Abstract

Abstract Nowadays CCTA has become the first line diagnostic tool in the clinical management of CAD thanks to its outstanding performance in assessing both the degree of stenosis and coronary plaques features, with crucial prognostic implications. Furthermore, CTCA allows an accurate quantification of epicardial fat, which has been shown to be a metabolic active tissue that by means of inflammatory mediators influences the development of high risk plaques and atrial fibrillation. A 70–years–old man underwent primary PCI for an acute STEMI. He was a former smoker with a history of obesity, hypertension, hypercholesterolemia and type II diabetes, without previous major cardiovascular events or significant comorbidities. The coronary angiography revealed diffuse coronary artery ectasia and a thrombotic total occlusion of the proximal portion of the RCA. After intravenous antiplatelet agent administration, balloon angioplasty was performed and three drug eluting stents were implanted. Furthermore, since the coronary angiography showed a calcific contour travelling parallel to the RCA course, in order to rule out a thrombosed coronary pseudoaneurysm, a CTCA was performed. CTCA unexpectedly revealed an enormous fibro–fatty plaque surrounded by a calcific shell in the RCA ostium–proximal segment, with the stents located at one border of the plaque, well expanded inside the vessel lumen. The post–procedural hospital stay was marked by new onset Atrial Fibrillation, unresponsive to pharmacological cardioversion. In contrast with coronary invasive angiography, CT was able to detect a very high plaque burden and a salient ubiquitary epicardial fat volume. In addition, at the site of the culprit lesion, CT showed huge plaque volume with an extreme eccentrically positive vessel remodeling, large low attenuation areas and spotty calcifications, all features known to predict adverse coronary events. This case shows how the combination of metabolic syndrome and ectopic fat accumulation fosters a milieu conducive for high risk atherosclerosis and its clinical complications.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call