The transmural passage of blood cells into myeloid sinusoids and the entry of platelets into the sinusoidal circulation; a scanning electron microscopic investigation

Scanning electron microscopic observations of rat bone marrow reveal that the sinusoidal wall is continuous and has no permanent patent apertures allowing free communication between the extravascular and intravascular myeloid compartments. Blood cells migrate into the sinusoids by perforating the endothelial cell body. Platelets are derived from long intrasinusoidal “proplatelet” processes which originate from the cell body of extravascularly located megakaryocytes. Proplatelet processes frequently occur in clusters, with the probability that all processes in a cluster arise from a single megakaryocyte. The release of platelets into the circulation may be initiated by local constriction along these processes, at which places either individual platelets or larger segments of proplatelet cytoplasm are pinched off. The larger segments may subsequently undergo further fragmentation into individual platelets.     

The coronary arteries in Marfan's syndrome. A morphologic study.

The coronary arteries of five hearts of patients known to have had Marfan's syndrome were studied microscopically. In four of the five cases the extramural coronary arteries showed structural changes consisting of accumulations of acid mucopolysaccharides and a concomitant disruption of the connective tissue elements. These changes closely resembled the changes that frequently occur in the aorta and that are generally described as "cystic medial necrosis". They are considered to be an important expression of wall weakening. In one case a laceration, probably traumatic, of a coronary artery led to formation of an "incomplete dissecting aneurysm." "Cystic medial necrosis" was found once in the proximal segment of the sinus nodal artery and once in the musculoelastic layer of a coronary artery that reached the atrioventricular node from the ventricular septum by perforating the anulus fibrosus. However, in contrast to findings in a previous report, the intramural coronary arteries were otherwise unaffected. The clinical significance of these data is as yet unknown particularly since these alterations are intramural and initially do not cause narrowing of the lumen. Nevertheless, the possibility of coronary arterial involvement by the metabolic disorder of Marfan's syndrome should always be considered during clinical assessment of this lesion.     

Differential diagnosis of the tetralogy of Fallot (author's transl)

The differential diagnosis of the tetralogy of Fallot includes three main types of condition: 1) Malformations which differ from Fallot in their extent, such as interventricular communications of type IV and pulmonary atresia with an open septum. 2) Malposition of the large vessels with pulmonary stenosis (double opening in the right ventricle, complete or corrected transposition). 3) Malformations associating an intraventricular shunt and another type of pulmonary stenosis (double chambered ventricle, interventricular membranous and muscular communication, common atrioventricular canal, single ventricle). An analysis of the findings in angiographic images can provide precise differential diagnosis of these pseudo-Fallots.