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The properties of the pacemaker current I(F)in human ventricular myocytes are modulated by cardiac disease

E Cerbai1, L Sartiani, P DePaoli

  • 1Department of Preclinical and Clinical Pharmacology, and Center of Molecular Medicine (CIMMBA), University of Firenze, Viale G. Pieraccini 6, 50139 Florence, Italy.

Journal of Molecular and Cellular Cardiology
|February 22, 2001
PubMed

Insights

The pacemaker current (If) is overexpressed in human heart failure cells, with higher functional expression in ischemic cardiomyopathy than dilated cardiomyopathy. This suggests disease etiology influences If expression, not cell size.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Electrophysiology

Background:

  • The pacemaker current (If) plays a role in heart rhythm and may contribute to arrhythmogenesis in failing human hearts.
  • The impact of cardiac disease on If expression remains unclear.

Purpose of the Study:

  • To investigate the functional expression and properties of the If current in human ventricular myocytes from healthy and failing hearts.
  • To compare If expression in failing hearts due to ischemic and dilated cardiomyopathy.

Main Methods:

  • Patch-clamp electrophysiology was used to record If in human ventricular myocytes.
  • Cells were isolated from control donor hearts and explanted failing hearts (ischemic and dilated cardiomyopathy).
  • Membrane capacitance was measured to normalize current density.

Main Results:

  • If was present in all failing myocytes and 76% of control myocytes.
  • If amplitude was significantly greater in failing hearts (ischemic and dilated) compared to controls.
  • If density was highest in ischemic cardiomyopathy, followed by dilated cardiomyopathy and control, indicating disease-specific modulation.
  • Activation curves were shifted to more positive potentials in failing hearts, and I-V slopes differed between disease types.

Conclusions:

  • The If current is overexpressed in human ventricular myocytes from failing hearts.
  • Functional If expression is modulated by the etiology of heart failure, being higher in ischemic than dilated cardiomyopathy.
  • The observed changes in If are not solely related to the degree of cell hypertrophy.

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