Key result
Myocardial infarction slows skeletal muscle phosphocreatine recovery more than twofold without hemodynamic compromise in rats.
Why the study?
The effects of experimental myocardial infarction on skeletal muscle bioenergetics and mitochondrial function were not fully understood, especially in the absence of heart failure.
Does experimental myocardial infarction without haemodynamic compromise alter skeletal muscle bioenergetics in rats?
Population
Rats with experimental myocardial infarction (12 +/- 3% LV volume) without heart failure or hypertrophy
Comparison
Infarcted rats vs non-infarcted control rats
Design
Preclinical experimental study
Follow-up
4 weeks post-operatively
Authors
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Small experimental MI without HF spares rat skeletal muscle bioenergetics; leaves open effects in clinical heart failure.
Does experimental myocardial infarction without haemodynamic compromise alter skeletal muscle bioenergetics in rats?
Absolute Event Rate: 1.6% vs 0.7%
Myocardial infarction can induce mitochondrial abnormalities in skeletal muscle even in the absence of overt haemodynamic compromise or heart failure.
Thompson et al. (1994) studied Myocardial infarction. Experimental myocardial infarction vs. Control was evaluated on Rate of phosphocreatine recovery (half-time in minutes). Experimental myocardial infarction in rats markedly slowed the rate of skeletal muscle phosphocreatine recovery (half-time 1.6 vs 0.7 min) in the absence of haemodynamic compromise.
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