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.

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.

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

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.

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.