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Inferior endocardial C cushion

Septum Septum secundum . primum

Valve of inferior vena cava

Sinus Venarum Septum Spurium
Valve of coronary sinus
Atrioventricular Valve Development

Figure 11.12 Ventral view of coronal sections through the heart at the level of the atrioventricular canal to show development of the venous valves. A. 5 weeks. B. Scanning electron micrograph of a similar-staged mouse heart showing initial formation of the septum primum; septum spurium is not visible. Note the atrioventricular canal (arrow). C. Fetal stage. The sinus venarum (blue) is smooth walled; it derives from the right sinus horn. Arrows, blood flow. D. High magnification of the interatrial septum (arrows) of a mouse embryo at a stage similar to C. The foramen ovale is not visible.

Figure 11.12 Ventral view of coronal sections through the heart at the level of the atrioventricular canal to show development of the venous valves. A. 5 weeks. B. Scanning electron micrograph of a similar-staged mouse heart showing initial formation of the septum primum; septum spurium is not visible. Note the atrioventricular canal (arrow). C. Fetal stage. The sinus venarum (blue) is smooth walled; it derives from the right sinus horn. Arrows, blood flow. D. High magnification of the interatrial septum (arrows) of a mouse embryo at a stage similar to C. The foramen ovale is not visible.

the inferior vena cava, and (b) the valve of the coronary sinus (Fig. 11.12C ). The crista terminalis forms the dividing line between the original trabeculated part of the right atrium and the smooth-walled part (sinus venarum), which originates from the right sinus horn (Fig. 11.12C).

Formation of the Cardiac Septa

The major septa of the heart are formed between the 27th and 37th days of development, when the embryo grows in length from 5 mm to approximately 16 to 17 mm. One method by which a septum may be formed involves two

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Figure 11.13 A and B. Septum formation by two actively growing ridges that approach each other until they fuse. C. Septum formed by a single actively growing cell mass. D, E, and F. Septum formation by merging of two expanding portions of the wall of the heart. Such a septum never completely separates two cavities.

Figure 11.13 A and B. Septum formation by two actively growing ridges that approach each other until they fuse. C. Septum formed by a single actively growing cell mass. D, E, and F. Septum formation by merging of two expanding portions of the wall of the heart. Such a septum never completely separates two cavities.

actively growing masses of tissue that approach each other until they fuse, dividing the lumen into two separate canals (Fig. 11.13, A and B). Such a septum may also be formed by active growth of a single tissue mass that continues to expand until it reaches the opposite side of the lumen (Fig. 11.13C). Formation of such tissue masses depends on synthesis and deposition of extracellular matrices and cell proliferation. The masses, known as endocardial cushions, develop in the atrioventricular and conotruncal regions. In these locations they assist in formation of the atrial and ventricular (membranous portion) septa, the atrioventricular canals and valves, and the aortic and pulmonary channels.

The other manner in which a septum is formed does not involve endocar-dial cushions. If, for example, a narrow strip of tissue in the wall of the atrium or ventricle should fail to grow while areas on each side of it expand rapidly, a narrow ridge forms between the two expanding portions (Fig. 11.13,D and E). When growth of the expanding portions continues on either side of the narrow portion, the two walls approach each other and eventually merge, forming a septum (Fig. 11.13 F). Such a septum never completely divides the original lumen but leaves a narrow communicating canal between the two expanded sections. It is usually closed secondarily by tissue contributed by neighboring proliferating tissues. Such a septum partially divides the atria and ventricles.

CLINICAL CORRELATES Endocardial Cushions and Heart Defects

Because of their key location, abnormalities in endocardial cushion formation contribute to many cardiac malformations, including atrial and ventricular septal defects and defects involving the great vessels (i.e., transposition of the great vessels and tetralogy of Fallot). Since cells populating the conotrun-cal cushions include neural crest cells and since crest cells also contribute extensively to development of the head and neck, abnormalities in these cells, produced by teratogenic agents or genetic causes, often produce both heart and craniofacial defects in the same individual.

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