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Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome.

Abstract

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

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  • Publisher Full Text
  • Authors+Show Affiliations

    Division of Cardiology, University of South Alabama, College of Medicine, Mobile 36617, USA.

    Source

    MeSH

    Cardiomyopathies
    Child
    Echocardiography, Three-Dimensional
    Heart
    Hemodynamics
    Humans
    Obesity
    Obesity, Morbid
    Syndrome
    Ventricular Function

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    11307864

    Citation

    Alpert, M A.. "Obesity Cardiomyopathy: Pathophysiology and Evolution of the Clinical Syndrome." The American Journal of the Medical Sciences, vol. 321, no. 4, 2001, pp. 225-36.
    Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci. 2001;321(4):225-36.
    Alpert, M. A. (2001). Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. The American Journal of the Medical Sciences, 321(4), pp. 225-36.
    Alpert MA. Obesity Cardiomyopathy: Pathophysiology and Evolution of the Clinical Syndrome. Am J Med Sci. 2001;321(4):225-36. PubMed PMID: 11307864.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. A1 - Alpert,M A, PY - 2001/4/20/pubmed PY - 2001/5/5/medline PY - 2001/4/20/entrez SP - 225 EP - 36 JF - The American journal of the medical sciences JO - Am. J. Med. Sci. VL - 321 IS - 4 N2 - Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death. SN - 0002-9629 UR - https://www.unboundmedicine.com/medline/citation/11307864/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9629(15)34671-1 DB - PRIME DP - Unbound Medicine ER -