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Left ventricular function and remodeling after myocardial infarction in aging rats
T E Raya1, M Gaballa, P Anderson
1Department of Pathology, University of Alabama, Birmingham 35294-0019, USA.
The American Journal of Physiology
|January 22, 1998
Summary
Aging impairs left ventricular (LV) function and increases fibrosis. However, older rats with myocardial infarction (MI) show similar LV remodeling and function compared to younger rats, indicating age does not worsen long-term MI outcomes.
Area of Science:
- Cardiovascular Physiology
- Aging Research
- Cardiac Remodeling
Background:
- Aging significantly alters left ventricular (LV) structure and function, distinct from younger hearts.
- Baseline LV function, including relaxation and systolic performance, declines with age.
- Myocardial fibrosis and myocyte size increase in aged hearts.
Purpose of the Study:
- To investigate how aging influences LV hemodynamics and remodeling following myocardial infarction (MI).
- To compare the functional and structural adaptations to MI in young versus aged rats.
- To understand the interaction between aging and MI on cardiac compensatory mechanisms.
Main Methods:
- Fischer 344 Brown Norway rats of different ages (7, 12, 18, and 23 months) were subjected to sham procedures or MI.
- Left ventricular (LV) function, hemodynamics, and cardiac remodeling were assessed 5 months post-MI.
- Isometric myocardial function was evaluated using papillary muscles from 12- and 23-month-old sham rats.
Main Results:
- Aging led to decreased baseline LV systolic function, increased myocyte cross-sectional area (CSA), and fibrosis.
- Post-MI, both young and aged rats exhibited impaired LV function and increased volumes.
- Crucially, no significant differences in LV systolic function or remodeling were observed between young and aged rats after MI.
- Myocyte hypertrophy and fibrosis increased post-MI in younger rats but not in older rats, suggesting a negative interaction of aging and MI.
Conclusions:
- Baseline cardiac function declines with age, characterized by reduced systolic performance and increased fibrosis.
- Despite pre-existing fibrosis and limited compensatory hypertrophy in aged rats, long-term adaptations to MI are comparable to younger adults.
- Aging does not exacerbate the functional or structural consequences of MI in the long term, suggesting resilience in the aged heart's response to injury.