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J Am Coll Cardiol, 2007; 50:940-949, doi:10.1016/j.jacc.2007.04.086
(Published online 20 August 2007). © 2007 by the American College of Cardiology Foundation |
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* Harvard Medical School, Boston, Massachusetts
Massachusetts General Hospital, Boston, Massachusetts
InfraReDx, Inc., Burlington, Massachusetts
William Beaumont Hospital, Royal Oak, Michigan
|| Columbia University Medical Center and the Cardiovascular Research Foundation, New York, New York
¶ CV Path, Gaithersburg, Maryland.
Manuscript received December 22, 2006; revised manuscript received March 13, 2007, accepted April 3, 2007.
* Reprint requests and correspondence: Mr. Pavan K. Cheruvu, 104 Toxteth Street, #4, Brookline, Massachusetts 02446. (Email: pavan_cheruvu{at}hms.harvard.edu).
Objectives: Our purpose was to quantify the frequency and distribution of suspected vulnerable lesions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coronary artery autopsy specimens.
Background: Most acute coronary events and sudden death are believed to arise from rupture of a TCFA followed by thrombosis. Although there is general agreement that clinical events are usually caused by focal lesions, there is considerable debate over the relative importance of focal versus systemic factors in the pathogenesis of atherosclerosis.
Methods: We longitudinally sectioned coronary arteries from 50 whole hearts taken from patients (mean age 73 years, 64% men) dying of cardiovascular (n = 33), noncardiovascular (n = 13), and unknown (n = 4) causes. A total of 3,639 longitudinal segments of length 3 mm were sectioned from 148 arteries, accounting for 10.9 m of total tissue length. Specimens were classified on the basis of histology and computer-aided morphometry.
Results: Twenty-three TCFA and 19 ruptured plaques were found (mean ± SD: 0.46 ± 0.95 and 0.38 ± 0.70 per heart, respectively), and these lesions accounted for only 1.6% and 1.2%, respectively, of the total length of the coronary tree examined in patients dying of cardiovascular causes. The majority of TCFA and ruptured plaque localized in the proximal third of the major coronary arteries, and in 92% of cases these lesions clustered within 2 or fewer nonoverlapping 20-mm segments.
Conclusions: The suspected precursors of rupture-mediated thrombosis occur in a limited, focal distribution in the coronary arteries.
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