Inflammation contributes to many of the characteristics of plaques implicated in the pathogenesis of acute coronary syndrome. Moveover, inflammatory pathways not only regulate the properties of plaques that precipitate acute coronary syndromes but also modulate the clinical consequences of the thrombotic complications of atherosclerosis.
Vascular inflammation has been recognized as one of the key factors in the pathogenesis of acute coronary syndromes (ACS). It is known that elevated plasma inflammatory biomarkers such as high sensitivity C-reactive protein and Interleukin-6 are associated with cardiovascular events. Recently peri-coronary adipose tissue (PCAT) attenuation by computed tomography angiography has emerged as a marker specific for coronary artery inflammation. Recent studies demonstrated that high PCAT attenuation was associated with increased cardiac mortality6 and progression of no culprit plaque. Current results strongly suggest that not only plaque morphology but also inflammation plays an important role in the development of ACS. Anti-inflammatory therapy may have additional value in those subjects with high PCAT attenuation for the prevention of ACS and cardiac death.
