Computed tomography and nuclear medicine for the assessment of coronary inflammation: clinical applications and perspectives

Abstract

There is increasing evidence that in patients with atherosclerotic cardiovascular disease (ASCVD) under optimal medical therapy, a persisting dysregulation of the lipid and glucose metabolism, associated with adipose tissue dysfunction and inflammation, predicts a substantial residual risk of disease progression and cardiovascular events. Despite the inflammatory nature of ASCVD, circulating biomarkers such as high-sensitivity C-reactive protein and interleukins may lack specificity for vascular inflammation. As known, dysfunctional epicardial adipose tissue (EAT) and pericoronary adipose tissue (PCAT) produce pro-inflammatory mediators and promote cellular tissue infiltration triggering further pro-inflammatory mechanisms. The consequent tissue modifications determine the attenuation of PCAT as assessed and measured by coronary computed tomography angiography (CCTA). Recently, relevant studies have demonstrated a correlation between EAT and PCAT and obstructive coronary artery disease, inflammatory plaque status and coronary flow reserve (CFR). In parallel, CFR is well recognized as a marker of coronary vasomotor function that incorporates the haemodynamic effects of epicardial, diffuse and small-vessel disease on myocardial tissue perfusion. An inverse relationship between EAT volume and coronary vascular function and the association of PCAT attenuation and impaired CFR have already been reported. Moreover, many studies demonstrated that 18F-FDG PET is able to detect PCAT inflammation in patients with coronary atherosclerosis. Importantly, the perivascular FAI (fat attenuation index) showed incremental value for the prediction of adverse clinical events beyond traditional risk factors and CCTA indices by providing a quantitative measure of coronary inflammation. As an indicator of increased cardiac mortality, it could guide early targeted primary prevention in a wide spectrum of patients. In this review, we summarize the current evidence regarding the clinical applications and perspectives of EAT and PCAT assessment performed by CCTA and the prognostic information derived by nuclear medicine.

Relationship between peri-coronary inflammation and coronary vascular function in patients with suspected coronary artery disease

“…Previous studies have confirmed that FAI reflects peri-coronary inflammation and is associated with vulnerable plaques and inflammatory activities ( 1 , 17 ). Moreover, the paracrine-mediated regulation of vascular homeostasis by PCAT has been reported in a study ( 18 ). In cases of CAD or microvascular dysfunction, radical oxygen species generated in response to regional ischemia can trigger the activation of EAT-driven inflammatory signals by releasing chemokines and inflammatory cytokines, which exert local effects on the underlying coronaries and myocardium ( 18 ).…”

“…Moreover, the paracrine-mediated regulation of vascular homeostasis by PCAT has been reported in a study (18). In cases of CAD or microvascular dysfunction, radical oxygen species generated in response to regional ischemia can trigger the activation of EAT-driven inflammatory signals by releasing chemokines and inflammatory cytokines, which exert local effects on the underlying coronaries and myocardium (18). The possible mechanism is that coronary artery inflammation in patients with impaired coronary blood flow may disrupt the role of PCAT in regulating vascular tension caused by focal inflammation.…”

Epicardial and Pericoronary Adipose Tissue, Coronary Inflammation, and Acute Coronary Syndromes

“…Higher CT attenuation in EAT indicates the presence of enlarged adipocytes and infiltration of pro-inflammatory M1 macrophages, indicating inflammation [46,52]. CT attenuation of the surrounding PCAT has prognostic significance in CAD, as elevated attenuation is associated with reduced coronary flow reserve [18,19,53], while a pericoronary fat attenuation index (pFAI) exceeding a specific threshold has been predictive of both all-cause and cardiac mortality [54]. Utilizing the pFAI could potentially improve risk assessment and guide targeted prevention strategies for individuals at higher risk [52].…”