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Electrical remodeling in pressure-overload cardiac hypertrophy: role of calcineurin

Z Wang1, W Kutschke, K E Richardson

  • 1Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa, USA.

Circulation
|October 3, 2001
PubMed

Insights

Heart myocyte hypertrophy alters electrical activity, particularly in subendocardial cells, due to increased calcium currents. This study reveals calcineurin

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology
  • Molecular Cardiology

Background:

  • Myocyte hypertrophy is common in heart disease.
  • Its impact on cardiac electrical remodeling remains unclear.
  • Regional differences in myocyte electrical properties are not well understood.

Purpose of the Study:

  • To investigate the contribution of myocyte hypertrophy to electrical remodeling in the left ventricle.
  • To explore the regional differences in electrophysiological responses to pressure overload.
  • To identify the underlying ionic and molecular mechanisms.

Main Methods:

  • Utilized a mouse model of pressure overload induced by surgical thoracic aortic banding.
  • Performed electrophysiological studies, including voltage-clamp recordings on dissociated myocytes.
  • Investigated the role of calcineurin using cyclosporin A inhibition.

Main Results:

  • Pressure overload induced greater action potential duration prolongation in subendocardial myocytes, amplifying repolarization dispersion.
  • Hypertrophied myocytes showed increased peak L-type Ca(2+) current density and accelerated recovery from inactivation.
  • Calcineurin inhibition prevented hypertrophy and normalized electrophysiological changes, including L-type Ca(2+) current.

Conclusions:

  • Upregulation of Ca(2+) current and calcineurin mediates regional electrophysiological variations in hypertrophied ventricles.
  • These findings suggest a partial uncoupling between structural and electrical remodeling during hypertrophy.
  • The study highlights the role of calcineurin in mediating hypertrophic cardiac remodeling and electrical changes.
Abstract

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