Key result
Carvedilol significantly improved ejection fraction (65.6% vs 55.45%) and attenuated myocardial fibrosis in rats with acute myocardial infarction via Smad3 inactivation and miR-29b upregulation.
Population
Male SD rats with left anterior descending surgery-induced acute myocardial infarction model, and rat…
Comparison
Carvedilol at low, medium, or high doses vs Sham surgery control and untreated LAD…
Design
Preclinical, randomized into several groups
Follow-up
4 weeks
Authors
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Should not change post-MI care; hypothesis-generating for carvedilol's Smad3/miR-29b effects in humans.
Absolute Event Rate: 65.6% vs 55.45%
p-value: p=<0.05
Carvedilol attenuates post-MI myocardial fibrosis and cardiac remodeling in rats via a mechanism involving Smad3 inactivation and miR-29b upregulation.
Zhu et al. (2013) studied Acute myocardial infarction-induced myocardial fibrosis (n=40). Carvedilol vs. Saline (untreated AMI model) was evaluated on Ejection fraction (EF) (p=<0.05). Carvedilol significantly improved ejection fraction (65.6% vs 55.45%) and attenuated myocardial fibrosis in rats with acute myocardial infarction via Smad3 inactivation and miR-29b upregulation.
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