January 5, 2007Journal of Hypertension
Therapeutic effects of angiotensin II type 1 receptor blocker at an advanced stage of hypertensive diastolic heart failure
Key result
A 3-week administration of olmesartan significantly decreased left ventricular end-diastolic pressure and attenuated hypertrophy, fibrosis, and diastolic dysfunction in rats with advanced DHF.
Why the study?
Does olmesartan improve left ventricular diastolic dysfunction and remodeling in a rat model of advanced hypertensive diastolic heart failure?
Population
Dahl salt-sensitive rats fed an 8% NaCl diet from age 7 weeks, n=12, at age 17 weeks with established left…
Comparison
Olmesartan 0.6 mg/kg per day for 3 weeks. vs Untreated control group.
Design
Preclinical, Randomly divided into two groups
Follow-up
3 weeks
Authors
Discussion
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Implication
Does not support clinical use in human DHF; leaves open translation of ARB effects from advanced rat models.
Structured PICO
Does olmesartan improve left ventricular diastolic dysfunction and remodeling in a rat model of advanced hypertensive diastolic heart failure?
P
Population
12 Dahl salt-sensitive rats with advanced hypertensive diastolic heart failure, randomized at 17 weeks of age to ARB therapy or no treatment for 3 weeks.
I
Intervention
Olmesartan 0.6 mg/kg per day (subdepressor dose) for 3 weeks.
C
Comparator
Untreated control group.
O
Outcome
Left ventricular end-diastolic pressure, left ventricular hypertrophy, fibrosis, and diastolic dysfunction.surrogate
Olmesartan attenuates diastolic dysfunction, hypertrophy, and fibrosis in a rat model of advanced hypertensive diastolic heart failure, independent of its blood pressure-lowering effects.
Cite This Study
Nishio et al. (2007) studied hypertensive diastolic heart failure (n=12). Angiotensin II type 1 receptor blocker (olmesartan) vs. untreated was evaluated on left ventricular end-diastolic pressure, hypertrophy, fibrosis and diastolic dysfunction. A 3-week administration of olmesartan significantly decreased left ventricular end-diastolic pressure and attenuated hypertrophy, fibrosis, and diastolic dysfunction in rats with advanced DHF.