Abstract Body (Do not enter title and authors here):

Introduction: Advances in coronary computed tomography angiography (CCTA) have enhanced the possibilities for assessment and quantification of coronary artery disease (CAD). Using data from the CCTA arm of the PRECISE randomized trial (non-acute chest pain needing testing), we examined the extent and diffuseness of coronary plaque burden using novel CCTA-derived metrics.

Methods: All stable, symptomatic patients from the PRECISE randomized trial who underwent CCTA for evaluation of suspected CAD and had ≥50% diameter stenosis in at least one vessel were included, N=196. 3-vessel CAD patterns were assessed using FFR_CT and AI-enabled quantitative plaque analysis (Heartflow). Nadir FFR_CT was defined as total drop in FFR_CT across the entire vessel. The FFR_CT drop over a stenosis was termed stenosis FFR_CT (sFFR_CT). The decrement in FFR_CT due to diffuse disease was termed diffuse FFR_CT (dFFR_CT) and defined as 1 – nadir FFR_CT – sFFR_CT. Patients were stratified into four groups (NoHEM, FOC, DIF and FOC+DIF) using cohort medians of 0.10 (sFFR_CT) and 0.13 (dFFR_CT) (Table). The Seattle Angina Questionnaire (SAQ) was used to assess symptoms.

Results: No hemodynamic disease (NoHEM), FOC, DIF and FOC+DIF were present in 21.5%, 28.6%, 29.6% and 20.4% of patients respectively. Clinical characteristics were similar between groups (Table). FOC and DIF+FOC had the lowest FFR_CT nadir values as well as the highest stenosis FFR_CT (both p<0.001). Per-patient total plaque volume (TPV, mm³) was higher in FOC and DIF+FOC compared to NoHEM and DIF (p=0.008; Figure). Per-patient noncalcified plaque volume (NCPV, mm³) followed a similar pattern (p=0.004), although % NCPV did not differ (0.86). Per-patient calcified plaque volume (CPV, mm³) and %CPV did not differ between groups (p=0.12 and 0.86).

Conclusion: CCTA allows for a more refined CAD plaque burden categorization by separating the FFR_CT losses due to focal stenoses and diffuse CAD. Patients with focal or mixed (focal and diffuse) CAD phenotypes were not distinguishable by clinical characteristics, risk burden or angina severity. However, they exhibited higher plaque volumes, particularly noncalcified plaque, than those with no NoHEM or only diffuse disease. Further studies are necessary to examine the prognostic and therapeutic implications of these findings.