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Role of apoptosis in pressure-overload cardiomyopathy

Amedeo Anselmi1, Mario Gaudino, Alfonso Baldi

  • 1Division of Cardiac Surgery, Department of Cardiovascular Medicine, Catholic University, Rome, Italy. amedeo.anselmi@aliceposta.it

Journal of Cardiovascular Medicine (Hagerstown, Md.)
|February 28, 2008
PubMed

Insights

Pressure overload causes left ventricular hypertrophy, which can lead to heart failure. This review explores the role of myocardial apoptosis in pressure-overload cardiomyopathy development.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pathophysiology

Background:

  • Left ventricular hypertrophy initially compensates for pressure overload, preserving ejection fraction.
  • Progressive ventricular dilation and heart failure occur despite normalized pressure overload.
  • Mechanisms of pressure-overload cardiomyopathy remain unclear, impacting prognosis.

Purpose of the Study:

  • To review experimental and clinical evidence on myocardial apoptosis in pressure-overload cardiomyopathy.
  • To elucidate cellular and molecular mechanisms underlying maladaptive hypertrophy.

Main Methods:

  • Literature review of experimental and clinical studies.
  • Analysis of data on myocardial apoptosis in pressure-overload models and patients.

Main Results:

  • Apoptosis is implicated in the maladaptive response of the myocardium.
  • Cellular and molecular derangements contribute to cardiomyopathy progression.
  • Evidence suggests apoptosis plays a significant role in heart failure development.

Conclusions:

  • Myocardial apoptosis is a key factor in the progression of pressure-overload cardiomyopathy.
  • Understanding apoptosis mechanisms is crucial for therapeutic strategies.
  • Further research is needed to fully establish the role of apoptosis in heart failure.

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