Key result
Progression of congestive heart failure in post-myocardial infarction mice involves slowing of cardiomyocyte contraction, with reduced posterior wall shortening velocity (1.2 vs 1.9 cm/s in sham).
Why the study?
Does heart failure progression in postinfarction mice alter cardiomyocyte Ca2+ release and contraction?
Population
Mice with congestive heart failure following induction of myocardial infarction, examined at early and…
Comparison
Induction of myocardial infarction to model… vs Sham-operated mice.
Design
Preclinical
Follow-up
10 weeks
Authors
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Hypothesis-generating for post-MI HF mechanisms in mice; leaves open translation to human cardiomyocyte function.
Does heart failure progression in postinfarction mice alter cardiomyocyte Ca2+ release and contraction?
Absolute Event Rate: 1.2% vs 1.9%
In postinfarction mice, declining myocardial function during heart failure progression involves slowing of cardiomyocyte contraction and Ca2+ release without a reduction in contraction magnitude.
Mørk et al. (2009) studied Congestive heart failure post-myocardial infarction. Myocardial infarction induction vs. Sham operation was evaluated on Posterior wall shortening velocity (cm/s). Progression of congestive heart failure in post-myocardial infarction mice involves slowing of cardiomyocyte contraction, with reduced posterior wall shortening velocity (1.2 vs 1.9 cm/s in sham).
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