In mice with fatty artery buildup, a quick burst of stress (like cold, a toxin, and a blood pressure drug) caused 3 out of 4 fragile plaques to burst, but only if the plaque was already weak — strong plaques didn’t break.
Scientific Claim
In apolipoprotein E-knockout mice fed a high-fat diet and subjected to carotid collar placement, short-term combination stimulation with lipopolysaccharide, phenylephrine, and cold exposure is associated with a 75% rate of plaque rupture in vulnerable plaques at 14 weeks, but no rupture in stable plaques at 6 weeks, suggesting that plaque vulnerability and acute stressors jointly determine rupture events.
Original Statement
“In total, 75% (18/24) of vulnerable plaques, but no stable plaques, showed rupture characteristics.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study reports observed frequencies of rupture under experimental conditions without implying causation or generalizability. The language 'associated with' is appropriate for this animal model.
Evidence from Studies
Supporting (1)
Scientists made mice with clogged arteries and stressed them with cold, a toxin, and a drug — and 75% of the weak plaques broke open, but the strong ones didn’t. This shows that both weak plaques and sudden stress are needed to cause a rupture.