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Isolated myocyte contractile function is normal in postinfarct remodeled rat heart with systolic dysfunction
1Department of Cardiology, University of Minnesota School of Medicine, VA Medical Center, Minneapolis 55417, USA. anand001@maroon.tc.umn.edu
Circulation
|December 24, 1997
Summary
Postinfarction ventricular remodeling involves myocyte lengthening, not slippage. Remote noninfarcted myocytes maintain normal function, suggesting other factors cause global heart dysfunction after myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Cardiac Remodeling Research
- Myocardial Infarction Studies
Background:
- Postinfarction ventricular remodeling is a known complication.
- The mechanisms driving remote noninfarcted myocardium dysfunction remain unclear.
Purpose of the Study:
- To investigate serial changes in left ventricular (LV) structure and function post-myocardial infarction.
- To correlate global cardiac changes with myocyte structural and functional alterations in remote myocardium.
Main Methods:
- Serial assessment of global LV structure and function in rat hearts post-myocardial infarction (MI) and sham operations.
- Isolation and functional assessment of myocytes from remote LV and RV myocardium.
- Correlation of myocyte dimensions and function with global LV remodeling and dysfunction.
Main Results:
- MI rats exhibited significant cardiac remodeling, increased heart weight-to-body weight ratio, and elevated LV volumes.
- Global LV dysfunction was evident, with impaired pressure development.
- Isolated LV and RV myocytes showed significant lengthening and widening, correlating with LV volume and function changes.
- Despite structural changes, isolated myocytes displayed normal contractile function and Ca2+ handling.
Conclusions:
- Postinfarct remodeling primarily involves myocyte lengthening, not slippage.
- Normal contractile function of isolated remote myocytes suggests myocyte contractile abnormalities are not the primary cause of global dysfunction.
- Reduced myocyte mass and nonmyocyte factors (e.g., wall stress, altered geometry) are likely key contributors to postinfarct LV dysfunction.