Turning ACS outside in: linking perivascular adipose tissue to acute coronary syndromes

ACUTE CORONARY SYNDROME (ACS) typically occurs when an atherosclerotic plaque suddenly destabilizes in a patient with previously stable coronary artery disease (CAD) (7). Tradition-ally, the research emphasis in this area has focused on pathol-ogy occurring within the vessel lumen and the intima. The prevailing concept is that CAD pathology progresses “inside out ” with endothelial dysfunction, infiltration of inflammatory cells, transcytosis of cholesterol-rich atherogenic lipoproteins from plasma to the intima, oxidative modification, foam cell formation, and smooth muscle pleiocytosis, subsequently lead-ing to stable plaque growth (23, 24). Plaque rupture at the shoulder region of atherosclerotic lesions allows the precarious exposure of prothrombotic and proinflammatory mediators, thereby triggering ACS with its attendant morbidity and mor-tality. These concepts have been recently challenged by report