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The anatomy of tetralogy of Fallot with pulmonary stenosis

E VEN THOUGH, AS STATED BY LEV AND ECKNER, hearts from no two patients are exactly the same, it is the characteristic anatomy that permits the instant recognition of the tetralogy of Fallot. The characteristic morphology had been recognised and illustrated long before Fallot realised that a constellation of 4 anatomic lesions was seen in the majority of specimens coming into his autopsy service from patients with ‘‘la maladie bleue’’. According to Marquis, it was the Danish monk, Steno, also known as Stensen, who first described the association of lesions, having observed the findings in an ectopic heart from a fetus. More recently, attempts have been made to identify one of the four anatomic features as being paramount. Thus, some have argued that it is underdevelopment of the subpulmonary infundibulum that was the primary feature, stating that this part of the heart was ‘‘too narrow, too shallow, and too short’’. Whilst the infundibulum is unequivocally narrow and hypoplastic, measurements of its length in series of hearts, when compared to the length of the normal infundibulum, have shown that, rather than being too short, the infundibulum is often longer than normal. It can, nonetheless, be short, or even absent, in selected specimens, as we will show in our subsequent discussions. In our own early studies, we suggested that anterocephalad deviation of the insertion of the muscular outlet septum relative to the septomarginal trabeculation was the key feature. This hypothesis was confounded by two observations. First, that the outlet septum could be deviated in antero-cephalad fashion without producing subpulmonary obstruction, as in the Eisenmenger defect. Second, that in some hearts, there can be subpulmonary obstruction when the outlet septum is fibrous, rather than muscular. Our further studies have now identified anatomic features that do prove pathognomonic for the lesion. These involve anterocephalad deviation of the outlet septum, be it muscular or fibrous, but require an associated malformation of the septoparietal trabeculations, these being the muscular bars which reinforce the parietal wall of the right ventricle. It is on the basis of the squeeze produced between the malaligned outlet septum, or its fibrous remnant, and the septoparietal trabeculations that we now identify the morphologic entity of tetralogy of Fallot. In the discussions that follow, we will show how the building blocks of the normal right ventricular outflow tract become divorced one from the other in the setting of tetralogy of Fallot. Recognition of these building blocks as individual entities permits distinction of the clinically significant variations to be found in the lesion.