Key result
Furosemide and ramipril equivalently attenuated reactive hypertrophy, improved left ventricular systolic function, and significantly reduced cardiac ACE and remodeling in post-infarction rats.
Why the study?
Does furosemide, ramipril, or their combination improve cardiac remodeling and RAS activity in a rat model of post-infarction chronic heart failure?
Population
Spontaneously hypertensive rats with myocardial infarction produced by coronary artery ligation
Comparison
Ramipril, furosemide, or combination therapy for… vs Untreated rats with myocardial infarction
Design
Preclinical, Randomly assigned
Follow-up
6 weeks
Authors
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Does not change post-MI HF therapy; leaves open whether furosemide attenuates remodeling in patients.
RCT
randomly assigned
Does furosemide, ramipril, or their combination improve cardiac remodeling and RAS activity in a rat model of post-infarction chronic heart failure?
In a rat model of post-infarction heart failure, furosemide and ramipril significantly reduced cardiac ACE and remodeling, suggesting diuretics work favorably without interfering with the effects of ACE inhibitors.
Seeland et al. (2003) conducted an RCT in chronic heart failure post-myocardial infarction. Furosemide, ramipril, or combination vs. untreated rats was evaluated on cardiac ACE mRNA and activity, reactive hypertrophy, and left ventricular systolic function. Furosemide and ramipril equivalently attenuated reactive hypertrophy, improved left ventricular systolic function, and significantly reduced cardiac ACE and remodeling in post-infarction rats.
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