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Atherosclerosis is a chronic, progressive, inflammatory disease causing multiple lesions in the intima of large and medium-sized arteries.1 A minority of atherosclerotic lesions referred to as vulnerable plaques (VPs) may suddenly precipitate thrombosis, leading to life-threatening events such as acute myocardial infarction and ischemic stroke. The most common VP is the rupture-prone type, also known as thin-cap fibroatheromas, which are characterized by a large necrotic core with a thin and inflamed fibrous cap, outward remodeling mitigating luminal obstruction, neovascularization, plaque hemorrhage, adventitial inflammation, and a “spotty” pattern of calcifications.2 Among these features, inflammation and angiogenesis are believed to be critical by degrading the plaque matrix (proteolytic enzymes secreted by macrophages) and expanding the necrotic core (intraplaque hemorrhage from leaky microvessels). Both inflammation and angiogenesis are known to be associated with tissue edema, but because edema is difficult to detect in dehydrated, paraffin-embedded pathological specimens, it has escaped attention as a possible VP marker.Cardiovascular magnetic resonance (CMR) with a T2-weighted short-tau inversion recovery sequence (T2-STIR) is an established technique for the visualization of myocardial edema as a measure of the area-at-risk in patients with acute myocardial infarction.3 Our own unpublished observations indicate that T2-STIR CMR often reveals localized coronary edema in the culprit artery of patients with acute myocardial infarction, indicating that VPs may be visualized by CMR. This is a novel finding, and there are no prior references to the use of this technique for the …

First In Vivo Demonstration of Coronary Edema in Culprit Lesion of Patient With Acute Coronary Syndrome by Cardiovascular Magnetic Resonance