About 1850, Dittrich of Erlangen, by his studies of inflammation of the heart during intra-uterine life, quite diverted public opinion from the older views of the subject. Peacock's earlier studies preceded this work by a few years, and a few years later came Meyer,1 who greatly extended the scope and influence of the inflammatory theory of Dittrich. Ten years later commenced the clinical recognition of congenital heart defects, and especially the anatomical changes in congenital narrowing of the pulmonary artery, by Von Dusch and by Mannkopff,2 and by Stoelker.3 Friedberg had, however, as early as 1844, published his studies of the stages of development of the circulatory organs in the human embryo, and had in accordance therewith divided the malformation of the heart into three groups, corresponding to the three periods of the heart's growth. This was the classification adopted quite independently by Peacock of London in his first publication in 1857. It was not until after Dittrich's studies4 and Meyer's that any distinctive cause was assigned for the failure to develop.
1 Virch. Arch., Bd. xii., 1857.
2 Ann. des Charité-Krankenh. zu Berl., 1863.
3 Diss., Bern, 1865.
4 See Dorsch's (his student) dissertation, Die Herzmuskelentzundung als Ursache angeborner Herzcyanose, Erlangen, 1855.
Carl Heine,5 and also Halbertsma, proposed a classification based on the quantitative and qualitative differences. Under the first division the former placed such changes as absence of the heart, deficiency of individual parts, abnormal smallness, atresia, and fissures; and, in the other direction, duplication of the heart as a whole or in its individual parts, and abnormal largeness. The qualitative differences were deviations of form, of position, and of the arrangement of the great vessels.
5 Angeborene Atresie d. Ostium arteriosum dextrum, Beitrag z. Lehre v. d. angeborenen Herzanomalium, Tübingen, 1861.
Peacock's classification in his earlier edition (1858) was partly on the basis of the time at which arrest of development occurs, and partly on the degree of impediment to the circulation and the functions of the heart. In his second edition he adheres to the same classes, with slight modifications, thus: 1. Arrest of development early in foetal life (fourth to sixth week; heart with two or three cavities; single or imperfectly divided arterial trunk); 2. Arrests at a later period (sixth to twelfth week; imperfect auricular or ventricular septa; imperfect or misplaced vessels); 3. Those after the third foetal month (closure and patency of foetal passages; irregularities of valves, cavities, etc.).
Kussmaul (1865) published a very important work on malformations due to defects of the pulmonary artery,6 and these malformations he considers under two general groups—viz. those having their origin before the ventricular septum closes, and those occurring after this period. His most valuable contribution to the subject is the importance which attaches to the distinction between primary and secondary defects or arrests of development—i.e. between an original alteration of growth or morbid condition, and those which follow from it as a necessary consequence. Of his classification, and of the importance of pulmonary artery malformations, a further description will be given.
6 Ueber angeborene Enge und Verschluss der Lungenarterienbahn, Freiburg, i. B.