Abstract
Purpose
Perivascular epicardial adipose tissue (PEAT) has been linked to underlying coronary artery disease (CAD) and proposed to modulate adjacent atherosclerotic plaque formation. In vitro and ex vivo studies support bilateral influence of adipose tissue and vessel wall. Therefore, we quantified PEAT volume and composition and its dynamics in a low coronary risk patient cohort with a semi-automate software in serial CT exams.
Methods and materials
We retrospectively included 120 patients (27% females) from a tertiary care hospital who underwent serial cardiac CT angiographies with a low cardiovascular risk profile. All coronary CTs 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 in a 5mm radius for each coronary artery (PEAT). Coronary plaques were quantified using a semi-automated software and compared to progression, stability of regression between the two scans. The measurements were compared on a per-patient and per-vessel basis between plaque-naïve and diseased vessels.
Results
Of 120 patients (32% female), 59.2%) had atherosclerotic plaque formation. After 36 months mean follow-up, 22 (18.3%) showed a CAD regression plaques, 39 (32.5%) had stable coronary arteries and 49 (40.8%) progressive CAD. Total EAT volume decreased by −15.6±37.2 mm3 in the regressive group, increased by 2.7±30.6mm3 in the stable group and by 24.3±37.1mm3 in the progressive CAD group (p=0.003).
Per-vessel analysis showed a significant decrease of perivascular EAT attenuation in patients with CAD regression (−3.8±7.6 HU) compared to CAD stable (1.2±9.1 HU) and CAD progressive patients (3.5±8.2 HU, p<0.0001). Mean sulcus EAT attenuation did not show a significant change at follow-up (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 correlated to adjacent plaque and support a direct bilateral influence.
Change per-vessel-basis (n=360)
Funding Acknowledgement
Type of funding source: None
Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice
