Key result
Deletion of the angiotensin II type 1a receptor reduced the incidence of atherosclerotic plaque rupture from 72% to 24% in ApoE-/- mice (P<0.01).
Why the study?
Does deletion of the AT1a receptor prevent atherosclerotic plaque rupture in ApoE-/- mice?
Does deletion of the AT1a receptor prevent atherosclerotic plaque rupture in ApoE-/- mice?
Absolute Event Rate: 24% vs 72%
p-value: p=<0.01
Genetic deletion of the AT1a receptor significantly reduces the incidence of atherosclerotic plaque rupture in a mouse model, suggesting a crucial role for AT1a in plaque vulnerability.
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Should not change practice; hypothesis-generating for AT1a blockade in human plaque vulnerability.
Aono et al. (2012) studied Atherosclerotic plaque rupture. Deletion of the Angiotensin II Type 1a Receptor vs. ApoE(-/-) mice (without AT1a deletion) was evaluated on Incidence of plaque rupture at 4 days after cuff placement (p=<0.01). Deletion of the angiotensin II type 1a receptor reduced the incidence of atherosclerotic plaque rupture from 72% to 24% in ApoE-/- mice (P<0.01).
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