Plaque Stability on Statins Bolstered by ‘Good’ Type of Calcification
Statin therapy has long been thought to cut the risk for ischemic coronary events, in part by stabilizing atherosclerotic plaques that are vulnerable to rupture, which would trigger thrombosis, and in part by depleting lesions of lipid and other soft components.
But it might be that statins, with a certain amount of irony, also intensify the process of plaque calcification, a familiar marker of increased risk. Statin therapy might raise the density of lesion calcifications in a way that makes rupture less likely, suggests a study of plaque size and composition by serial coronary CT angiography (CTA).
Two CTA scans were obtained at least 2 years apart on more than 2500 coronary lesions in 857 patients in an international registry, 64% of whom had been on statin therapy continuously throughout that time. The remainder had not been on a statin at any time between scans.
Not unexpectedly, there were signs that plaques in statin-treated patients progressed in volume more slowly than those not exposed to the drugs. But CTA caught other changes over time based on the density of lesion components, as visualized and measured by within-lesion variation in gray-scale signal attenuation.
In general, coronary plaques in statin-treated patients transformed from containing calcium at low densities to showing predominantly higher-density calcifications. Meanwhile, plaques with the lowest calcium densities progressed in volume at the highest rate, and those containing the densest calcium showed the slowest progression.
In other words, the findings might partly account for the way statin therapy lowers atherothrombotic risk, in that they suggest statins make plaques progressively less vulnerable by “increased densification” of calcium and diminishing softer components, Alexander R. van Rosendael, MD, told theheart.org | Medscape Cardiology.
“We very nicely saw that the plaques that are considered the highest-risk, the low-attenuation plaques, actually decrease. And probably parts of them will become this very dense calcium,” said van Rosendael, New York–Presbyterian Hospital and Weill Cornell Medicine, New York City. “We believe that this partially explains why statins work.”
The analysis, based on the Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging (PARADIGM) registry, was published online August 18 in JAMA Cardiology, with van Rosendael as lead author.