Key result
Treatment with 17b-estradiol or the ERα agonist 16α-LE2 slowed the progression of myocardial hypertrophy and reduced systolic dysfunction, but significantly decreased the 9-week survival rate to 58.3% compared to 92.3% with placebo.
Why the study?
Does estrogen, an ERα agonist, or raloxifene improve cardiac hypertrophy and function in a mouse model of pressure overload?
Does estrogen, an ERα agonist, or raloxifene improve cardiac hypertrophy and function in a mouse model of pressure overload?
Absolute Event Rate: 58.3% vs 92.3%
p-value: p=<0.05
E2 and the ERα agonist 16α-LE2 attenuated the progression of myocardial hypertrophy and systolic dysfunction in a pressure overload mouse model, but were associated with significantly increased mortality.
No takes yet. Share an insight, caveat, or question.
May improve hypertrophy and function yet raise mortality in pressure-overload mice; leaves open net benefit and translational relevance of ERα agonism.
Westphal et al. (2012) studied Pressure overload induced cardiac hypertrophy (n=52). 17b-estradiol (E2) and 16a-LE2 vs. Placebo was evaluated on Survival rate at 9 weeks (p=<0.05). Treatment with 17b-estradiol or the ERα agonist 16α-LE2 slowed the progression of myocardial hypertrophy and reduced systolic dysfunction, but significantly decreased the 9-week survival rate to 58.3% compared to 92.3% with placebo.
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