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Reduced force generating capacity in myocytes from chronically ischemic, hibernating myocardium
Virginie Bito1, Jolanda van der Velden, Piet Claus
1Division of Experimental Cardiology, University Hospital Gasthuisberg and University of Leuven, Belgium.
Circulation Research
|January 20, 2007
Summary
Hibernating myocardium exhibits reduced contractile force due to less myofibrillar protein per cell volume, replaced by glycogen and mitochondria. This cellular remodeling may slow functional recovery after revascularization.
Area of Science:
- Cardiology
- Cellular Biology
- Biochemistry
Background:
- Hibernating myocardium displays contractile dysfunction linked to local factors and intrinsic cellular remodeling.
- Previous research suggested potential defects in myofilament calcium responsiveness as a cause.
Purpose of the Study:
- To investigate the cellular mechanisms underlying contractile dysfunction in hibernating myocardium.
- To determine if myofilament Ca2+ responsiveness is altered in hibernating myocytes.
Main Methods:
- Isolated single myocytes from control and hibernating porcine hearts.
- Measured isometric force development after direct myofilament activation.
- Analyzed protein expression, phosphorylation, and cellular ultrastructure via electrophoresis, immunoblotting, and electron microscopy.
Main Results:
- Maximal isometric force was significantly reduced in hibernating myocytes.
- Ca2+ sensitivity, force redevelopment rate, and protein expression/phosphorylation were unchanged.
- Hibernating myocytes showed decreased myofilament density (57.1% vs 69.9%) and increased glycogen/mitochondria.
Conclusions:
- Reduced force in hibernating myocardium stems from decreased myofibrillar protein density per cell volume.
- Glycogen and mitochondria accumulation contributes to this cellular remodeling.
- These structural changes may impede functional recovery upon revascularization.
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