Reciprocal communication of pericoronary adipose tissue and coronary atherogenesis.

Objective: Pericoronary adipose tissue (PCAT) has been linked to underlying coronary artery disease (CAD) and proposed to modulate adjacent atherosclerotic plaque formation over pro-inflammatory pathways. In vitro and ex vivo studies support the bilateral communication of adipose tissue and vessel wall. We quantified PCAT and its dynamics in a low coronary risk cohort with a semi-automated software in serial coronary computed tomography angiography (CTA).

Methods: We retrospectively included patients from a tertiary care hospital who underwent serial coronary CTA with a low cardiovascular risk profile. All examinations were evaluated in a standardized approach: epicardial adipose tissue (EAT) volume and attenuation was quantified in total, in the atrioventricular (RCA, LCX) or interventricular (LAD) sulcus and within a 5 mm radius for each coronary artery (PCAT). Coronary plaques were quantified using a semi-automated software and compared for progression, stability or regression.

Results: Of 120 patients (27% females), 59.2% showed atherosclerotic plaques. After 36 months mean follow-up, 22 (18.3%) showed plaque regression, 39 (32.5%) were stable and 49 (40.8%) were progressive. Total EAT volume decreased by -15.6 ± 37.2 mm³ in the regressive group, increased by 2.7 ± 30.6 mm³ in the stable group and by 24.3 ± 37.1 mm³ in the progressive group (p = 0.003). Per-vessel analysis showed a significant decrease of PCAT attenuation in patients with CAD regression (-3.8 ± 7.6HU) compared to the stable (1.2 ± 9.1HU) and progressive group (3.5 ± 8.2HU, p < 0.0001). Mean sulcus EAT attenuation did not show a significant change (p = 0.135).

Conclusion: Epicardial adipose tissue volume is mutually changing with the progression or regression of coronary artery disease. Perivascular but not epicardial attenuation levels correlate to adjacent plaque and support a direct bilateral influence.