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Behavioral risk factors of chronic heart failure

  • Ram B. Singh
  • , Tomko Komatsu
  • , Masaichi Changil Lee
  • , Shaw Watanabe
  • , Sarah O. Nwozo
  • , Takeshi Kiyoi
  • , Masaki Mogi
  • , Shikha S. Gaur
  • , Rashmi Gautam
  • , Garima Tyagi
  • , Manal M.A. Smail
  • , Aminat G. Magomedova
  • , Sudha R. Yelluri
  • , R. K. Agarval
  • , A. V. Sotnikov
  • , A. V. Gordienko
  • , D. V. Nosovich
  • , N. V. Birukova
  • Halberg Hospital and Research Institute
  • Kanagawa Dental University
  • Life Science Promoting Association
  • University of Ibadan
  • Ehime University
  • Saraswati Institute of Medical Sciences
  • Mahatma Jyotiba Phule Rohilkhand University
  • Lomonosov Moscow State University
  • National University, San Diego
  • Technomed Holdings LLC Publishing House
  • Military Medical Academy, Saint Petersburg
  • Pirogov Russian National Research Medical University

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

There is evidence that behavioral risk factors, such diets rich in refined carbohydrates, sugar trans-fat and saturated fat and salt, the lack of mastication during eating, sedentary behavior, tobacco intake, alcoholism, and mental stress, are important risk factors of cardio-metabolic diseases including heart failure (HF).These health behaviors are known to predispose risk factors for HF: obesity, hypertension, metabolic syndrome, diabetes mellitus, and coronary artery disease. The exact mechanisms of how sugar and tobacco damage the cardiac cells are not known. However, it seems that oxidative stress, resulting in inflammation and immune deficiency, is common in the pathogenesis of HF. Free radicals are known to damage the cell membranes causing development of intracellular Ca2+ overload, activation of proteases and phospholipases, and alterations in cardiac gene expression. These biochemical alterations result in the changes in the molecular structure, and function of different subcellular organelles of the heart, with pathological subcellular remodeling, leading to HF. Since cardiac hypertrophy impairs the relationship between ATP demand and production, mitochondrial bioenergetics must keep up with the cardiac hypertrophic phenotype. The roles of mitochondrial proteomic and energetic remodeling in cardiac hypertrophy are of significant importance. The temporal and causal relationships between mitochondrial failure with increased energy demand can facilitate progression to cardiac decompensation. It is possible that the maladaptive effect of sustained neuroendocrine signals on mitochondria may lead to bioenergetic fading, which contributes to the progression from cardiac hypertrophy to HF. It seems that persistent and continuous pathological signals in the cardiac cells induce cardiac hypertrophy, which is associated with increased risk for sudden death or progression to HF, irrespective of the initial cause of hypertrophy. These cardiac alterations, although considered adaptive, become maladaptive, leading to cardiac failure if prolonged for a long duration. Since cardiac imaging can identify early cardiac hypertrophy, there is an unmet need to examine the significance of behavioral risk factors in the early diagnosis of HF.

Original languageEnglish
Title of host publicationPathophysiology, Risk Factors, and Management of Chronic Heart Failure
PublisherElsevier
Pages41-52
Number of pages12
ISBN (Electronic)9780128229729
ISBN (Print)9780128231111
DOIs
StatePublished - 1 Jan 2024

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Cardiac
  • cardiomyocyte
  • diet
  • lifestyle
  • oxidative stress

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