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10.1016/j.amjcard.2008.03.007

http://scihub22266oqcxt.onion/10.1016/j.amjcard.2008.03.007
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C5500213!5500213!18514634
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suck abstract from ncbi


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pmid18514634      Am+J+Cardiol 2008 ; 101 (11A): 89E-103E
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  • Nutritional and Anti-Inflammatory Interventions in Chronic Heart Failure #MMPMID18514634
  • Kalantar-Zadeh K; Anker SD; Horwich TB; Fonarow GC
  • Am J Cardiol 2008[Jun]; 101 (11A): 89E-103E PMID18514634show ga
  • Five million individuals with chronic heart failure (CHF) in the United States have poor clinical outcomes including high death rates. Observational studies have indicated a reverse epidemiology of traditional cardiovascular risk factors in CHF; in contrast to trends seen in the general population, obesity and hypercholesterolemia are associated with improved survival. The temporal discordance between the overnutrition (long-term killer) and undernutrition (short-term killer) not only can explain some of the observed paradoxes but also may indicate a role for malnutrition, inflammation and oxidative stress that result in cachexia contributing to poor survival in CHF. Diminished appetite or anorexia may be both a cause and a consequence of this so-called malnutrition-inflammation-cachexia (MIC) or wasting syndrome in CHF. Neurohumoral activation, insulin resistance, cytokine activation and survival selection resultant genetic polymorphisms may also contribute to the prominent inflammatory and oxidative characteristics of this population. In CHF patients with wasting, nutritional strategies may be a promising therapeutic approach in CHF, especially if the provision of additional protein and energy also includes nutrients with anti-inflammatory and anti-oxidant properties. Regardless of the etiology of anorexia, appetite stimulating agents especially with anti-inflammatory properties such as megesterol acetate or pentoxyphylline may be appropriate adjuncts to dietary supplementation. Understanding the factors that modulate the MIC and wasting and their associations with clinical outcomes in CHF may lead to the development of nutritional strategies that alter the pathophysiology of CHF and improve outcomes
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