Impact of statins on progression of coronary artery calcium composition and density as assessed by noncontrast CT.
Authors
Affiliations (8)
Affiliations (8)
- Monash Health, Clayton, VIC, Australia.
- Department Medicine, Division of Artificial Intelligence in Medicine), Imaging and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
- Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
- Department of Cardiac Sciences, University of Calgary, Calgary, AB, Canada.
- British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
- Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
- Monash Victorian Heart Institute Victorian Heart Hospital, 631 Blackburn Road, Clayton, VIC, 3168, Australia.
- Monash Victorian Heart Institute Victorian Heart Hospital, 631 Blackburn Road, Clayton, VIC, 3168, Australia. [email protected].
Abstract
The effect of statins on progression of coronary artery calcium (CAC) density as measured by noncontrast computed tomography (CT) remains unknown. We examined the association of statin therapy with temporal changes in compositional calcium density using quantitative assessment of CAC scoring CT. This was a retrospective, single-center study of asymptomatic individuals undergoing serial CAC scoring CT. Scans were analyzed using a fully automated deep learning model, with quantification of total CAC volume and volumes of calcium compositional subtypes stratified by Hounsfield unit (HU) density: 130-199; 200-299; 300-399; ≥400 HU. Of 316 patients (58.4 ± 10.1 years; 49.1% male) with CAC present at baseline and rescanned at a mean interval of 3.8 ± 1.7 years, 175 (55.4%) patients were statin-treated and 141 (44.6%) patients were statin-naive. In patients exhibiting only low-density calcium (130-199 HU) at baseline, statin therapy was associated with a temporal decrease in CAC volume (β - 0.05[-0.09 to - 0.02]; p < 0.05). Among patients with ≥ 2 calcium compositional subtypes at baseline, statin therapy was associated with a greater temporal increase in volumes of each density stratum (130-199 HU: β 0.05[0.00-0.11]; 200-299 HU: β 0.11[0.07-0.14]; 300-399 HU: β 0.11[0.07-0.16]; ≥400 HU: β 0.11[0.06-0.16]; all p < 0.05). Similar results were observed for changes in relative proportions of each density stratum (all p < 0.001). In asymptomatic individuals undergoing serial CAC scoring CT, statin therapy was associated with a shift toward denser calcium, considered a more stable phenotype. Assessment of CAC density may capture more unique aspects of plaque progression and stability beyond traditional CAC scoring.