![]() Valvar aortic stenosis is generally caused by incomplete or abnormal development of the aortic valve (bicuspid or unicuspid morphology, poorly defined cusps, hypoplastic aortic annulus). A prominent muscle bundle (muscle of Moulaert) on the left ventricular free wall can also contribute to LVOTO by projecting into the left ventricular outflow tract (LVOT). Subvalvar LVOTO is related to the posterior and leftward malalignment of the conal or outflow septum, the most commonly associated anomaly in IAA. Several anatomic substrates for LVOTO can be identified in IAA at a subvalvar, valvar, or supravalvar level, or as a combination of the three (multilevel stenosis). Despite excellent peri-operative survival, successful IAA repair can be complicated by left ventricular outflow tract obstruction (LVOTO), which may be present preoperatively or may (re-)occur during follow-up. The preferred treatment of IAA consists of a single-staged biventricular repair with closure of the ventricular septal defect (VSD) and reconstruction of the arch. IAA is defined as a lack of luminal continuity between the ascending and the descending thoracic aorta. Interrupted aortic arch (IAA) is a rare congenital lesion comprising approximately 1.5% of all congenital heart disease. In patients with a borderline left ventricular outflow tract that undergo a primary repair, these (pre-) operative predictors can provide guidance for optimal surgical decision-making and for close monitoring during follow-up of patients at increased risk for developing left ventricular outflow tract obstruction after corrective surgery. Anatomic and surgical risk factors for left ventricular outflow tract obstruction were the presence of an aberrant right subclavian artery, use of a pulmonary homograft or polytetrafluoroethylene interposition graft for aortic arch repair, and the presence of a small- or medium-sized ventricular septal defect. Manifestation of postoperative left ventricular outflow tract obstruction was associated with a smaller pre-operative size of the aortic root (sinus of Valsalva), sinotubular junction, and aortic annulus. Postoperative left ventricular outflow tract obstruction requiring an intervention was common, with an incidence ranging between 14 and 38%. From the 44 potentially relevant studies, eight studies met the inclusion criteria. Studies that reported echocardiographic and/or clinical predictors for left ventricular outflow tract obstruction in infants that underwent biventricular repair of interrupted aortic arch were included. A systematic search of the literature was performed across the PubMed and EMBASE databases. The aim of this review is to summarize reported risk factors for left ventricular outflow tract obstruction after corrective surgery for interrupted aortic arch. Identification of patients at risk for obstruction is important to facilitate clinical decision-making and monitoring during follow-up. Left ventricular outflow tract obstruction is an important complication after interrupted aortic arch repair and subsequent interventions may adversely affect survival. ![]()
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