Department of Anatomy and Developmental Biology, School of Biomedical Sciences, Monash University, Clayton, VIC 3800, Australia.
Eur Heart J. 2010 Aug;31(16):2058-66. doi: 10.1093/eurheartj/ehq104. Epub 2010 May 7.
Pre-term birth affects 10-12% of live births and occurs when the myocardium is still developing; therefore, the final structure of the myocardium could be altered. We hypothesized that, in response to pre-term birth, structural remodelling occurs within the myocardium which enables the immature heart muscle to adapt to the haemodynamic transition at birth but results in persistent alterations in its structure. Our objective was to determine how pre-term birth alters the final structure of the myocardium.
Using sheep, pre-term birth was induced at 0.9 of term; hearts were examined at 9 weeks after term-equivalent age, when cardiomyocyte proliferation and maturation have ceased. In pre-term lambs, we found that cardiomyocytes of both ventricles and the interventricular septum were hypertrophied. Cardiomyocyte maturation in pre-term lambs was altered in that there was a greater proportion of mononucleated, polyploid (4n) cardiomyocytes in both ventricles compared with controls; importantly, induction of polyploidy is associated with irreversible stress-related changes in DNA. We also found a six- to seven-fold increase in collagen deposition, usually accompanied by lymphocytic infiltration.
We conclude that pre-term birth leads to remodelling of the myocardium that alters its final structure. This may programme for long-term cardiac vulnerability.
早产影响 10-12%的活产儿，发生在心肌仍在发育的时候；因此，心肌的最终结构可能会发生改变。我们假设，为了适应早产，心肌内会发生结构重塑，使未成熟的心肌能够适应出生时的血液动力学转变，但会导致其结构持续改变。我们的目的是确定早产如何改变心肌的最终结构。
使用绵羊，在妊娠 0.9 时诱导早产；在相当于足月后 9 周时检查心脏，此时心肌细胞增殖和成熟已经停止。在早产羔羊中，我们发现两个心室和室间隔的心肌细胞都发生了肥大。早产羔羊的心肌细胞成熟发生了改变，与对照组相比，两个心室中有更大比例的单核、多倍体（4n）心肌细胞；重要的是，多倍体的诱导与与 DNA 相关的不可逆应激变化有关。我们还发现胶原沉积增加了六到七倍，通常伴有淋巴细胞浸润。
我们得出结论，早产导致心肌重塑，改变了其最终结构。这可能会为长期的心脏脆弱性编程。
