Neonatal intima formation in the human coronary artery

被引:87
作者
Ikari, Y
McManus, B
Kenyon, J
Schwartz, SM
机构
[1] Univ Washington, Dept Pathol, Seattle, WA 98195 USA
[2] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada
关键词
intima; proliferating cell nuclear antigen; monoclonality; infants; left anterior descending coronary artery;
D O I
10.1161/01.ATV.19.9.2036
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:2036 / 2040
页数:5
相关论文
共 36 条
[1]  
Benditt E P, 1976, Ann N Y Acad Sci, V275, P96, DOI 10.1111/j.1749-6632.1976.tb43342.x
[2]  
BENDITT EP, 1977, AM J PATHOL, V86, P693
[3]  
CAMPBELL GR, 1990, ADV EXP MED BIOL, V273, P147
[4]   HEPARAN SULFATE-DEGRADING ENZYMES INDUCE MODULATION OF SMOOTH-MUSCLE PHENOTYPE [J].
CAMPBELL, JH ;
RENNICK, RE ;
KALEVITCH, SG ;
CAMPBELL, GR .
EXPERIMENTAL CELL RESEARCH, 1992, 200 (01) :156-167
[5]   EXTRACELLULAR MATRIX-SMOOTH MUSCLE PHENOTYPE MODULATION BY MACROPHAGES [J].
CAMPBELL, JH ;
KALEVITCH, SG ;
RENNICK, RE ;
CAMPBELL, GR .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1990, 598 :159-166
[6]   CYTOGENETIC ANALYSIS REVEALS CLONAL PROLIFERATION OF SMOOTH-MUSCLE CELLS IN ATHEROSCLEROTIC PLAQUES [J].
CASALONE, R ;
GRANATA, P ;
MINELLI, E ;
PORTENTOSO, P ;
GIUDICI, A ;
RIGHI, R ;
CASTELLI, P ;
SOCRATE, A ;
FRIGERIO, B .
HUMAN GENETICS, 1991, 87 (02) :139-143
[7]  
Chung IM, 1998, AM J PATHOL, V152, P913
[8]   KINETICS OF CELLULAR PROLIFERATION AFTER ARTERIAL INJURY .4. HEPARIN INHIBITS RAT SMOOTH-MUSCLE MITOGENESIS AND MIGRATION [J].
CLOWES, AW ;
CLOWES, MM .
CIRCULATION RESEARCH, 1986, 58 (06) :839-845
[9]  
CLOWES AW, 1983, LAB INVEST, V49, P327
[10]   LONG-TERM BIOLOGICAL RESPONSE OF INJURED RAT CAROTID-ARTERY SEEDED WITH SMOOTH-MUSCLE CELLS EXPRESSING RETROVIRALLY INTRODUCED HUMAN GENES [J].
CLOWES, MM ;
LYNCH, CM ;
MILLER, AD ;
MILLER, DG ;
OSBORNE, WRA ;
CLOWES, AW .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (02) :644-651