Reciprocal communication of pericoronary adipose tissue and coronary atherogenesis

Abstract

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 mm 3 in the regressive group, increased by 2.7 ± 30.6 mm 3 in the stable group and by 24.3 ± 37.1 mm 3 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.

The correlation of pericoronary adipose tissue with coronary artery disease and left ventricular function

“…Hoshino et al [ 40 ] mentioned that FAI was associated with cardiac mass, and some studies have reported a correlation between LV function and EAT [ 51 , 52 ]; notably, these results are similar to ours. In addition, studies have shown that LV dysfunction and increased FAI (> 70.1 HU) can significantly increase the cardiac mortality [ 42 , 53 ]. Our results suggest that cardiac mortality caused by increased FAI may be due to changes in LV function.…”

To Explore the Influencing Factors of Pericoronary Adipose Tissue and Noninvasive Fractional Flow Reserve on the Progression of Coronary Heart Disease Based on 320-Slice Coronary CTA

“… 13 , 14 Pericoronal adipose tissue-FAI can be regarded as a quantitative index of PCAT density changes; many studies believe that it has a certain relationship with major adverse cardiac events (MACEs) and that it can be used as a standard to measure the changes of perivascular inflammatory microenvironment. 15 , 16 It is believed that EAT may be related to the progression of coronary atherosclerotic plaque, but there are few studies related to the relationship between PCAT and coronary atherosclerosis. Therefore, this study got rid of the exploration of EAT.…”

The Correlation of Pericoronary Adipose Tissue with Coronary artery disease and left ventricular function

“…This may be because coronary artery and myocardium has no obvious boundary, and the PCAT can release cytokines reach myocardium and coronary artery through paracrine signaling mechanisms, which results in the changes of myocardial and left ventricular function [34] . In addition, studies have shown that left ventricular dysfunction and increased FAI (> 70.1HU) can signi cantly increase the cardiac mortality [31,35] . Our results suggest that cardiac mortality caused by increased FAI may be due to changes in left ventricular function.…”