McGill H C
Arteriosclerosis. 1984 Sep-Oct;4(5):443-51. doi: 10.1161/01.atv.4.5.443.
In concluding this eclectic review, I believe that we can say with certainty that coronary atherosclerosis has its origins in childhood, at least by age 10 and possibly earlier. Endothelial changes follow lipid accumulation, but, with present methods, there is no evidence that endothelial injury precedes lipid accumulation. Proliferation is a prominent feature of accelerated experimental atherosclerosis, but we do not see evidence that proliferation is a major feature of early naturally occurring human atherosclerosis. The prominence of the monocyte-macrophage in the earliest detectable lesions of atherosclerosis in childhood justifies the current interest in monocyte biology. Hyperlipidemia, in the sense of the average high levels common in our population, seems almost certain to contribute to accelerated atherogenesis in children, but conclusive proof is still lacking. Mild hypertension in children, or even the high range of normal blood pressure, may accelerate the transition of innocuous childhood fatty streaks to more ominous fibrous plaques. The putative relationship of adult coronary heart disease risk factors to the childhood lesions of atherosclerosis is largely based on extrapolation from adult data. Direct evidence bearing on these relationships, however difficult to obtain, would be helpful in designing and promoting effective preventive regimens for children.
在总结这篇兼收并蓄的综述时，我认为我们可以肯定地说，冠状动脉粥样硬化始于儿童期，至少在10岁时就已出现，甚至可能更早。内皮变化继发于脂质积聚，但就目前的方法而言，没有证据表明内皮损伤先于脂质积聚。增殖是实验性动脉粥样硬化加速发展的一个突出特征，但我们并未发现增殖是早期自然发生的人类动脉粥样硬化的主要特征的证据。单核细胞 - 巨噬细胞在儿童期最早可检测到的动脉粥样硬化病变中的突出表现，证明了目前对单核细胞生物学的关注是合理的。从我们人群中常见的平均高水平来看，高脂血症似乎几乎肯定会促进儿童动脉粥样硬化的加速发展，但仍缺乏确凿证据。儿童的轻度高血压，甚至是正常血压的上限，都可能加速无害的儿童脂肪条纹向更危险的纤维斑块的转变。成人冠心病危险因素与儿童动脉粥样硬化病变之间的假定关系，很大程度上是基于从成人数据推断而来。然而，关于这些关系的直接证据，无论多么难以获得，都将有助于设计和推广针对儿童的有效预防方案。
