What does this research mean for the field?

Long-term AT1-receptor blockade does not regress left ventricular hypertrophy in rats with persistent systolic pressure overload, but it improves left ventricular end-diastolic pressure and normalizes left ventricular ACE mRNA levels. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

Determine whether chronic AT1 receptor blockade regresses left ventricular hypertrophy and alters left ventricular ACE expression in rats with pressure-overload aortic stenosis.

March 18, 1997Circulation

Angiotensin AT 1 Receptor Inhibition

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Why the study?

Does AT1-receptor blockade regress hypertrophy and modify left ventricular ACE expression in rats with ascending aortic stenosis?

Population

184 rats (145 with ascending aortic stenosis, 39 sham-operated)

Comparison

AT1-receptor blocker BMS-186295 50 mg.kg-1.d-1… vs Amlodipine 2.5 mg.kg-1.d-1, no drug, or sham…

Design

Preclinical, randomized

Follow-up

15 weeks

Authors

EWEllen O. WeinbergHeart Failure / Cardiomyopathy MLMin Ae LeeBrigham and Women's Hospital MWMarilyn J. WeignerProvidence College

Discussion

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Implication

AT1 blockade may improve hemodynamics without regressing LVH in pressure-overload rats; leaves open translation to human disease.

Key Points

Determine whether chronic AT1 receptor blockade regresses left ventricular hypertrophy and alters left ventricular ACE expression in rats with pressure-overload aortic stenosis.
Rats with surgically induced ascending aortic stenosis were randomized 6 weeks post-surgery to 15 weeks of BMS-186295 (50 mg/kg/d, n=49), amlodipine (2.5 mg/kg/d, n=48), or no drug (n=48), alongside sham-operated controls (n=39).
Left ventricular mass, myocyte cross-sectional area, in vivo hemodynamics, and ACE mRNA levels via ribonuclease protection assay were measured.
Neither BMS-186295 nor amlodipine regressed hypertrophy compared to untreated controls (left ventricular/body weight ratio: 2.78 ± 0.08 vs 2.81 ± 0.20 mg/g, P = NS; systolic pressure: 189 ± 9 and 188 ± 16 vs 193 ± 8 mm Hg, P = NS).
Both BMS-186295 and amlodipine significantly reduced left ventricular end-diastolic pressure (11.0 ± 1.7 and 11.5 ± 1.8 mm Hg vs 14.8 ± 2.3 mm Hg in untreated LVH; P = NS vs 7.0 ± 0.5 mm Hg in sham) and normalized elevated left ventricular ACE mRNA levels.

Structured PICO

Does AT1-receptor blockade regress hypertrophy and modify left ventricular ACE expression in rats with ascending aortic stenosis?

Population

184 rats (145 with ascending aortic stenosis, 39 sham-operated)

Intervention

AT1-receptor blocker BMS-186295 50 mg.kg-1.d-1 for 15 weeks

Comparator

Amlodipine 2.5 mg.kg-1.d-1 (positive control), no drug, or sham operation

Outcome

Left ventricular/body weight ratio and left ventricular ACE mRNA levelssurrogate

In a rat model of pressure overload, AT1-receptor blockade improved hemodynamics and normalized ACE expression without regressing left ventricular hypertrophy.

Cite This Study

Weinberg et al. (1997) studied this question.

synapsesocial.com/papers/6a1befaeea84844e355f31ee https://doi.org/10.1161/01.cir.95.6.1592

Topics

Hypertension management Echocardiography

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Angiotensin AT 1 Receptor Inhibition

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Angiotensin AT 1 Receptor Inhibition

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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