While the concept of plaque `vulnerability' implies a propensity towards thrombosis, the term vulnerable was originally intended to provide a morphologic description consistent with plaques that are prone to rupture. It is now known that the etiology of coronary thrombi is diverse and can arise from entities of plaque erosion or calcified nodules. These findings have prompted the search for more definitive terminology to describe precursor lesions associated with rupture, now referred to as thin-cap fibroatheromas. This review focuses on the thin-cap fibroatheroma, as a specific cause of acute coronary syndromes. To put these issues into current perspective, we need to revisit some of the older literature describing plaque morphology in stable and unstable angina, acute myocardial infarction, and sudden coronary death. The morphology, frequency, and precise location of these thin-cap fibroatheromas are further discussed in detail. Potential mechanisms of fibrous cap thinning are also addressed, in particular emerging data, which suggests the role of cell death “apoptosis” in cap atrophy.
From the *Departments of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC; † Cell Biology, Harvard Medical School, Boston, Massachusetts; ‡ Molecular Cardiology, Hahnemann University, Philadelphia, Pennsylvania; and § Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Correspondence to Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, 6825, 16 th Street NW, Washington, DC 20306-6000; e-mail: firstname.lastname@example.org