Reciprocal communication of pericoronary adipose tissue and coronary atherogenesis.

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). 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. 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). 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.

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