34 C. W. M. Poynter 



(1857), Mallwo (i860), Heine (1861), Hickman (1869), Hunter (1869), 

 Peacock (1873), Barlow (1876), Pott (1878), Smith (1880), Tooth (1883), 

 Gevaert (1885), Bury (1887), Habershon (1888), Cadet de Gassecourt 

 (1890), White (1891), Saunders (1892), Boquet (1893), Bornier (1907), 

 Hebb (1913). 



§ XI. 



VI. ABNORMALITIES OF THE PULMONARY TRUNK 



A and B. Pulmonary Stenosis and Atresia 



Anomalous development, leading to partial or complete closure 

 of the pulmonary artery, is of frequent occurrence among con- 

 genital heart irregularities. In this study it is present in almost 

 34 per cent, of all cases. A variety of conditions is found ; the 

 artery may simply be smaller than normal or the stenosis may be 

 confined to the orifice, the semilunar valves may be grown to- 

 gether so that only a minute opening remains or closed forming 

 an obstructive diaphragm, the artery may be shrunken to form 

 a fibrous cord or be entirely wanting. 



The presence of this anomaly in conjunction with others of the 

 heart has long been recognized. Morgagni (1728) considered 

 the condition congenital and believed that it was responsible for 

 the persistence of the foramen ovale by the stagnation of blood 

 in the right ventricle. As already pointed out, Hunter saw a 

 connection between the stenosed artery and defective ventricular 

 septum. 



Many observers have considered that the condition resulted 

 from foetal endocarditis and, although this cause is not now gen- 

 erally accepted, it is impossible to prove that certain cases are not 

 produced by an early inflammatory reaction. Peacock and Ro- 

 kitansky looked on the condition as the result of error in devel- 

 opment of the aortic septum. It seems to me that Keith (1909) 

 has offered the most satisfactory explanation in his classification 

 of the cases as partial or complete arrest of developmental expan- 

 sion of the infundibulum. 



Cases of complete obstruction of the pulmonary artery may be 

 compensated for by defective ventricular septum, open ductus 

 arteriosus or, more rarely, enlarged bronchial arteries. Cyanosis 



