Is there an anatomic basis for subvalvular right ventricular outflow tract obstruction after an arterial switch...

The study was initiated by reports on right ventricular outflow tract obstruction in complete transposition of the great arteries after an arterial switch repair. We investigated 39 heart specimens with native, unoperated transposition of the great arteries. Of these, 14 hearts had a ventricular septal defect; 25 had an intact ventricular septum. In each heart specimen the narrowest site of the subaortic outflow tract was measured and compared with the circumference of the aortic orifice. Obstruction was considered to be present if the outflow tract circumference was less than that of the aortic orifice. In addition, the diameter of the ascending aorta immediately above the level of the valve orifices was measured and compared with that of the pulmonary trunk. An obstruction was present in the subaortic right ventricular outflow tract of two hearts (5.1%): one of the obstructions, in a neonatal heart with intact ventricular septum, was caused by a prominent supraventricular crest and anterior trabeculations; the other obstruction was an additional extensive muscular hypertrophy, in the heart of a 13-year-old patient with a similar anatomy, and a septal defect. A mismatch between the diameters of the ascending aorta and the pulmonary trunk was present in 15 of 32 hearts measured. Our observations and a review of the literature confirm that subvalvular right ventricular outflow tract obstruction in hearts with native transposition of the great arteries is infrequent. Nevertheless, the anatomic characteristics of the right ventricular outflow tract are such that the tract is intrinsically narrow and muscular hypertrophy may easily lead to obstruction. After an arterial switch operation, subvalvular obstruction could be caused by dynamic processes analogous to those observed after relief of isolated pulmonary valve stenosis. Anatomic subvalvular obstruction could be due to either an obstruction that was not identified before operation or (a purely speculative hypothesis) subtle degrees of mismatch in size between the proximal aorta and the pulmonary trunk, which may be considered irrelevant at time of operation but may also set into pace a process of ongoing adaptive infundibular hypertrophy.