Coronary CT angiography derived pericoronary inflammation and bespoke cardiovascular risk prediction in the lipid clinic: beyond the calcium score

Abstract

Abstract Background Dyslipidaemia promotes atherosclerosis. Genetic dyslipidaemias, Familial Hypercholesterolaemia (FH) being the most common, are associated with heightened risk of coronary artery disease (CAD) and premature major adverse cardiovascular events (MACE). However, this risk is both heterogeneous and modifiable with treatment. CT coronary imaging can identify subclinical atherosclerosis, enabling personalised risk stratification and treatment targets. Coronary artery calcium scoring (CACS) is current first-line in European guidelines for asymptomatic patients. However, calcification occurs late in CAD pathogenesis and CACS has low specificity in young patients with severe FH. CT coronary angiography (CTCA) assesses non-calcific plaque and high-risk plaque (HRP) features unappreciable with CACS. Additionally, the pericoronary fat attenuation index (FAI) measures inflammation on routine CTCA and is the strongest non-invasive imaging biomarker of risk of fatal MI. Purpose To quantify and compare the reclassification of subclinical atherosclerosis burden in Lipid Clinic patients assessed via CACS vs CTCA with FAI analysis. Methods Analysis of a prospectively maintained clinical database of asymptomatic Lipid Clinic patients with both CACS and CTCA imaging from May 2019 to December 2020. CACS was reported with the standardised Agastston criteria and compared with (i) the CTCA-derived Coronary Artery Disease – Reporting and Data System (CAD RADS) grading of anatomical stenosis, including a modifier for HRP features, and (ii) FAI analysis. Significance was defined as two-tailed p75th percentile vs age and sex matched controls) was seen in 6/27 (22%) patients with none to mild calcification on CACS and 6/28 (21%) patients with none to mild CAD on CTCA, of whom 3/7 (43%) had HRP. High FAI was seen in all groups of calcification severity and CAD RADS score (Figure 2). The proportion with high FAI was higher in CAD RADS 0 vs CAD RADS 4, and CACS severity was not associated with level of inflammation (p=0.94). High FAI was observed in 16% of patients on treatment, suggesting treatment failure. This included patients with CACS ranging from 0 to severe (>400), and CAD RADS of minimal (1) to severe (4). Conclusion CTCA re-stratifies CAD presence and severity vs CACS in a high-risk, asymptomatic patient group and identified a high proportion of patients with HRP features. FAI provides incremental value in identification of patients at risk of future MACE regardless of CACS grade, including patients without evidence of overt CAD. Identifying high FAI on treatment may imply treatment failure. Funding Acknowledgement Type of funding sources: None.