Statin Users See Good Changes in Atherosclerotic Plaques

While statin therapy didn’t curb overall atherosclerotic plaque progression on serial coronary CT angiography, it was associated with plaques transforming to a lower-risk composition.

Statin use was associated with volume decreases in low-attenuation plaque and fibro-fatty plaque and greater progression of high-density calcium plaque and very dense 1K plaque. In contrast, untreated coronary lesions increased in volume over time for all calcified and noncalcified plaque types alike.

Coronary lesions without low-attenuation plaque or fibro-fatty plaque at baseline changed after statin therapy to include more dense calcium, reported Jeroen Bax, MD, PhD, of Leiden University Medical Center in The Netherlands, and collaborators of the PARADIGM study in JAMA Cardiology.

Moreover, increasing calcium density was associated with slower overall plaque progression — a finding in line with prior work tying 1K plaque, with its very dense calcium, with a reduced risk of acute coronary syndrome.

“Atherosclerotic features associated with ruptured plaques are large necrotic cores with an inflamed and thin fibrous cap. However, plaque features hypothesized to contribute to plaque stability are small necrotic cores that have been replaced by sheets of calcification,” Bax and colleagues wrote.

PARADIGM included 857 patients (mean age 62.1 years, 63.0% men) undergoing serial coronary CT angiography 2 or more years apart in 2013-2016, and was conducted at 13 sites in seven countries.

Images of 2,458 coronary lesions were assessed, over two-thirds of which were in patients treated with statins.

Plaque composition was categorized according to calcium content on CT angiography: low attenuation (-30 to 75 Hounsfield units [HU]), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1,000 HU), and 1K (>1,000 HU).

Based on study results, plaques with growing attenuation over 700 HU “may have protective implications, but this hypothesis requires further study,” Bax and colleagues noted.

The observational study left room for unmeasured confounding. As such, the authors were unable to claim that statin use directly causes compositional plaque changes.