Effect of statin therapy on coronary inflammation assessed by pericoronary adipose tissue computed tomography attenuation

Abstract

Aims: Pericoronary adipose tissue (PCAT) attenuation on coronary computed tomography angiography (CCTA) is an imaging biomarker of coronary inflammation. The natural history of PCAT attenuation remains unknown. High-intensity statin therapy has pleiotropic anti-inflammatory effects. We sought to assess temporal changes in PCAT attenuation in patients with and without statin therapy.

Methods and results: This was a multicentre observational study that included consecutive patients with stable coronary artery disease (CAD) undergoing clinically indicated serial CCTA with identical scan parameters ≥ 12 months apart between May 2013 and July 2022. Using semi-automated software, PCAT attenuation was measured on a per-lesion level (PCATlesion) and per-patient level around the proximal right coronary artery (PCATRCA). Of the 96 patients (57 ± 11 years, 60% male), 34 patients were not on a statin at baseline or follow-up (statin-naive), 26 patients were commenced on a statin after the baseline scan (statin-commenced), and 34 patients were on a statin at both time points (statin-continued). There was no significant difference between the groups for age, sex, body mass index (BMI), and prevalence of traditional cardiovascular risk factors except for dyslipidaemia (25.0% vs. 34.6% vs. 64.7%, P < 0.01 for trend). At a median follow-up of 3.8 years, there was a significant reduction in PCATlesion in the statin-commenced (-79.4 ± 11.7 to -86.5 ± 10 HU, P < 0.001) and the statin-continued (-83.5 ± 8.5 to -90.6 ± 8.5 HU, P = 0.001) groups. Meanwhile, no significant difference in PCATlesion was observed in the statin-naïve group (-84.4 ± 9.7 to -86.6 ± 9.5, P = 0.1). Multivariate analysis showed statin intensity and LDL change to be independently associated with percentage change of PCATlesion, after correcting for cardiovascular risk factors, changes in body weight, and coronary artery calcium score.

Conclusion: Statin therapy was associated with a reduction in PCATlesion, while no significant change in PCATlesion was observed without statin therapy. If validated in larger studies, PCAT attenuation could potentially be used to monitor the response of the coronary arteries to statins and guide treatment.

Keywords: atherosclerosis; coronary computed tomography angiography; inflammation; pericoronary adipose tissue; statin.

Graphical Abstract

A schematic overview of the main study aims and findings, with a representative image demonstrating a case example of changes in PCAT attenuation in a patient commenced on statin after the baseline CCTA. CACS, coronary artery calcium score, CCTA, coronary computed tomography angiography; HU, Hounsfield units; PCAT, pericoronary adipose tissue.

Figure 1

Patient selection and study design. Flow chart showing inclusion and exclusion criteria for the three cohorts.

Figure 2

Changes in PCAT_lesion attenuation value across the three groups with different statin intake histories. There was significant reduction in PCAT_lesion in the statin-commenced (−77.5 ± 12.4 to −84.9 ± 10.6 HU, P < 0.0001) and statin-continued groups (−78.5 ± 11.2 to −83.5 ± 12.5 HU P = 0.0003). No significant change was seen in the statin-naïve group (−81.9 ± 10.5 to −84.0 ± 10.7, P = 0.1).

Figure 3

Baseline and follow-up PCAT_lesion attenuation maps on CCTA. PCAT around the coronary plaque is shown in cross-section (upper panels) and curved multi-planar views (lower panels) in case examples of patients who are statin-naïve (A) and statin-commenced (B).

Figure 4

Changes in PCAT_RCA across the three groups with different statin intake histories. There was a significant reduction in PCAT_RCA in all three cohorts. The statin-commenced cohort has the greatest reduction (−75.6 ± 9.5 to −84.3 ± 8.5 HU, P < 0.0001), followed by the statin-continued cohort (−76.2 ± 9.7 to −80.2 ± 10.2, P = 0.03), and with the statin-naïve cohort having the lowest change (−78.8 ± 9.4 to −83.3 ± 7.9 HU, P < 0.01).