In mice prone to clogged arteries, a daily dose of atorvastatin made the dangerous, rupture-prone plaques much less common—even though the overall blockage didn’t get smaller.

The drug reduced the number of inflammatory immune cells inside the artery plaques by nearly 40%, which also made the plaques less fatty and changed their collagen structure.

The drug lowered the activity of enzymes that break down the structural fibers in plaques, which may help keep plaques from rupturing.

Atorvastatin helps make the new blood vessels inside artery plaques less leaky by helping support cells stick better and sealing gaps between vessel lining cells, which may stop bleeding inside the plaque.

Atorvastatin helps the support cells (pericytes) wrap around new blood vessels in plaques more tightly, making them stronger and less likely to leak.

A common cholesterol drug called atorvastatin can reduce the growth of leaky new blood vessels inside artery plaques, even when it doesn’t lower cholesterol much—this might help prevent plaques from bursting.