Cellular mechanisms of myocardial infarct expansion.
Population
Rat hearts with infarct expansion 1, 2, and 3 days after coronary ligation, and 7 human hearts.
Comparison
Myocardial infarction vs Sham-operated control hearts and hearts without…
Design
Preclinical
Follow-up
1 to 3 days
Authors
Discussion
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Implication
Myocyte slippage may drive post-MI thinning; hypothesis-generating for cell-retention therapies pending human confirmation.
Structured PICO
P
Population
Rat hearts with infarct expansion 1, 2, and 3 days after coronary ligation, and 7 human hearts (5 from patients who died within 3 days of infarction, 2 from patients without coronary disease).
I
Intervention
Myocardial infarction (coronary ligation in rats, spontaneous in humans)
C
Comparator
Sham-operated control hearts (rats) and hearts without coronary disease (humans)
O
Outcome
Cellular mechanisms of wall thinning and dilatation (transmural cell count, cell density, myocyte cross-sectional area, sarcomere length)surrogate
Myocardial infarct expansion and wall thinning are primarily driven by a decrease in the number of cells across the ventricular wall (myocyte slippage) rather than just cell stretch or rupture.
Cite This Study
Weisman et al. (1988) studied this question.