The molecular and cellular pathophysiology of heart failure

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M R Piano1, M Bondmass, D W Schwertz

  • 1Department of Medical-Surgical Nursing, University of Illinois at Chicago College of Nursing, 60612, USA.

Heart & Lung : the Journal of Critical Care
|March 11, 1998
PubMed

Insights

Heart failure affects 465,000 Americans annually, impacting all demographics. This review details the epidemiology and cellular pathophysiology of heart failure, including myocyte changes during compensated and decompensated stages.

Area of Science:

  • Cardiology
  • Cellular Biology
  • Pathophysiology

Background:

  • Heart failure affects 465,000 individuals annually in the U.S.
  • It is a significant cause of morbidity and mortality across all demographics.
  • Current understanding extends beyond the cardiorenal-neurohumoral model to include myocyte alterations.

Purpose of the Study:

  • To review the epidemiology of heart failure.
  • To explore the cellular pathophysiology of heart failure.
  • To discuss the transition from compensated to decompensated heart failure.

Main Methods:

  • Literature review of epidemiological data.
  • Analysis of cellular mechanisms in heart failure.
  • Examination of neurohormonal and cytokine involvement.

Main Results:

  • Cellular changes include myocyte hypertrophy and abnormalities in calcium homeostasis.
  • Cytoskeletal architecture changes are observed.
  • Neurohormonal overexpression (norepinephrine, angiotensin II) and cytokines contribute to decompensation.

Conclusions:

  • Heart failure involves complex cellular changes affecting myocyte structure and function.
  • These changes occur during both compensated and decompensated stages.
  • The transition to decompensation is linked to neurohormonal and inflammatory factors.

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