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Morphogenetic Differences of Secundum Atrial Septal Defects

机译:继发性房间隔缺损的形态学差异

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It is generally considered that the development of secundum atrial septal defect (ASDII) or oval fossa defect is the result of excessive resorption of the embryological atrial septum primum, but this does not seem to explain all defects. We investigated 58 postmortem hearts with an ASDII and 22 normal hearts from patients ranging in age from 1 day to 49 years. The different structures of the oval fossa were examined. In 86% of the specimens, the defects were the result of a malformation of the valvula foraminis ovalis or embryological atrial septum primum, and in 14% an absent superior limbus (septum secundum) was the cause of the interatrial communication. The “septum primum” ASDs were divided into four subgroups based on the degree of deficiency of the septum primum and position of the ostium secundum within the septum primum. We conclude that the morphogenesis of ASDII is variable and both septum primum and septum secundum defects occur, which may be relevant in view of genetic studies that may lead to further differentiation of patients with and without genetically determined ASDIIs.
机译:通常认为,继发性房间隔缺损(ASDII)或卵圆形窝缺损的发展是过度吸收胚胎学房间隔初生的结果,但这似乎不能解释所有缺损。我们调查了年龄从1天到49岁的58例ASDII死后心脏和22例正常心脏。检查了卵圆窝的不同结构。在86%的标本中,缺损是由于卵圆形凹口畸形或胚胎学的房间隔缺损所致,而在14%的标本中,上缘缺如(继发性脓疱)是造成房间通讯的原因。根据隔垫的缺损程度和隔垫内的仲皮孔的位置,将“隔垫” ASD分为四个亚组。我们得出的结论是,ASDII的形态发生是可变的,并且都发生了中隔初生和隔隔缺损,这可能与遗传学研究相关,因为遗传学研究可能导致有和没有遗传学确定的ASDIIs的患者进一步分化。

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