Neonatal intima formation in the human coronary artery

Neonatal intima formation in the human coronary artery
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DOI:
10.1161/01.atv.19.9.2036
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发表时间:
1999-09-01
影响因子:
8.7
通讯作者:
Schwartz, SM
Schwartz, SM
中科院分区:
医学1区
文献类型:
--
作者:
Ikari, Y;McManus, B;Schwartz, SM

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所有人类的冠状动脉中都会出现内膜肿块,在以后的生活中由于脂质的局灶性积累或由此产生的对损伤的反应而变得动脉粥样硬化。我们评估了 91 名妊娠 17 周至产后 23 个月患者的尸检标本中左冠状动脉前降支近端内膜肿块形成的时间过程。妊娠30周前很少发现内膜;然而,在妊娠 36 周至出生期间,至少观察到一些内膜细胞的频率增加至 35%。出生后 3 个月,所有患者的冠状动脉位置均出现内膜肿块。出生后平均内膜/中膜比率为0.1,并持续增加到出生后第二年。增殖细胞核抗原染色表明,内侧平滑肌细胞的复制在出生前较高,但在出生至 2 岁时下降。然而,内膜的复制指数仍保持在2%至5%,因此,围产期出现的冠状内膜细胞可能是在内侧平滑肌复制后通过迁移而产生的,如颈动脉球囊损伤模型中所见。总之,冠状动脉内膜的形成是一个快速的过程,从围产期或产后期开始。考虑到成人病变的克隆性和病变形成后期缺乏增殖,有趣的是推测这一事件可能构成晚年动脉粥样硬化的基础。
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.