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Cardiac cachexia is a syndrome that has received increased attention in recent years. Although an association between proteolysis and cardiac cachexia has been proposed, the direct influence of oxidative stress on the process has not been demonstrated. In the present study, the right (RH) and left (LH) hearts (atrium and ventricle of each side of the heart) were collected from rats at the 5th and 10th days after phosphate buffer (control) orWalker-256 solid tumour implantation. Immediately after sacrifice, cachexia was determined in tumour-bearing animals by the formula: [(inicial body weight-final body weight+tumour weight+weight gain of control group)/(initial body weight+body mass gain of control group)]×100%; RH and LH were stored until use. Oxidative stress and proteolysis were determined in each collected sample. In addition, heart samples were collected from a separate set of animals to determine the thickness of the left and right ventricles. Cachexia values increased over time after tumour implantation from 6.85% at the 5th day to 17.76% at the 10th day. There was no significant difference in LH wet weight and ventricle thickness compared with the control, where as RH wet weight (0.109±0.09g at the 5th day and 0.093±0.09g at the 10th day) and thickness (420±16μm at the 5th day and 279±08μm at the 10th day) were significantly decreased at both time points when compared with control values (0.153±0.06g and 607±21μm, respectively). tert-Butyl-stimulated chemiluminescence analysis revealed a significant increase in the LH and decrease in the RH oxidative stress profiles. Carbonylated proteins increased in the LH (140%, p0.05) and RH (100%, p0.05) at the 5th day, and significantly decreased in both sides on the 10th day compared to controls. Chemotrypsin-like, caspase-like, and calpain-like activities were evaluated by chemiluminescence, and only calpain-like activity was found to increase at the 5th day in the RH. In the LH, all proteolytic activities systems were decreased when compared with controls. Together, these results demonstrate that oxidative stress appears to play a different role in mass modulation on the LH and RH. The proteolytic systems evaluated herein also appear to have different effects on the responses developed during cardiac cachexia in the two sides of the heart.

Hintergrund: Die Pathophysiologie der kardialen Kachexie ist zurzeit nicht vollständig geklärt. Wir untersuchten den Zusammenhang zwischen rechtsventrikulärer (RV) und hepatischer Funktion und kardialer Kachexie. Methoden: Wir schlossen 118 Patienten mit linksventrikulärer Ejektionsfraktion (LVEF) ≤40% ein und unterteilten diese in drei Gruppen: Patienten in New York Heart Association (NYHA)-Klasse II (n=59), NYHA-Klasse III ohne Kachexie (n=41) und NYHA-Klasse III mit Kachexie (n=18). Bei allen Patienten wurden Blutanalysen, Echokardiographie und Spiroergometrie durchgeführt. Ergebnisse: Eine eingeschränkte systolische RV-Funktion (tricuspid annular plane systolic excursion [TAPSE] ≤15 mm) bestand bei 80% der kachektischen Patienten. Beim Vergleich der Patienten in NYHA-Klasse II mit nicht-kachektischen und mit kachektischen Patienten in NYHA-Klasse III fanden wir einen kontinuierlichen Abfall der systolischen RV-Funktion (Median TAPSE 19 [Interquartilsabstand; IQR: 16-23] mm vs. 16 [IQR: 13-19] mm vs. 14 [IQR: 9-15] mm; Kruskal-Wallis p10 mmHg: 6.8 vs. 27.5 vs. 75.0%; p, Background: The mechanisms involved in cardiac cachexia remain poorly understood. We examined the association of right ventricular (RV) and hepatic dysfunction with cardiac cachexia. Methods: We prospectively enrolled 118 patients with left ventricular ejection fraction (LVEF) ≤40% who were subgrouped as follows: New York Heart Association (NYHA) class II (n=59), NYHA class III without cachexia (n=41) and NYHA class III with cachexia (n=18). All patients underwent blood collection, echocardiography and exercise testing. Results: Reduced systolic RV function (tricuspid annular plane systolic excursion [TAPSE] ≤15 mm), was present in 80% of cachectic patients. When comparing NYHA class II patients vs. non-cachectic and cachectic NYHA class III patients we found a stepwise decrease in systolic RV function (median TAPSE 19 [interquartile range; IQR: 16-23] mm vs. 16 [IQR: 13-19] mm vs. 14 [IQR: 9-15] mm, respectively; Kruskal-Wallis p10 mmHg: 6.8 vs. 27.5 vs. 75.0%, respectively; p

Commentary on Rautiainen S, Levitan EB, Mittleman MA, et al. Total antioxidant capacity of diet and risk of heart failure: a population-based prospective cohort of women. Am J Med 2013;126:494–500.[OpenUrl][1][CrossRef][2][PubMed][3] Heart failure is a syndrome comprising symptoms such as breathlessness alongside objective evidence of cardiac dysfunction. This is a common condition with a considerable economic impact on health services.1 Nutritional intake and status appear to be important in heart failure. Non-intentional weight loss in the setting of heart failure (cardiac cachexia) is an independent predictor of … [1]: {openurl}?query=rft.jtitle%253DAm%2BJ%2BMed%26rft.volume%253D126%26rft.spage%253D494%26rft_id%253Dinfo%253Adoi%252F10.1016%252Fj.amjmed.2013.01.006%26rft_id%253Dinfo%253Apmid%252F23561629%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1016/j.amjmed.2013.01.006&link_type=DOI [3]: /lookup/external-ref?access_num=23561629&link_type=MED&atom=%2Febnurs%2F17%2F3%2F72.atom

Background There are a myriad of proteins responsible for modulation of expenditure of energy. Angiotensin II (Ang II) is a vital component of renin-angiotensin system that affects blood pressure and also linked to both cachexia and obesity via fat and muscle metabolism. Previous research suggests that the direct action of Ang II is on the brain, via angiotensin II type 1 receptor protein, affecting food intake and energy expenditure. The objective of the study is to investigate the effect of 1-sarcosine (SAR)-Ang II infusion on energy expenditure and metabolism in a rat model of congestive heart failure cachexia. Methods Adult female rats of the Sprague Dawley strain (n = 33) were used (11 pair-fed control, 12 ad libitum and 10, 1-sarcosine–angiotensin II-infused rats). Body weight, faecal excretion, feed intake (in grams), water intake (in milliliters) and urine excreted were recorded daily. The measurements were recorded in three different periods (4 days prior to surgery, “pre-infusion”; day of surgery and 5 days postsurgery, “infusion period”; days 7 to 14, “recovery” period). Different analytical methods were used to measure energy expenditure per period, uncoupling protein 3 mRNA expression, crude protein and adipose tissue body composition. Results During the infusion period, the SAR–Ang II group experienced rapid weight loss (p

Cancer cachexia is defined as a multifactorial syndrome of involuntary weight loss characterized by an ongoing loss of skeletal muscle mass and progressive functional impairment. It is postulated that cardiac dysfunction/atrophy parallels skeletal muscle atrophy in cancer cachexia. Cardiotoxic chemotherapy may additionally result in cardiac dysfunction and heart failure in some cancer patients. Heart failure thus may be a consequence of either ongoing cachexia or chemotherapy-induced cardiotoxicity; at the same time, heart failure can result in cachexia, especially muscle wasting. Therefore, the subsequent heart failure and cardiac cachexia can exacerbate the existing cancer-induced cachexia. We discuss these bilateral effects between cancer cachexia and heart failure in cancer patients. Since cachectic patients are more susceptible to chemotherapy-induced toxicity overall, this may also include increased cardiotoxicity of antineoplastic agents. Patients with cachexia could thus be doubly unfortunate, with cachexia-related cardiac dysfunction/heart failure and increased susceptibility to cardiotoxicity during treatment. Cardiovascular risk factors as well as pre-existing heart failure seem to exacerbate cardiac susceptibility against cachexia and increase the rate of cardiac cachexia. Hence, chemotherapy-induced cardiotoxicity, cardiovascular risk factors, and pre-existing heart failure may accelerate the vicious cycle of cachexia-heart failure. The impact of cancer cachexia on cardiac dysfunction/heart failure in cancer patients has not been thoroughly studied. A combination of serial echocardiography for detection of cachexia-induced cardiac remodeling and computed tomography image analysis for detection of skeletal muscle wasting would appear a practical and non-invasive approach to develop an understanding of cardiac structural/functional alterations that are directly related to cachexia.

International audience; Since cardiac cachexia could be associated with alterations in muscular mitochondrial metabolism, we hypothesized that the expected alterations in the activities of mitochondrial oxidative enzymes could be associated with changes in mitochondrial protein synthesis in oxidative skeletal muscles. Cardiac cachexia was provoked in male rats by the ligation of the left coronary artery. Six cachectic and 6 control rats were age-paired, and their food intake was observed. The synthesis of mitochondrial proteins was measured by [1-13C]-valine infusion in soleus, tibilais, myocardium, and liver. Muscles (soleus, gastrocnemius, and tibialis anterior), heart, kidneys, liver, and visceral adipose tissue were weighed. Mitochondrial cytochrome c oxydase IV as well as citrate synthase and myosin ATPase activities were measured. As expected, decreased food intake was observed in the cachectic group. Heart, kidney, and liver weights were higher in the cachectic group, while the visceral adipose tissue weight was lower (P < .01). No changes in muscle weights were observed. Soleus mitochondrial proteins fractional synthesis rate was higher in the cachectic group (P = .054). Cytochrome c oxydase IV activity was reduced (P = .009) and increased (P = .038) in the soleus and liver of the cachectic rats, respectively. No change in citrate synthase activity was observed. Myosin ATPase activity was reduced in the gastrocnemius of the cachectic group (P < .01). Mitochondrial protein synthesis is increased in the soleus of rats with cardiac cachexia, suggesting a compensatory mechanism of the impaired oxidative mitochondrial function. Further work should assess whether the mitochondrial protein synthesis is altered in chronic heart failure patients with cardiac cachexia, and whether this is the cause or the consequence of cachexia.

Objectives: Our study aims to determine the role of serum adiponectin in chronic heart failure (CHF) and cardiac cachexia (CC). Methods: Ninety consecutive patients were included in the study. Patients were divided into three groups: 30 CHF patients with CC, 30 CHF patients without CC, and 30 healthy individuals. Adiponectin levels were measured through human ELISA kits. Results: Levels of serum adiponectin were significantly higher in the CHF patients with cachexia in comparison with the other groups (CHF with CC: 58.4 ± 15.5 ng/ml vs. CHF without CC: 24 ± 6.7 ng/ml and controls: 7.7 ± 3.4 ng/ml; p = 0.001). Serum adiponectin was negatively correlated with BMI, high-sensitivity C-reactive protein, and hemoglobin (r = -0.37, p = 0.02; r = -0.29, p = 0.02; r = -0.18, p = 0.03, respectively) in the CHF patients with cachexia. Additionally, serum adiponectin levels were positively correlated with B-type natriuretic protein levels, left ventricle end-diastolic and end-systolic diameters (r = 0.36, p = 0.02; r = 0.46, p = 0.01; r = 0.49, p = 0.006, respectively) in the CHF patients with cachexia. Conclusion: Our findings suggest that adiponectin may play a critical role in the pathogenesis of cardiac remodeling and anemia in CC.

Heart failure (HF) is the main cause of mortality and morbidity in Western countries. Although evidence-based treatments have substantially improved outcomes, prognosis remains poor with high costs for health care systems. In patients with HF, poor dietary behaviors are associated with unsatisfactory quality of life and adverse outcome. The HF guidelines have not recommended a specific nutritional strategy. Despite the role of micronutrient deficiency, it has been extensively studied, and data about the efficacy of supplementation therapy in HF are not supported by large randomized trials and there is limited evidence regarding the outcomes. The aim of the present review is to analyze the state-of-the-art of nutritional deficiencies in HF, focusing on the physiological role and the prognostic impact of micronutrient supplementation.

Groen BB, Res PT, Pennings B, Hertle E, Senden JM, Saris WH, van Loon LJ. Intragastric protein administration stimulates overnight muscle protein synthesis in elderly men. Am J Physiol Endocrinol Metab 302: E52-E60, 2012. First published September 13, 2011; doi:10.1152/ajpendo.00321.2011.-The loss of skeletal muscle mass with aging has been attributed to an impaired muscle protein synthetic response to food intake. Therefore, nutritional strategies are targeted to modulate postprandial muscle protein accretion in the elderly. The purpose of this study was to assess the impact of protein administration during sleep on in vivo protein digestion and absorption kinetics and subsequent muscle protein synthesis rates in elderly men. Sixteen healthy elderly men were randomly assigned to an experiment during which they were administered a single bolus of intrinsically L-[1-(13)C] phenylalanine-labeled casein protein (PRO) or a placebo (PLA) during sleep. Continuous infusions with L-[ring-(2)H(5)] phenylalanine and L-[ring-(2)H(2)] tyrosine were applied to assess in vivo dietary protein digestion and absorption kinetics and subsequent muscle protein synthesis rates during sleep. We found that exogenous phenylalanine appearance rates increased following protein administration. The latter stimulated protein synthesis, resulting in a more positive overnight whole body protein balance (0.30 +/- 0.1 vs. 11.8 +/- 1.0 mu mol phenylalanine.kg(-1).h(-1) in PLA and PRO, respectively; P < 0.05). In agreement, overnight muscle protein fractional synthesis rates were much greater in the PRO experiment (0.045 +/- 0.002 vs. 0.029 +/- 0.002%/h, respectively; P < 0.05) and showed abundant incorporation of the amino acids ingested via the intrinsically labeled protein (0.058 +/- 0.006%/h). This is the first study to show that dietary protein administration during sleep is followed by normal digestion and absorption kinetics, thereby stimulating overnight muscle protein synthesis. Dietary protein administration during sleep stimulates muscle protein synthesis and improves overnight whole body protein balance. These findings may provide a basis for novel interventional strategies to attenuate muscle mass loss.

The importance of the preoperative nutritional status of cardiothoracic surgical patients in determining outcomes is demonstrated and discussed. Demographic, anthropometric, and biochemical changes in patients undergoing cardiothoracic surgery increase the importance of identifying those at risk for postoperative complications resulting from malnutrition. The interrelationships of chronic heart failure, cardiac cachexia, nutritional status, and nutritional support are identified and emphasized. The complexities of myocardial energetics and metabolism are outlined together with the nutrient needs for patients undergoing cardiac, pulmonary, or other intrathoracic operative procedures.

WOS: 000290783400039, PubMed ID: 21376408, …

Guideline; Journal Article; Review; Patients with cardiac disease can develop two types of malnutrition: cardiac cachexia, which appears in chronic congestive heart failure, and malnutrition due to the complications of cardiac surgery or any other type of surgery in patients with heart disease. Early enteral nutrition should be attempted if the oral route cannot be used. When cardiac function is severely compromised, enteral nutrition is feasible, but supplementation with parenteral nutrition is sometimes required. Sustained hyperglycemia in the first 24 hours in patients admitted for acute coronary syndrome, whether diabetic or not, is a poor prognostic factor for 30-day mortality. In critically-ill cardiac patients with stable hemodynamic failure, nutritional support of 20-25 kcal/kg/day is effective in maintaining adequate nutritional status. Protein intake should be 1.2-1.5 g/kg/day. Routine polymeric or high protein formulae should be used, according to the patient's prior nutritional status, with sodium and volume restriction according to the patient's clinical situation. The major energy source for myocytes is glutamine, through conversion to glutamate, which also protects the myocardial cell from ischemia in critical situations. Administration of 1 g/day of omega-3 (EPA+DHA) in the form of fish oil can prevent sudden death in the treatment of acute coronary syndrome and can also help to reduce hospital admission for cardiovascular events in patients with chronic heart failure. Yes El paciente con patología cardíaca puede presentar 2 tipos de desnutrición: la caquexia cardíaca, que aparece en situaciones de insuficiencia cardíaca congestiva crónica, y una malnutrición secundaria a complicaciones de la cirugía cardíaca o de cualquier cirugía mayor realizada en pacientes con cardiopatía. Se debe intentar una nutrición enteral precoz si no se puede utilizar la vía oral. Cuando la función cardíaca esté profundamente comprometida la nutrición enteral es posible, pero a veces precisará suplementación con nutrición parenteral. La hiperglucemia aguda sostenida en las primeras 24 h en pacientes ingresados por síndrome coronario agudo, sean o no diabéticos, es un factor de mal pronóstico en términos de mortalidad a los 30 días. En el paciente crítico cardíaco con fallo hemodinámico en situación estable, un soporte nutricional de 20-25 kcal/kg/día es eficaz para mantener un estado nutricional adecuado. El aporte proteico debe ser de 1,2-1,5 g/kg/día. Se administrarán fórmulas poliméricas o hiperproteicas habituales, según la situación nutricional previa del paciente, con restricción de sodio y volumen según su situación clínica. La glutamina es la mayor fuente de energía para el miocito, vía conversión a glutamato, protegiendo además a la célula miocárdica de la isquemia en situaciones críticas. La administración de 1 g/día de ω-3 (EpA+DHA), en forma de aceite de pescado, puede prevenir la muerte súbita en el tratamiento del síndrome coronario agudo y también puede contribuir a una disminución de los ingresos hospitalarios, por eventos cardiovasculares, en la insuficiencia cardíaca crónica.

心臓悪液質は, 心臓弁膜症の末期像であり, 術後管理に難渋し手術成績も不良な疾患群である. われわれは, 僧帽弁を主病変とし, るいそうを伴い, 術前NYHAがIV度, さらに, うっ血による肝機能障害を認める症例10例を心臓悪液質と定義し, 術後人工呼吸管理日数の違い (I群; 5日以上, 5例, II群; 4日以内, 5例) により2群に分け, 術前, 術後管理について検討した. 両群とも術前1週間前と術後にIVHを行い, I群の2例に術後経管栄養を行った. 術前より呼吸管理を要したのはI群の2例であった. その結果, 病脳期間が長いほど, 術後長期の人工呼吸管理が必要とする傾向にあったが, 術後カテコラミン使用量, 術後経過, 予後は両群間に差はなかった. これらのことより, 心臓悪液質症例に対しても, 術前, 術後の栄養, 呼吸, 循環管理を行えば, 通常の弁膜症症例と同様に手術ができると考えられた.

Our understanding of the pathophysiology of chronic heart failure (CHF) has significantly advanced over the last 15 years from the historic haemodynamic model of mere pumping failure to a much more complex approach including multiple body systems. The concept of neuroendocrine activation is the cornerstone of the current pathophysiological understanding as well as of the therapeutic approaches that are available today. On this basis, the treatment of CHF has made significant advances over the last two decades. Moreover, treatments for acute cardiac events have improved considerably. As a consequence of effective acute and chronic therapy and a steadily growing population of the aged, a growing number of patients live for prolonged periods in a state of compensated cardiac failure. As a result not only a significant increase in prevalence numbers of CHF can be observed giving rise to the word of an epidemic proportion in the development on heart failure. Also clinical features and complications of a long-term disease progression are increasingly coming to the fore in the clinical presentation of patients. With growing understanding of the complexity of CHF pathophysiology and modern therapy starting to adopt to tailored treatment strategies of specific aspects in patients subgroups a broader and more differentiated perspective on the patients might be required with.

Cardiac cachexia, the loss of lean body mass that affects a large proportion of patients with chronic heart failure, is associated with increased morbidity and mortality. The pathophysiology of cardiac cachexia is complex and multifactorial, but recent studies are providing new information that is helping to clarify the pathophysiology and new targets for treatment.New attention is being paid to developing a definition as well as a clinically relevant way to diagnose this syndrome. The adverse clinical effects of cachexia are being emphasized by new research on the obesity paradox, suggesting that cardiac cachexia is such a detrimental process that obesity actually confers a survival benefit. This information is useful in developing practical approaches to managing body weight and lean tissue in chronic heart failure patients and may provide therapeutic targets. New mechanisms and pathways that mediate cardiac cachexia are being identified and appear to act by increasing energy requirements, reducing energy intake, impairing nutrient absorption, and causing metabolic alterations.Recent studies have helped to better delineate multifactorial mechanisms in the pathophysiology of cardiac cachexia that may lead to more effective treatments to address this common and important syndrome in patients with chronic heart failure.

Chronic heart failure (CHF) is an enormous medical and communal burden. The syndrome is common, carries a grim prognosis and severely impacts quality of life. Those patients who develop cardiac cachexia combat both important disability and a poor outlook. Muscle wasting is a critical component of cachexia. The pathophysiological determinants are numerous and some of them are common to other chronic severe illnesses. There is increasing awareness, however, that heart failure related myopathy is a distinct entity, characterized by specific functional, structural and morphologic changes and the involvement of several neurohormonal pathways, catabolic processes, a pro-inflammatory environment and increased oxidative stress. Although clear-cut evidence based solutions for the problem are not readily available, the modulating effects of regular exercise in CHF patients suggest that physical training should at least be incorporated in the essentially multi-disciplinary approach.

The patients with heart failure (HF) often exhibit some degree of muscle wasting restricted to the lower limbs. This loss of tissue may become more extensive in some patients, usually when their HF is more advanced, and may affect all body compartments. The underlying metabolic causes are very complex and differ from patient to patient. Three essential contributors are dietary deficiency and loss of nutrients through the digestive tract and metabolic dysfunction. The development of cachexia is an ominous sign and new drugs will be added into our therapeutic armamentarium to fight against cardiac cachexia in the near-future.

Extreme loss of body tissue in association with severe illness has been observed by physicians since ancient Greek times. The term ‘cachexia’ was the label for a ‘signum mali ominis’ in various, mostly fatal, diseases. Observing the chronicity of the course of a disease, cachexia was recognised as a severe complication indicating end-stage disease and poor quality of life. As modern treatment helps to prevent early death for an increasing number of chronic diseases, growing interest is focussed on chronic complications such as cachexia. Nevertheless, observation and clinical documentation of this condition go back as long as medical science itself. Pioneering studies on the reasons and mechanisms of cachexia were performed several decades ago. These studies provide fundamental insights and guidance towards a better understanding of cachexia.

Cachexia (body wasting) in patients with cardio-vascular illness usually develops when patients have chronic heart failure (CHF). As an increasing public health problem and a leading cause of morbidity and mortality worldwide, CHF is associated with a poor prognosis [1]. The onset of cachexia in CHF patients (cardiac cachexia) is a serious complication of their disease and even worsens the prognosis of the underlying disease [2]. This connection between advanced heart failure and significant weight loss has long been recognised. The earliest report dates back to the school of medicine of Hippocrates some 2300 years ago. The term ‘cachexia’ is of Greek origin and derives from the words kakos (bad) and hexis (condition). The term ‘cardiac cachexia’ was first used in 1860 by Mauriac [3].

Imagine you have a choice. Tomorrow, you can either be dead, or you can choose a 1% chance of survival. For most of us, it's an easy decision; the odds of survival aren't good, but they are better than certain death. Now imagine that you are trying to persuade a patient not to receive cardiopulmonary resuscitation (CPR). ‘It almost certainly would not work, would only prolong the dying process,’ you explain. But CPR could work: there is perhaps a 1% chance of surviving to see another day. Why would patients choose not to receive it? However, despite most people's clear preference for continued life, the collective experience of clinicians is that CPR should not always be performed, and in many groups of patients, should only rarely be attempted. Individual physicians are required to respect this experience, while at the same time maintaining a high-quality doctor-patient relationship and providing realistic choices to seriously ill patients. The preference not to provide CPR in many circumstances exists for good reasons. I remember clearly my first night working in the emergency department as a second year medical student. A very frail man suffering from cardiac cachexia and severe COPD arrived soaked in sweat and labouring to breathe. He became unconscious as he entered the final stages of dying. ‘Do you want us to resuscitate him?’ the family was hurriedly asked in a back room, away from his suffering. ‘Yes,’ they replied. I remember his eyes as he looked about uncomprehendingly after he was intubated and regained consciousness. He died a few days later in the intensive care unit (ICU). Life sustaining technology is seductive. What was happening had seemed completely wrong, but this perception lessened when I took hold of the ambi-bag and breathed life back in his sodden lungs. Although patients may not …

The onset of cardiac cachexia is characterized by a defined severe weight loss in patients with advanced chronic heart failure and it predicts an increased mortality in these patients. Recent studies with potential therapeutics investigated the effects and efficiency of beta-blockers, ghrelin, or ghrelin-agonists in cachexia. These and other new studies, like the influence of heart transplantation on cardiac cachexia, give prospect into potential therapeutic options in the future. General aim of the treatment strategy is to prevent the onset and retard the progress of cachexia. This could be achieved by modifying the metabolic, neurohormonal and immune system abnormalities, e.g. with beta-blockers and angiotensin-converting enzyme inhibitors. However, these alterations interact in a complex pathophysiological process, which is supposed to end in a vicious circle and thereby the wasting process is further promoted. To interrupt this, an early start of therapy is important to decelerate the development of cardiac cachexia. Many further investigations are needed to find out more about the pathophysiological pathways, to confirm the previous results, and to evaluate new therapeutics.

There is no agreed definition for cachexia, and this hampers research and treatment. This Viewpoint emphasizes the importance of definitive cut-off limits for weight loss over time, and the need for straightforward diagnostic criteria. The authors suggest cut-off values for cardiac cachexia but acknowledge that the values might differ in other conditions.

Purpose of review This review focuses on the prognostic implications and therapeutic approaches in cardiac cachexia - a syndrome that has been recognized for a long time, although it has only received increased attention lately. Recent findings Cardiac cachexia is a common and serious complication of chronic heart failure and associated with very poor prognosis, yet is often recognized by the clinicians only at late stage. Approximately 15% of heart failure patients will develop cardiac cachexia, defined by a 6% non-edematous, non-voluntary weight loss over a period of 6 months. Several studies have demonstrated that cardiac cachexia is a multi-factorial disease, which involves increased neurohormonal activity and immune abnormalities, resulting in hormonal and metabolic catabolic/anabolic imbalance of the body, leading to the loss of fat and lean mass and ultimately death. So far, there are no standardized therapies available for this disease. Summary Cardiac cachexia in heart failure patients is under-recognized and there is currently no causal therapy available. Several interesting treatment options exist, however, which have emerged recently, including appetite stimulants, hormones and 'classical' drugs, such as beta-blockers and ACE inhibitors.

[Graphic][1] ![Graphic][2] A case of idiopathic giant atrium is described. The patient died of cardiac cachexia at the age of 80 years. Although she was diagnosed as having atrial fibrillation and cardiomegaly at the age of 40 years, she had not complained of any symptoms and did not … [1]: /embed/graphic-1.gif [2]: /embed/graphic-2.gif

Ghrelin is a novel growth-hormone-releasing peptide isolated from the stomach that has been identified as an endogenous ligand for the growth-hormone secretagogue receptor. This peptide results in a positive energy balance by stimulating food intake and inducing adiposity through growth-hormone-independent mechanisms. In addition, ghrelin has several cardiovascular effects, as indicated by the presence of its receptor in blood vessels and ventricles of the heart. Infusion of ghrelin decreases systemic vascular resistance and increases cardiac output in patients with heart failure. Furthermore, repeated administration of ghrelin improves cardiac structure and function, and attenuates the development of cardiac cachexia in rats with heart failure. These results suggest that ghrelin has therapeutic potential in the treatment of severe chronic heart failure.

Cachexia has been known to physicians since ancient Greek times as a 'signum mali ominis' in various diseases indicating end stage disease and poor quality of life. Cardiac cachexia is recently receiving growing attention as modern treatment options prevent early death from cardiac events and more patients live with chronic compensated heart failure. Nevertheless, observation and clinical documentation of this condition go back as long as medical science itself. Pioneering studies on the reasons and mechanisms of cachexia were performed several decades ago. These studies provide fundamental insights and guidance towards a better understanding of cachexia. This review presents an overview of early thoughts and milestone studies on metabolic abnormalities and cachexia in chronic heart failure.

Made available in DSpace on 2016-07-07T12:33:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2014. Added 1 bitstream(s) on 2016-07-07T12:43:14Z : No. of bitstreams: 1 ISSN1179-8475-2014-05-319-326.pdf: 248626 bytes, checksum: 651f1c9697e32bdce2840926092fed98 (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Cachexia and muscle wasting are frequently observed in heart failure patients. Cachexia is a predictor of reduced survival, independent of important parameters such as age, heart failure functional class, and functional capacity. Muscle and fat wasting can also predict adverse outcome during cardiac failure. Only more recently were these conditions defined in International Consensus. Considering that heart failure is an inflammatory disease, cardiac cachexia has been diagnosed by finding a body weight loss .5%, in the absence of other diseases and independent of other criteria. Muscle wasting has been defined as lean appendicular mass corrected for height squared of 2 standard deviations or more below the mean for healthy individuals between 20 years and 30 years old from the same ethnic group. The etiology of heart failure-associated cachexia and muscle wasting is multifactorial, and the underlying physiopathological mechanisms are not completely understood. The most important factors are reduced food intake, gastrointestinal alterations, immunological activation, neurohormonal abnormalities, and an imbalance between anabolic and catabolic processes. Cachexia and muscle wasting have clinical consequences in several organs and systems including the gastrointestinal and erythropoietic systems, and the heart, previously affected by the primary disease. We hope that a better understanding of the mechanisms involved in their physiopathology will allow the development of pharmacological and nonpharmacological therapies to effectively prevent and treat heart failure-induced cachexia and muscle wasting before significant body weight and muscle wasting occurs. Universidade Federal de Mato Grosso do Sul, Faculdade de Fisioterapia Universidade Estadual Paulista, Departamento de Clínica Médica, Faculdade de Medicina de Botucatu FAPESP: 2012/21687-1 FAPESP: 2012/50512-5

predicts length of stay, 14.6% of the variability in LOS was attributed to preoperative nutrition and inotropes, (R50.14; p!.001) The nutritional coefficient was -0.288 (p-value 5 0.001) and inotrope use coefficient was 0.246 (p-value 5 0.013) (Fig. A). There was a trend towards higher costs for patients with a serum albumin !3g/dL (HR .85; p!.07). Patients on inotropes had a 38% higher admission cost (HR 1.38; p!.001). Patients on inotropes with a serum albumin greater than 3g/dL had 22% (HR .78; p!.024) lower admission costs than those who were malnourished. The addition of inotropes to a malnourished patient had 54% higher admission costs (HR 1.54; p!.001). In contrast, patient’s receiving MCS with normal serum albumin and the addition of inotropes did not significantly add to costs (HR 1.25; p!.068). Conclusion: We identified a novel finding in patients undergoing durable MCS. Cardiac cachexia compounded the length of stay in the heart failure population receiving mechanical circulatory support. We suggest a thorough nutritional assessment prior to MCS placement. Nutritional status may assist surgeons and cardiologist in choosing the optimal timing of intervention to shorten LOS and resource utilization.