Key result
In AT1A-KO mice with induced myocardial infarction, treatment with spironolactone (20 mg/kg per day) almost normalized LV remodeling, cardiac dysfunction, and cardiac gene expression.
Why the study?
Does spironolactone improve post-MI LV remodeling in angiotensin II type 1A receptor-knockout mice?
Population
Wild-type and angiotensin II type 1A receptor-knockout mice subjected to acute myocardial infarction by…
Comparison
Spironolactone (20 mg/kg per day) vs Untreated AT1A-KO mice and WT mice
Design
Preclinical
Follow-up
28 days
Authors
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May warrant targeting Ang II-independent pathways post-MI; leaves open clinical translation pending human data.
Does spironolactone improve post-MI LV remodeling in angiotensin II type 1A receptor-knockout mice?
Spironolactone normalizes post-MI LV remodeling in AT1A-KO mice, demonstrating that cardiac aldosterone plays a critical role in Ang II-independent remodeling.
Katada et al. (2005) studied Myocardial Infarction. Spironolactone vs. Untreated AT1A-KO mice and wild-type mice was evaluated on Left ventricular (LV) geometry, hemodynamics, and cardiac gene expression. In AT1A-KO mice with induced myocardial infarction, treatment with spironolactone (20 mg/kg per day) almost normalized LV remodeling, cardiac dysfunction, and cardiac gene expression.
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