The intimal thickening on the posterior aortic wall is composed of small number of dedifferentiated smooth muscle cells (SMC). Some of these cells are in apoptosis. On the anteromedial wall, the intima and media are composed of proliferated SMC and small number of SMC which exhibit contractile phenotype. In all parts of the aortic wall, there is a large number of pseudocysts with large amount of mucins, without presence of inflammatory cells.
Both procedures are effective for coarctation repair in young infants. Risk of recoarctation is a function of the complex anatomy of the arch, while residual ductal tissue may play a significant role.
Some foam cells develop from monocyte-macrophage lineage (CD68-immunoreactive), while others originate from smooth muscle cells (vimentin and S-100-immunoreactive). Coarctation of the aorta is characterised by a diminution in cell numbers (apoptosis) as well as their dedifferentiation from contractile to synthetic phenotype.
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