Knauth Alison, McCarthy Karen P, Webb Sandra, Ho Siew Yen, Allwork Sally P, Cook Andrew C, Anderson Robert H
The Children's Hospital, Boston, MA, USA.
Cardiol Young. 2002 Jul;12(4):364-72. doi: 10.1017/s104795110001297x.
We describe the structure of, and suggest an etiology for, the interatrial communication which can occur through the mouth of the coronary sinus. Based on the study of human embryos, we propose that the defect is best explained by dissolution of the wall of the coronary sinus adjacent to the left atrium, permitting shunting between the atriums through the right atrial orifice of the sinus.
An interatrial communication across the mouth of the coronary sinus defect was first described in 1965 by Raghib and colleagues, its existence being predicated on the basis of incomplete formation of the left "atriovenous fold". Their hypothesis implies that the coronary sinus never develops, and thus the atrial septum itself is incomplete.
We have studied the development of the coronary sinus in a series of human embryos. Based on this work, we present the anatomical findings in 6 specimens with varying degrees of dissolution of the walls of the coronary sinus, and ten specimens with isomerism of the right atrial appendages, in which the sinus has never been formed.
The coronary sinus defect is not a hole within the atrial septum, but a communication between the atriums through the mouth of the sinus. There was a range of defects in our series of specimens with usual atrial arrangement, extending from complete absence of the walls which normally separate the coronary sinus from the left atrium, to small fenestrations between this vessel and the left atrial cavity. In the hearts with isomerism of the right atrial appendages, however, we never observed an orifice of the coronary sinus. Thus, a coronary sinus defect cannot exist in this setting.
Our findings indicate that the defect requires initial formation of the walls of the coronary sinus, but with subsequent dissolution of the wall adjacent to the left atrium. This produces a communication between the atriums through the mouth of the sinus.
我们描述了可通过冠状窦口出现的房间隔交通的结构,并提出了其病因。基于对人类胚胎的研究,我们认为该缺损最好的解释是冠状窦毗邻左心房的壁溶解,从而允许心房之间通过窦的右心房口进行分流。
1965年,拉吉卜及其同事首次描述了跨越冠状窦口缺损的房间隔交通,其存在基于左“房室襞”形成不完全。他们的假设意味着冠状窦从未发育,因此房间隔本身不完整。
我们研究了一系列人类胚胎中冠状窦的发育。基于这项工作,我们展示了6例冠状窦壁有不同程度溶解的标本以及10例右心耳异构(其中窦从未形成)标本的解剖学发现。
冠状窦缺损并非房间隔内的一个孔,而是心房之间通过窦口的交通。在我们一系列正常心房排列的标本中存在一系列缺损,范围从通常分隔冠状窦与左心房的壁完全缺失,到该血管与左心房腔之间的小窗孔。然而,在右心耳异构的心脏中,我们从未观察到冠状窦口。因此,在这种情况下不可能存在冠状窦缺损。
我们的研究结果表明,该缺损需要冠状窦壁最初形成,但随后毗邻左心房的壁溶解。这会通过窦口在心房之间产生交通。