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

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.

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 lowered levels of two key inflammation signals in the blood, showing it reduces body-wide inflammation even when cholesterol doesn’t change.

The drug lowered the levels of chemical signals (MCP-1 and CX3CL1) that attract immune cells to plaques, and also reduced the number of receptors on blood cells that respond to those signals.

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.