Author + information
- Received June 16, 2005
- Revision received October 10, 2005
- Accepted October 24, 2005
- Published online April 18, 2006.
- ↵⁎Reprint requests and correspondence:
Dr. Renu Virmani, CVPath, International Registry of Pathology, 19 Firstfield Road, Gaithersburg, Maryland 20878.
The majority of patients with acute coronary syndromes (ACS) present with unstable angina, acute myocardial infarction, and sudden coronary death. The most common cause of coronary thrombosis is plaque rupture followed by plaque erosion, whereas calcified nodule is infrequent. If advances in coronary disease are to occur, it is important to recognize the precursor lesion of ACS. Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated. The non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrotic core with an overlying fibrous cap measuring <65 μm, containing rare smooth muscle cells but numerous macrophages. Thin cap fibroatheromas are most frequently observed in patients dying with acute myocardial infarction and least common in plaque erosion. They are most frequently observed in proximal coronary arteries, followed by mid and distal major coronary arteries. Vessels demonstrating TCFA do not usually show severe narrowing but show positive remodeling. In TCFAs the necrotic core length is approximately 2 to 17 mm (mean 8 mm) and the underlying cross-sectional area narrowing in over 75% of cases is <75% (diameter stenosis <50%). The area of the necrotic core in at least 75% of cases is ≤3 mm2. These lesions have lesser degree of calcification than plaque ruptures. Thin cap fibroatheromas are common in patients with high total cholesterol (TC) and high TC/high-density lipoprotein cholesterol ratio, in women >50 years, and in those patients with elevated high levels of high sensitivity C-reactive protein. It has only recently been recognized that their identification in living patients might help reduce the incidence of sudden coronary death.
The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army, the Department of the Air Force, or the Department of Defense. Dr. William A. Zoghbi acted as guest editor.
- Received June 16, 2005.
- Revision received October 10, 2005.
- Accepted October 24, 2005.
- American College of Cardiology Foundation
- Plaque rupture as the basis of ACS
- Location, length, and percent luminal narrowing of the TCFA
- Role of monocyte infiltration of the occlusive thrombus
- Plaque erosion as the basis of ACS
- Calcified nodule as the basis of ACS
- Coronary calcification
- Correlation of risk factors with ACS pathology