Even though the mice had fatty plaques and they burst, their blood fat levels didn’t change — meaning the rupture wasn’t caused by worse cholesterol, but by something else, like immune activity.

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.

The mice lost a little weight from the stress, but not more than they did from just eating a fatty diet — so the plaque bursts weren’t caused by extreme sickness or starvation.

The drug didn’t lower the mice’s overall cholesterol, so its benefits must come from something else—like reducing inflammation or cell death in plaques.

Mice treated with the drug had much smaller dead-cell areas in their artery plaques—almost half as big—which might mean their plaques are less likely to break open.

Before the plaque actually burst, 8 out of 10 had bleeding inside them — meaning bleeding happens before the cap breaks, and might be a warning sign.