European Heart Journal Advance Access originally published online on March 21, 2007
European Heart Journal 2007 28(8):1038-1039; doi:10.1093/eurheartj/ehm006
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New risk factors of heart failure?
Department of Internal Medicine and Cardiology
Halberg Hospital and Research Institute
Civil Lines
Moradabad-10
UP 244001
India
Tel: +91 591 2417437
Fax: +91 591 2411009
E-mail address: icn2005{at}sancharnet.in
Columbus Concept Institute
Bastogne
Belgium
Taiyo Kagaku
Yokkaichi
Japan
Safaric University
Kosice
Slovakia
Safaric University
Kosice
Slovakia
We appreciate very much Siirilä-Waris et al.1 for their excellent work on risk factors of heart failure. Progression of heart failure may be due to an initial cardiac injury, or mutation of the genetic programme, in association with activation of neurohormones and proinflammatory cytokines, resulting into immune activation, which worsens heart failure. Therefore, it may be proposed that any factor which can block neuroendocrine activation would be protective, whereas other factors that can enhance neurohormonal activity would be the risk factors of heart failure. Decreased heart rate variability, increased blood pressure variability, dyslipidemia, increased IL-6, IL-1, TNF-alpha, C-reactive protein, and adhesion molecules are other important determinants of mortality in patients of heart failure.2–4 Presence of coronary artery disease is also an important risk factor of mortality, which becomes worst if there is coexisting cardiac cachexia or obesity among these patients.
Apart from above risk factors, nutritional factors such as increased consumption of proinflammatory foods; refined starches and sugar, trans fatty acids, w-6 fatty acids, and saturated fat may enhance proinflammatory cytokines. Therefore eating proinflammatory foods could be an important cause of increased mortality in heart failure, because these patients have a pre-existing proinflammatory milieu.5–7 These foods may produce oxidative stress, free fatty acids, and proinflammatory substances, which result in endothelial dysfunction.6,7 Glucose ingestion in normal subjects is associated with increased superoxide generation in leukocytes and mononuclear cells, as well as with raised amount and activity of nuclear factor-
B (NF-B), a transcriptional factor regulating the activity of at least 125 genes, most of which are proinflammatory.5,6 Increased consumption of refined carbohydrates also causes an increase in two other proinflammatory transcription factor, activating protein-1 (AP-1), and Egr-1, the first regulating the transcription of matrix metallo-proteinases and the second modulating the transcription of tissue factor and plasminogen activator inhibitor-1. These adverse factors related to diet may worsen the prognosis in heart failure.
A mixed meal from a fast-food chain has also been shown to induce activation of NF-B associated with the generation of reactive oxygen species (ROS) by mononuclear cells.5,6 Superoxide anion appears to be an activator of at least two major proinflammatory transcription factor, NF-B and AP-1. These observations are consistent with previous findings, demonstrating that after oral or intravenous glucose challenges, in both normal subjects and patients with type 2 diabetes mellitus, there is an increased generation of ROS and raised circulating levels of proinflammatory cytokines, such as TNF-
, IL-6, and IL-18.5,6 In apparently healthy subjects, a single high-fat meal produces endothelial activation, as evidenced by increased concentrations of the adhesion molecules VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1), in association with raised plasma concentrations of IL-6 and TNF-.5–7 A high-fat meal may increase the circulating levels of IL-18, a proinflammatory cytokine supposed to be involved in plaque destabilization associated with the simultaneous decrease of circulating adiponectin, an adipocyte-derived protein with insulin sensitizing, anti-inflammatory, and antiatherogenic properties. Consumption of a high-fat meal together with vegetable foods rich in natural antioxidants largely prevent the negative effects on endothelial function.5,6 In particular, endothelial dysfunction acutely triggered by the consumption of a high-fat meal rich in saturated fatty acids is reduced by the simultaneous consumption of a vegetable serving including pepper (100 g), tomatoes (100 g), and carrots (200 g). It seems that these foods are slowly digested and absorbed without causing any significant increase in free radical stress and free fatty acids, which is a characteristic of Columbus foods (www.Columbus-concept.com) and therefore such foods may improve the prognosis in heart failure. Cytokines are known to worsen the neurons which worsen in presence of deficiency of w-3 fatty acids, responsible for the survival of neurons. Omega-3 fatty acids can regulate leptin gene expression and the concentrations of anandamides in the brain, which in turn binds to endogenous cannabinoid receptors and regulate food intake. It is possible that in the clinical trials in heart failure, using agents to inhibit TNF-alpha activity showed disappointing results, because proinflammatory effect of diet was not considered. It seems that anticytokine therapy in heart failure would work only in patients with proven proinflammatory status with due consideration to diet. Coenzyme Q10 and w-3 fatty acids or even anti-inflammatory foods and statins, because of their pleitropic effects, may prove beneficial in this setting. We would appreciate opinion of the authors of the above study about our comments.1
References
- Siirilä-Waris K, Lassus J, Melin J, Peuhkurinen K, Markku S, Nieminen MS. Harjola VP for the FINN-AKVA study group. (2006) Characteristics, outcomes and predictors of one year mortality in patients hospitalized for acute heart failure. Euro Heart J http://eurheartj.oxfordjournals.org/misc/terms.dtl.
- Pocock SJ, Wang D, Pfeffer MA, Yusuf S, McMurray JJ, Swedberg KB, Ostergren J, Michelson EL, Pieper KS, Granger CB. (2006) Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J 27:65–75.
[Abstract/Free Full Text] - Tavazzi L, Maggioni A, Lucci D, Cacciatore G, Ansalone G, Oliva F, Porcu M. (2006) Nationwide survey on acute heart failure in cardiology ward services in Italy. Eur Heart J 27:1207–1215.
[Abstract/Free Full Text] - Anker SD and von Hachling S. (2004) Inflammatory mediators in chronic heart failure. Heart 90:464–470.
[Free Full Text] - Singh RB, Pella D, DeMeester F. (2006) What to eat and chew in acute myocardial infarction. Eur Heart J 27:1628–1629.
[Free Full Text] - Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano G, D'Armiento M, D'Andrea F, Giugliano D. (2004) Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA 292:1440–1446.
[Abstract/Free Full Text] - Singh RB, Niaz MA, Agarwal P, Beegum R, Rastogi SS. (1995) Effect of antioxitant rich foods on plasma ascorbic acid, cardiac enzyme and lipid peroxide levels in patients hospitalized with acute myocardial infarction. J Am Diet Assoc 95:775–780.[CrossRef][ISI][Medline]
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