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Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2036-2040

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2036-2040.)
© 1999 American Heart Association, Inc.


Vascular Biology

Neonatal Intima Formation in the Human Coronary Artery

Yuji Ikari; Bruce M. McManus; Jennifer Kenyon; Stephen M. Schwartz

From the Department of Pathology (Y.I., S.M.S.), University of Washington, Seattle, and the Department of Pathology and Laboratory Medicine (B.M.M., J.K.), University of British Columbia, Vancouver, Canada.

Correspondence to Yuji Ikari, MD, Mitsui Memorial Hospital, Division of Cardiology, 1-Kanda-Izumi-cho, Chiyoda-ku, Tokyo 101, Japan.

Abstract—Intimal masses develop in the human coronary arteries of all humans, becoming atherosclerotic in later life either because of focal accumulation of lipid or the resulting response to injury. We evaluated the time course of formation of the intimal mass in the proximal left anterior descending coronary artery in autopsy specimens from 91 patients between 17 weeks' gestation and 23 months of postnatal age. Intima was rarely found before 30 weeks' gestation; however, the frequency with which at least some intimal cells were observed increased to 35% between 36 weeks' gestation and birth. By 3 months after birth, all patients had an intimal mass at this coronary location. The mean intima/media ratio was 0.1 just after birth and increased continuously to the second postnatal year. Replication of medial smooth muscle cells, indicated by proliferating cell nuclear antigen staining, was high before birth and decreased between birth and 2 years of age. However, the replication index of the intima remained at 2% to 5%. Thus, coronary intimal cells appearing in the perinatal period may arise by migration after replication of medial smooth muscle, as is seen in models of carotid artery balloon injury. In conclusion, formation of the coronary artery intima is a rapid process, beginning in the peripartum or postpartum period. Given the clonality of the adult lesion and the lack of proliferation in later stages of lesion formation, it is intriguing to speculate that this event may form the basis for atherosclerosis in later life.


Key Words: intima • proliferating cell nuclear antigen • monoclonality • infants • left anterior descending coronary artery




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