socio-economic status (5).

The term “malnutrition” is used to indicate a range of nutritional abnormalities (see Figure 1), but it is typically used to denote protein–energy undernutrition, which in cases of HF is caused by complex mechanisms (1, 6).

Figure 1.

A conceptual tree of nutritional disorders (18)

Guidelines proposed by the European Society of Cardiology (ESC) for treating acute and chronic HF refer to the need to monitor and prevent malnutrition in HF patients. However, the guidelines feature no strict nutritional recommendations for HF patients, who are at high nutritional risk as a group, nor do they offer any such recommendations for the poor nutritional status subgroup, for which high morbidity and mortality rates have been observed. Evidence is also lacking in terms of the safe and effective treatment of cardiac cachexia (7).

In the future, data is to be provided by the PICNIC Study, investigating whether nutritional interventions could modify the course of disease, rehospitalization rates, quality of life, and mortality in a group of HF patients (8). In line with guidelines set by the European Society of Clinical Nutrition and Metabolism (ESPEN), all patients should undergo nutritional risk assessment on hospitalization (9).

Despite risk stratification, only a small percentage of patients receive nutritional support. This is likely due to poor awareness of the medical, economic, and social consequences of the issue, and to inadequate hospital practices that either ignore nutritional status or contribute to an insufficient supply of nutrients (4).

In the context of multidisciplinary healthcare, recommended by the ESC and proven by research to offer multifaceted benefits, nutritional status should be systematically assessed in HF patients (1).

Epidemiology of malnutrition in heart failure

Evidence indicates that malnutrition very frequently co-occurs with chronic HF. The prevalence of malnutrition in this patient group is as high as 69%, regardless of age, sex or left ventricular ejection fraction (3). For hospitalized patients, the prevalence is approx. 50%, but may be higher, especially in the elderly (4, 10). This seems to hold special significance in the context of the frequent hospitalizations of HF patients, as this significantly increases nutritional risk. Moreover, malnutrition is found in 10–25% of patients undergoing cardiac surgery, which affects perioperative risk (11).

In patients with valvular heart disease, malnutrition is three times as frequent as in those with coronary heart disease. This is most likely due to underlying hemodynamic changes and an inflammatory response in this patient group. 80% of malnourished patients die or are rehospitalized within 12 months, versus 30% of patients with normal nutritional status (8).

Nutritional status disorders in the elderly

Nutritional deficiency in the elderly

Many elderly people over 60 years of age do not fulfill the daily requirements for micro- and macronutrient intake (12, 13, 14, 15, 16, 17). In a small study on a group of elderly patients >65 years of age, Yan et al. found that micronutrient intake was below recommended levels for a range of nutrients, e.g. vitamin E, vitamin D, fiber, and magnesium. For macronutrients, no such deficiency was found, as the average daily energy intake was approximately 2500 kcal/day (15).

Even though nutrition intake per se is in line with nutritional recommendations, nutrition requirements differ depending on age, sex, and energy expenditure. In a study by Power et al. it was found that elderly community-dwelling 64–93-year-olds did not have an adequate intake of calcium, magnesium, vitamins D and C, folate, zinc, and vitamin B6 (16).

Participants in the latter study were classified as overweight or obese based on their body mass index (BMI). However, BMI is not a complete measure of nutritional status, i.e. it is not sufficient to rule out or confirm poor nutritional status, and it is therefore important to determine nutritional status in accordance with clinical recommendations (18).

Nutritional disorders in the elderly

Elderly people with insufficient micro- and macronutrient intake can be expected to suffer from a range of nutritional disorders. Malnutrition, sarcopenia, and frailty are frequent problems among elderly patients, resulting in poor health outcomes. The prevalence of malnutrition and the risk of malnutrition, as determined by the Mini Nutritional Assessment (MNA), range between 2.7% and 19%, and between 28% and 58%, respectively (19, 20, 21, 22). Low protein and energy intake are key factors in the development of malnutrition.

The prevalence of sarcopenia, defined by loss of muscle mass and muscle strength (23), is up to 32%. Loss of muscle mass and strength leads to difficulties in walking, which in turn have a negative impact on daily physical functioning (24). As a consequence, sarcopenia contributes to disability, falls (24) and a low quality of life (25).

Furthermore, sarcopenia is closely related to frailty, which can be identified in patients fulfilling three out of five of the following criteria: weight loss, weakness, exhaustion, slowness, and low activity (26).

Nutritional status disorders in heart failure

Data from the Framingham Heart Study (FHS) provide many significant insights on the population of HF patients. Its results indicate that overweight and obese men and women are at a higher risk of HF than those with a normal body weight. However, the situation differed regarding the risk assessment in patients who already had HF. In this group, overweight and obesity were factors decreasing the risk of mortality. This observation has been corroborated by numerous studies and termed “the obesity paradox” (27).

A study by Casas-Vara (28) formed two hypotheses based on the above correlation.

Firstly that excess body fat contributes to a neutralization of tumor necrosis factor alpha (TNF-α) and lipopolysaccharides, and increases adipokine production. Secondly, excess body fat is correlated with other beneficial factors, such as young age, increased muscle mass, increased protein levels, increased muscle strength, and increased exercise tolerance. In the study, for patients with HF, obesity was correlated with better nutritional status, higher muscle mass, better immune capacity and better prognosis. Additionally, nutritional status worsened as New York Heart Association (NYHA) functional class and age increased. Patients with higher BMI values showed a better nutritional and functional status than those with a lower body mass index.

Some analyses suggest that the BMI, which is commonly used to determine nutritional status, and was used in the Framingham study and in formulating the obesity paradox, is not actually sensitive to malnutrition in patients with heart disease, as it does not reflect adequate energy intake in HF patients (2). Furthermore, in HF patients, the BMI may in fact mask malnutrition due to the frequent occurrence of edemas in this patient group. The presence of edemas in HF complicates the assessment of body weight loss over time (9).

Thus, other nutritional status criteria make better independent predictors of survival than the BMI. The BMI should not be used as the only criterion for assessment in a clinical setting (29). In a study by Gastelurrutia et al., malnutrition was found in 53% of patients with a normal body weight, 42% of overweight patients and 27% of obese patients (6).

HF is a clinical syndrome with a progressive course, often leading to cardiac cachexia, which in turn is a significant predictor of mortality in chronic HF, independent of age, NYHA functional class, and left ventricular ejection fraction (2, 30). Cardiac cachexia is defined as weight loss equal to at least 6% of initial body weight, occurring within the previous 6 – 12 months, which is unintentional and not caused by edema treatment (31). The prevalence of cardiac cachexia may depend on the diagnostic criteria used and on the functional class in HF (1).

The prevalence of cardiac cachexia is estimated at 12–15% for NYHA functional class II–III. The prevalence increases by 10% annually in NYHA class III–IV (32). It should be noted that the range of prevalence depends of the method for diagnosis. Several studies have demonstrated that using bioelectrical impedance vectorial analysis (BIVA) cachexia achieved till 47% in stable HF patients (33, 34).

Patients with cardiac cachexia are found to have higher concentrations of adiponectin and ghrelin, as well as higher levels of inflammatory markers such as interleukin 6 (IL-6) and TNF-α. TNF-α activation induces cell apoptosis and activates protein degeneration, and is also partly responsible for decreased blood flow in the muscles (1).

The interdependencies between metabolic and inflammatory markers, appetite-regulating hormones and actual nutritional status in chronic HF patients remain poorly understood (35).

Assessment of nutritional status in heart failure

Regarding prevention, the regular assessment of nutritional risk in HF may provide much prognostic data and help prevent negative outcomes (3). Nutritional status screening for hospitalized chronically-ill patients is essential in good clinical practice, offering a simple method for the effective identification of high nutritional risk groups (11). Though numerous research instruments are available, a clear indication of those instruments with the highest predictive value in HF is still lacking (3).

With no gold standard for assessing the nutritional status of HF patients, the prevalence of malnutrition in the study group depends on the diagnostic criteria and screening instruments used (9). Studies assessing nutritional risk in patients with HF have used the following research instruments: a) Subjective Global Assessment (SGA); b) Nutritional Risk Index (NRI); c) Nutritional Risk Screening; d) Malnutrition Universal Screening Tool (MUST); e) Controlling Nutritional Status (CONUT); f) Geriatric Nutritional Risk Index (GNRI); g) Prognostic Nutritional Index (PNI); and h) Mini Nutritional Assessment (MNA).

The latter questionnaire is recommended for the identification of high nutritional risk patients, especially among the elderly, by the ESPEN and other entities. In HF, this questionnaire may provide added value in identifying nutritional risk groups, alongside the BMI and unintentional weight loss assessment (36).

An algorithm for choosing the most relevant instrument for assessing nutritional risk in HF patient populations was presented by Sargeto et al. (29). In accordance with the algorithm, the MNA is an adequate instrument for the assessment of the nutritional status of those with advanced or acute HF, both in and out of hospital. MNA results are a good predictor of in-hospital and long-term mortality. What is more, it allows for a reliable assessment of eating habits and is easy and quick to complete. These aspects are important in screening. Furthermore, the MNA may be useful in planning prevention programs for elderly patients with concurrent frailty (5).

Biochemical markers of nutritional status

Body weight and composition are linked to biochemical parameters in patients with advanced chronic HF, and should be included in the prognosis for these patients. A low body weight and decreased values of the biochemical parameters of nutritional status are significant negative prognostic factors in chronic HF (37).

Biochemical tests allowing for the assessment and monitoring of nutritional status, may be used as a basis for nutritional interventions, and are highly reproducible and objective (38). Routine tests include albumin, transferrin and prealbumin measurements. Concentrations of these proteins decrease in the malnourished and ill, and protein deficiency occurring for any reason always negatively impacts prognosis, increasing mortality and the risk of complications (39). Blood albumin levels also enable the classification of malnutrition. Albumin levels of 3.4–3.0 g/dL indicate mild malnutrition, 2.9–2.1 g/dL — moderate, and below 2.1 g/dL — severe malnutrition (40).

Approximately 20% of patients are found to have low blood albumin (<3.5 g/dl) on admission to hospital. After a week of hospitalization, the number of hypoalbuminemic patients increases by 7.9% (41). Protein malnutrition is linked to the overproduction of TNF and other proinflammatory factors that intensify disease processes (42). It also contributes to hematopoietic factor deficiencies. Thus, in malnourished patients, decreased hemoglobin and hematocrit levels are observed, and anemia is a significant negative prognostic factor in chronic HF (43).

Due to a range of factors, transferrin is not a specific indicator of malnutrition, but because of its short half-life of 8 days, its concentration in the blood reflects dynamic changes in the patient's system. Normal transferrin levels range from 176 to 315 mg/dL. Severe malnutrition is indicated by values below 117 mg/dL (40). The 2-day half-life of prealbumin allows for the rapid monitoring of changes in peritoneal protein synthesis. This indicator is specific for impaired protein synthesis in the liver, which may contribute to malnutrition. Normal prealbumin levels range from 18 to 45 mg/dL, with values below 5 mg/dL indicating severe malnutrition (40).

Albumin levels indicate nutritional status over a longer period, while transferrin and prealbumin levels, along with fibronectin, which has a 4-hour half-life, and retinol-binding protein, with a half-life of 12 hours, are sensitive markers of rapid change in nutritional status, and are therefore particularly useful in monitoring the effectiveness of nutritional intervention. Out of these proteins, fibronectin is the one whose serum levels are the least affected by liver damage, which makes it especially useful in assessing nutritional status. Although C-reactive protein (CRP) is not strictly a marker of nutritional status, as an acute-phase protein it signals increased protein–energy demand and the possibility of cachexia (44).

In pathological states, a significant impairment of lipid metabolism occurs, justifying lipid profile testing for total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL) and triglycerides in chronic HF patients. Genetic tests, observation and interventions have shown the significance of lipid disorders, especially hypercholesterolemia and atherogenic dyslipidemia (high triglycerides, low HDL), in the development of HF (7, 45).

Useful biochemical markers of nutritional status also include electrolyte concentrations, e.g. sodium, potassium, magnesium, and calcium. Sodium regulates extracellular osmoticity, and sodium deficiency from malnutrition negatively affects the water balance in the body. Magnesium is a co-factor in numerous enzyme systems responsible for normal metabolic processes, and participates in maintaining membrane equilibrium, together with sodium and potassium ions. Magnesium and calcium are bound by albumins in the serum, therefore albumin concentrations must be considered when analyzing the concentrations of these ions (44).

Frailty and nutritional status in heart failure

Considering the increasing age of patients with HF, a specific approach to their treatment is required, with more attention paid to geriatric conditions, e.g. frailty. The identification of frailty in patients with HF is important from a clinical point of view, as this condition adversely affects the course of HF (46, 47, 48).

Frailty is defined as a multidimensional physiological syndrome which mainly occurs in people over 65 years of age. Although several definitions of frailty have been proposed recently, no single definition of this condition is as yet fully acceptable. One of the first frailty syndrome (FS) definitions, still frequently used in the clinical setting, was proposed in 2001 by Fried et al. (26) based on the Cardiovascular Health Study (CHS). In the study, the biological phenotype of frailty was identified, which incorporates such elements as build, nutritional status and psychomotor status. Five physical indicators of FS were identified: weight loss, sarcopenia, poor nutritional status, a low level of physical activity, and limited physical abilities; these constitute risk factors behind adverse outcomes in frail people.

The decline in muscle strength and mass with aging may be linked to physical frailty, falls, functional decline, and impaired mobility in very elderly people (exercise, training and nutritional supplementation for physical frailty in very elderly people) (49).

HF is associated with elevated resting metabolic rate and catabolic/anabolic imbalance (50). The prevalence of cachexia among patients with NYHA classes II–IV is 12–15%, and mortality in chronic HF patients with cardiac cachexia is 2–3 times higher than in non-cachectic subjects with this condition (51). Cardiac cachexia can be defined as weight loss >6% of a previous stable weight without evidence of fluid retention, during the past 6 months (52). Guidelines proposed by the ESC recommend assessing nutritional status. Anker et al. identified cachexia as a strong independent risk factor for mortality in patients with chronic HF, together with low peak oxygen consumption (51).

Many clinical features of cachexia, e.g. fatigue, muscle weakness, sarcopenia and inflammation, are also observed in frailty syndrome. While weight loss is crucial for the diagnosis of cachexia, it is not necessarily associated with frailty. Decrease in muscle mass can be counterbalanced by an increase in total body mass; this phenomenon is referred to as sarcopenic obesity, and results from a simultaneous decrease in muscle mass and increase in fat mass. Frailty consensus defines four possible treatments for FS: exercise (resistance and aerobic), caloric and protein support, vitamin D supplementation, and a reduction in polypharmacy (53). As mentioned previously, cachexia is an important feature of HF. Although there is no established treatment for cardiac cachexia, available data show the favorable effects of nutritional therapy, micronutrient supplementation, physical activity, neurohormonal blockade, immunomodulatory agents, anabolic steroids, and appetite stimulation (54).

Some studies on elderly individuals have shown low levels of vitamin D to be associated with limited physical activity and a high frailty index, both in patients with and without HF (55). Therefore, supplementation with vitamin D has a positive influence on muscle strength and balancing ability, as shown by extended walking distance and a reduced frequency of falls (56).

Consequences of malnutrition in heart failure

Malnutrition leads to a range of negative consequences in patients with chronic HF. Studies show associations between malnutrition and wound healing disorders, an increased rate of postoperative complications, and mortality (10).

Regarding cardiac surgery, it is assumed that perioperative nutritional support reduces postoperative complications. This is in line with the guidelines of the ESPEN, which state that patients at high nutritional risk undergoing major surgery should receive nutritional support starting 10–14 days before the planned procedure (11).

Patients at high nutritional risk are also at a higher risk of cardiovascular death, i.e. death from HF progression, myocardial infarction, cerebrovascular accident, other vascular conditions or sudden cardiac death, than patients not at risk of malnutrition. After adjusting for age, sex, NYHA functional class, and BNP level, malnutrition still remains an independent risk factor for mortality (3).

A study by Lourenco et al., investigating nutritional status and nutrient and energy intake in HF patients, found either reduced muscle mass or a risk of muscle mass reduction in nearly 40% of participants (11). Apart from a muscle mass decrease, patients with cardiac cachexia experience loss of fat and bone mass, jointly contributing to a lower body weight (1).

Malnutrition resulting in deteriorated musculoskeletal function affects patients' functional capacity, resulting in the risk of adverse events such as falls. Notably, falls are among the main causes of disability in the elderly population. In hospitalized patients, deteriorated functional capacity may be predicted by lower dynamometer grip strength test results, correlated with decreased total protein (4).

The literature often describes a link between the duration of hospitalization and HF patients' nutritional status: the risk of malnutrition increases together with the length of stay in hospital (10). In hospitalized patients, malnutrition estimated using the MNA questionnaire is correlated not only with an increased stay in hospital, but also with an increased risk of rehospitalization and of death, both in and out of hospital (8).

Mortality data for patients with cardiac cachexia are very unfavorable: 18% die within three months, 29% within six, and 50% within 18 months (30). In a study by Bonilla-Palomas et al. (36), the annual mortality rate for patients identified as malnourished in the MNA was 56%, versus 23.5% in the high nutritional risk group, and 11.3% in patients with normal nutritional status. The risk of complications such as bedsores, wound infections, pneumonia, and kidney failure in hospitalized patients is higher in high nutritional risk groups (9).

Nutritional recommendations

Nutritional support is currently considered an essential part of chronic HF treatment, aimed at improving patients' nutritional status, replenishing energy reserves, building skeletal muscle tissue, and enhancing physical fitness (1, 57). The understanding of links between HF and nutritional disorders allows for early prevention and interventions to improve the patients' health and prognosis. An individual approach to malnutrition diagnosis and treatment in HF patients is always required (58).

Interventions in HF patients are more difficult due to dealing with multimorbidity, as most of the available nutritional guidelines and recommendations are related to a single condition. Chronic co-morbidities in HF patients necessitate the modification of treatment, while the use of diuretics and anticoagulants may result in unfavorable interactions with some nutritional components. The use of loop diuretics contributes to decreased levels of potassium, sodium, and magnesium, and to hypoglycemia, hyperlipidemia, and hyperuricemia. Anticoagulant treatment can result in mucosal damage and gastrointestinal bleeding. Apart from insufficient nutrient intake, malnutrition can result from the treatment used. Even small doses of digoxin may cause food aversion, nausea, and vomiting. ACE inhibitors decrease appetite, resulting in drug-induced anorexia (59, 60, 61).

There is a clear association between oral dryness and the number of medicines taken. Furosemide used jointly with a beta-blocker increases the sensation of dryness, which may be most problematic at lunchtime. One complication present in HF patients is edema of the gastric mucosa and congestion in other internal organs, which decreases peristalsis, leading to appetite loss and constipation.

Limited physical activity, leading to constipation and poor appetite, is another factor contributing to eating disorders in HF patients. Gastrointestinal dysfunction may be related to aging, slower digestion and delayed gastric emptying. A peristalsis-stimulating diet and the use of mild laxatives are the most common methods for improving intestinal function. A properly balanced diet, as well as providing appetizing, high-calorie meals, lays the foundations for the prevention of malnutrition.

The daily calorie intake for patients with cardiac cachexia should amount to 25–30 kcal/kg/day (62). Carbohydrates should account for 50–55%, fats for 30–35%, and proteins for 15–20% of the total daily intake. Energy demand may depend on HF class. Patients in NYHA class III–IV show increased metabolism compared to healthy individuals. Protein intake is also higher in HF patients than in the general population, ranging from 1.1 g/kg dry body weight/day in patients with normal nutritional status to 1.5–2.0 g/kg dbw/day in malnourished patients with cardiac cachexia and patients with protein loss from nephropathy and/or intestinal absorption disorders (62, 63, 64).

Care must be taken with regard to hypo- and hyperalimentation. Excess energy supply is associated with physiological stress and increased serum levels of catecholamine and insulin, as well as impaired water and sodium absorption, hepatic dysfunction, and HF aggravation (57, 64, 65).

Excess energy supply from an unbalanced diet and excessive calorie intake may in some cases contribute to the development and progression of circulatory failure, via a mechanism of glucotoxicity and lipotoxicity.

Recommendations include limiting the intake of saturated and trans fats, cholesterol, and monosaccharides. In patients with HF, hyperglycemia leads to changes in the redox system, increasing oxidative stress and decreasing nitric oxide levels, resulting in endothelial dysfunction (60, 62).

Omega-3 supplementation is recommended by HF treatment guidelines as supportive treatment. Research suggests that omega-3 supplementation may enhance ventricular systolic function and physical fitness, and decrease the number of hospitalizations, inflammatory marker levels, and HF mortality (59, 60).

Patients with HF often have micronutrient deficiencies. This is mainly due to prolonged diuretic treatment, low micronutrient intake, and increased micronutrient loss. Mineral supplementation can reduce the symptoms and increase effort tolerance. Published studies demonstrate the positive impact of microelement supplementation on quality of life, compared with a placebo. However water-soluble vitamins should be prescribed with caution in patients receiving chronic diuretic treatment. The available studies suggest supplementing mineral elements, but no consensus has been established, and authors affirm the need for further studies (64, 66, 67).

Sodium intake restrictions are included in HF management guidelines. Divergent data from published studies do not allow for a determination of the optimum sodium intake in the daily diet. Sodium intake restriction seems most important in the diet of patients with NYHA classes III and IV, down to 0.8–1.6 grams in severe HF. For elderly patients, salt restriction is difficult to accept and negatively affects perceived quality of life. Thus, herbs are used as an alternative method of enhancing taste and increasing food intake. The best method for limiting salt intake is its removal from the table, in order that salt is not added to the dish.

Vitamin B1 deficiencies have been reported in patients with HF undergoing chronic diuretic treatment and in elderly patients with low body weight and severe co-morbidities (68, 69). Thiamine plays a role in the biochemical processes occurring in the heart, muscles, and the nervous system. A deficiency may intensify HF and deregulate oxygen metabolism. B1 supplementation improves left ventricular ejection fraction. It is suggested that its level is not only measured in malnourished patients; supplementation offers the highest number of benefits to patients with alcohol-induced heart disease (70).

The available literature suggests an association between cardiovascular disease and vitamin D deficiency (71). Such a deficiency may contribute to the development of cardiomyopathy, hypertension, and decreased systolic function; however, no studies are available that would suggest optimum doses of the vitamin for HF patients.

Iron is another element of which HF patients tend to have insufficient intake. This deficiency may result from a diet low in iron-rich foods, low assimilability, loss of iron due to gastrointestinal bleeding or impaired red blood cell production, deteriorating kidney function, and the treatment administered. Iron deficiency and anemia impair the transportation of oxygen to the cells, decrease renal perfusion, and increase the symptoms of renal insufficiency (loss of appetite, fatigue, edemas, and ischemia). Compensation for iron deficiency improves both heart and kidney function. Treatment for anemia includes supplementing iron and other nutrients which are lacking, as well as the use of erythropoiesis-stimulating agents. The intravenous administration of iron is believed to reduce symptom intensity, and the recommended dose is one ampule weekly for 4 consecutive weeks (72, 73, 74).

A low supply of iron, folate and vitamin B12 in the diet, combined with the use of acetylsalicylic acid, non-steroid anti-inflammatory drugs, and anticoagulants, increases the risk of anemia. The available studies report that it may affect 17% of HF patients, and that elderly patients with decreased hematocrit have 40% higher mortality than those with normal hematocrit values. Anemia intensifies HF symptoms, increases ischemia, and is an independent risk factor for mortality. Antioxidant depletion and an increase in free radicals in HF patients results from increased oxidative stress. The use of oxidative supportive therapy is tentatively discussed in HF treatment guidelines.

Magnesium is another element that is not sufficiently supplied, and its deficiency in HF patients increases fatigue (66), and may contribute to arrhythmias and decreased glucose tolerance (75). Zinc deficiencies, resulting from low intake and increased zinc elimination with urine, impair taste, appetite, and wound healing, and increase susceptibility to bedsores (2, 76).

Vitamin A and C deficiencies are linked to increasing hypoxia and endothelial cell apoptosis (76). In HF patient care, fluid intake must be monitored, as it should not exceed 1–1.5 liters per day. Fluid intake lower than 1 liter/day necessitates microelement supplementation (59, 65).

Nutritional therapy in heart failure

Treatment options for malnutrition and cachexia are limited. The hormonal and anti-inflammatory drugs available do not deliver satisfactory results (77).

The understanding of each patient's situation, and especially their diet and nutritional status, is essential for improving patient safety and control. Nutritional status can be improved by developing individual nutrition plans, using nutritional status assessment instruments, and raising awareness on proper nutrition.

Enteral nutrition is only administered to HF patients when oral food intake is impossible or when the amount of food consumed fulfills less than 65% of the required daily intake. Enteral nutrition requires the simultaneous implementation of a strategy for cardiac cachexia prevention and treatment.

Even parenteral nutrition administered to stabilize body weight does not prevent muscle mass loss or metabolic disorders.

Treatment should be started with small-gauge tubes, and then progress to larger ones; care must be taken to avoid excess fluid supply. Since smaller volumes are administered, the preparations must have adequate caloric content.

Parenteral nutrition is used to complement enteral nutrition, or in cases where sufficient nutrition can no longer be provided naturally. Hyperalimentation without proper caution can result in decompensated heart disease. Patients with HF have a low tolerance to large volumes administered through a central line, which is used more commonly than peripheral catheters.

Clinical implications

The assessment of nutritional status, nutritional requirements, and appetite should become a routine part of the overall health assessment of HF patients.

Preventing malnutrition and cachexia, as well as supplementing vitamins, minerals and energy intake is important for maintaining and improving HF patients' health, alleviating symptoms, and improving patients' daily functioning.

Consent for publication

All co-authors have agreed to the submission and publication of this manuscript.

Competing interests

The authors declare that they have no competing interests.

Ethical standard

This review paper is in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.