Abstract
Congenital heart diseases (CHD) or the process of their repair leads to an increased risk for adult cardiovascular disease compared with the general population [1]. The proliferation of intimal smooth muscle cells (SMCs), which causes intimal thickenings prior to any evidence of visible lipid deposition, was proposed to be the initial lesion of coronary atherosclerosis [2]. The increasing trend to consider intimal thickenings as possible pre-atherosclerotic lesions is based on the distribution of intimal hyperplasia in children and the localization of characteristic atherosclerotic lesions observed in adult humans [3].
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