Conditioned Nutritional Requirements: Therapeutic Relevance to Heart Failure

  • Michael J. Sole
  • Kursheed N. Jeejeebhoy
Part of the Progress in Experimental Cardiology book series (PREC, volume 9)


The advent of disease, genetic predisposition or certain drug therapies may significantly alter the recommended daily intake for specific nutrients published by government agencies and established in healthy people. That is the nutritional demands of a given physiological state or pathological process such as myocardial failure may result in “conditioned nutrient requirements or deficiencies” for the affected organ—in this case the myocardium and perhaps skeletal muscle. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in l-carnitine, coenzyme Q10, creatine and thiamine—nutrient co-factors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacological fashion but there has been no broad-based approach to nutritional supplementation in CHF to correct this complex of metabolic abnormalities. We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, co-enzyme Q10, carnitine, thiamine, creatine, vitamin E, C and selenium to cardiomyopathic hamsters, during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt and—dp/dt measured in a Langendorff apparatus. We also documented in carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume. These experiments suggest that a comprehensive restoration of adequate myocyte nutrition should be essential to any therapeutic strategy designed to benefit patients suffering from CHE Future studies in this area are of clinical importance.

Key words

dilated cardiomyopathy congestive heart failure nutrition oxidative stress energetics creatine carnitine taurine coenzyme Q10 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Vogt AM, Kubler W. 1998. Heart failure: is there an energy deficit contributing to contractile dysfunction? Basic Res Cardiol 93:1–10.PubMedCrossRefGoogle Scholar
  2. 2.
    Clark AL, Sparrow JL, Coates AJS. 1995. Muscle fatigue and dyspnea in chronic heart failure: two sides of the same coin? Eur Heart J 16:49–52.PubMedCrossRefGoogle Scholar
  3. 3.
    Freeman L, Roubenoff R. 1994. The nutrition implications of cardiac cachexia. Nutr Rev 52: 340–347.PubMedCrossRefGoogle Scholar
  4. 4.
    Broqvist M, Arnqvist H, Dahlstrom U, et al. 1994. Nutritional assessment and muscle energy metabolism in severe chronic congestive heart failure: effects of long-term dietary supplementation. Eur Heart J 15:1641–1650.PubMedGoogle Scholar
  5. 5.
    Arsenian MA. 1997. Carnitine and its derivatives in cardiovascular disease. Prog Cardiovasc Dis 40:265–286.PubMedCrossRefGoogle Scholar
  6. 6.
    Schonekess BO, Allard MF, Lopaschuk GD. 1995. Proprionyl L-carnitine improvement of hypertrophied heart function is accompanied by an increase in carbohydrate oxidation. Circ Res 77:726–734.PubMedCrossRefGoogle Scholar
  7. 7.
    Engel AG. 1986. Carnitine deficiency syndromes and lipid storage myopathies. In: Myology, Basic and Clinical. Engel AG, Banker BQ (editors) 1663–1696, Toronto: McGraw Hill Book Co.Google Scholar
  8. 8.
    Pepine CJ. 1991. The therapeutic potential of carnitine in cardiovascular disorders. Clin Ther 13: 2–18.PubMedGoogle Scholar
  9. 9.
    Littaru GP. 1995. Energy and Defence: Facts and Perspectives on Coenzyme Q10 in Biology and Medicien. 1–91. Rome: Casa Editrice Scientifica Internazionale.Google Scholar
  10. 10.
    Elmberger PG, Kalen A, Appelkvist EL, et al. 1987. In vitro and in vivo synthesis of dolichol and other main mevalonate products in various organs of the rat. Eur J Biochem 168:1–11.PubMedCrossRefGoogle Scholar
  11. 11.
    Folkers K, Vadhanavikit S, Mortensen SA. 1985. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q10. Proc Natl Acad Sci USA 82: 4240–4244.PubMedCrossRefGoogle Scholar
  12. 12.
    Seligman H, Halkin H, Rauchfleisch S, et al. 1991. Thiamine deficiency in patients with congestive failure receiving long-term furosemide therapy: a pilot study. Am J Med 91:151–156.CrossRefGoogle Scholar
  13. 13.
    Brady JA, Rock CL, Horneffer MR. 1995. Thiamine status, diuretic medications and the management of congestive heart failure. J Am Diet Assoc 95:541–544.PubMedCrossRefGoogle Scholar
  14. 14.
    Nascimben L, Ingwall JS, Pauletto P, et al. 1996. Creatine kinase system in failing and nonfailing human myocardium. Circulation 94:1894–1901.PubMedCrossRefGoogle Scholar
  15. 15.
    Neubauer S, Horn M, Cramer M, et al. 1997. In patients with cardiomyopathy the myocardial phosphocreatine/ATP ratio predicts mortality better than ejection fraction or NYHA class. Circulation 96:2190–2196.PubMedCrossRefGoogle Scholar
  16. 16.
    Huxtable RJ, Chubb J, Azari J. 1980. Physiological and experimental regulation of taurine content in the heart. Fed Proc 39:2685–2690.PubMedGoogle Scholar
  17. 17.
    Pion PD, Kittleson MD, Rogers QR, et al. 1987. Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 237:764–768.PubMedCrossRefGoogle Scholar
  18. 18.
    Azuma J, Sawamura A, Awata N. 1992. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J 56:95–99.PubMedCrossRefGoogle Scholar
  19. 19.
    Ball AMMM, Sole MJ. 1998. Oxidative stress and the pathogenesis of heart failure. Cardiol Clinics 16:665–675.CrossRefGoogle Scholar
  20. 20.
    Li RK, Sole MJ, Mickle DAG, et al. 1997. Vitamin E and oxidative stress in the heart of the cardiomyopathic Syrian hamster. Free Radical Biol Med 24:252–258.CrossRefGoogle Scholar
  21. 21.
    Keith M, Geranmayegan A, Sole MJ, et al. 1998. Increased oxidative stress in patients with congestive heart failure. J Am Coll Cardiol 31:1352–1356.PubMedCrossRefGoogle Scholar
  22. 22.
    Keith ME, Jeejeebhoy KN, Langer A, et al. 2001. A controlled clinical trial of vitamin E supplementation in patients with congestive heart failure. Am J Clin Nutr 73: 219–224.Google Scholar
  23. 23.
    Keith ME, Ball A, Jeejeebhoy KN, et al. 2001. Conditioned nutritional deficiencies in thecar-diomyopathic hamster heart. Can J Cardiol 17:449–458.PubMedGoogle Scholar
  24. 24.
    Sole MJ, Jeejeebhoy KN. 2000. Conditioned nutritional requirements and the pathogenesis and treatment of myocardial failure. Curr Opin Clin Nutr Metab Care 3:417–424.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2003

Authors and Affiliations

  1. 1.University of TorontoTorontoCanada

Personalised recommendations