Nutritional and anti-inflammatory interventions in chronic heart failure.
Currently, there are 5 million individuals with chronic heart failure (CHF) in the United States who 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 that malnutrition, inflammation, and oxidative stress may play a role that results in protein-energy wasting contributing to poor survival in CHF. Diminished appetite or anorexia and nutritional deficiencies 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 also may contribute to the prominent inflammatory and oxidative characteristics of this population. In patients with CHF and wasting, nutritional strategies including amino acid supplementation may represent a promising therapeutic approach, especially if the provision of additional amino acids, protein, and energy includes nutrients with anti-inflammatory and antioxidant properties. Regardless of the etiology of anorexia, appetite-stimulating agents, especially those with anti-inflammatory properties such as megesterol acetate or pentoxyphylline, may be appropriate adjuncts to dietary supplementation. Understanding the factors that modulate MIC and body 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.
Harold Simmons Center for Chronic Disease Research and Epidemiology, Los Angeles Biomedical Research Center at Harbor-UCLA, Torrance, California 90509-2910, USA. kamkal@ucla.edu
Kamyar
K
Kalantar-Zadeh
Stefan D
SD
Anker
Tamara B
TB
Horwich
Gregg C
GC
Fonarow
D000596:Amino Acids / Q000008:administration & dosage; D000855:Anorexia / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D000975:Antioxidants / Q000627:therapeutic use; D019167:Appetite Stimulants / Q000494:pharmacology; D002100:Cachexia / Q000453:epidemiology / Q000503:physiopathology / Q000517:prevention & control; D015897:Comorbidity; D019587:Dietary Supplements; D004357:Drug Synergism; D016166:Free Radical Scavengers / Q000627:therapeutic use; D006333:Heart Failure / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D044342:Malnutrition / Q000503:physiopathology; D019290:Megestrol Acetate / Q000494:pharmacology; D044623:Nutrition Therapy; D010431:Pentoxifylline / Q000627:therapeutic use; D011110:Polymorphism, Genetic / Q000502:physiology
D000596:Amino Acids; D000975:Antioxidants; D019167:Appetite Stimulants; D016166:Free Radical Scavengers; D010431:Pentoxifylline; D019290:Megestrol Acetate