MINI-SYMPOSIUM

Pathologic assessment of the vulnerable human coronary plaque

F D Kolodgie¹, R Virmani¹, A P Burke¹, A Farb¹, D K Weber¹, R Kutys¹, A V Finn², H K Gold²

¹ The Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC, USA
² Cardiac Unit, Department of Internal Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA

Correspondence to:
Correspondence to:
Renu Virmani MD
Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, 6825 16th Street, NW, Washington, DC 20306–6000, USA; virmani@afip.osd.mil

Keywords: coronary plaque; thin cap fibroatheroma

The first 150 words of the full text of this article appear below.

Despite significant strides towards an understanding of the initiation and progression of atherosclerosis and the influence of risk factors, coronary heart disease remains the principal killer in the western world.¹ If progress in the field is to continue in the 21st century, one must focus on high risk patients with lesions that are vulnerable to thrombosis together with the triggering mechanisms that cause plaques to rupture at a precise location and time. Although animal studies have helped define the molecular mechanisms of atherosclerosis, a convincing model of plaque rupture still does not exist. Therefore, the development of future treatments targeted against plaque instability is contingent upon our ability to confidently recognise precursor lesions likely to thrombose; this will be primarily achieved via improved imaging modalities.

Insights into the mechanisms of coronary thrombosis extend from detailed analyses of underlying plaque morphologies in necropsy specimens from sudden death victims.^2,3 In 50–75% of . . . [Full text of this article]

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