We report our experience with transcatheter patent ductus arteriosus (PDA) closure in premature infants and compare patients grouped by the device used for closure: the Microvascular Plug, “MVP” (Medtronic, Minneapolis, MN); Micro Plug Set, “Micro Plug” (KA Medical, Minneapolis, MN); and Amplatzer Piccolo Occluder, “Piccolo” (Abbot, Santa Clara, CA). We also report trends in device selection over time. Studies examining outcomes according to device selection for PDA closure in premature infants are lacking. We performed a retrospective review of all percutaneous PDA closures in premature infants at a single center (June 2018–May 2021). Patients were grouped by initial device selected for PDA closure (intention to treat). Institutional Review Board approval was obtained. 58 premature infants [MVP (n = 25), Micro Plug (n = 25), and Piccolo (n = 8)] underwent successful transcatheter PDA closure (mean gestational age 27 weeks 2 days; mean weight at procedure 1.4 kg; mean age at procedure 28 days). Pre-procedural demographics, procedural data, and follow-up data were similar between groups. There were no significant procedural adverse events. Three devices (2 MVP, 0 Micro Plug, 1 Piccolo p = 0.27) embolized after the procedure. One other device was removed for concern for aortic obstruction. Device selection evolved with a clear trend toward the Micro Plug device over time. Demographic, procedural, and follow-up data were similar between the MVP, Micro Plug, and Piccolo groups. The Micro Plug did not require exchange for suboptimal fitting or embolize and became our preferred device in most cases.
Background. Fontan-associated liver disease is a well-known sequela following the Fontan procedure for patients living with single-ventricle heart disease. Pulmonary vasodilators, such as phosphodiesterase type 5 inhibitors, have emerged as a potential therapeutic option for lowering central venous pressures by reducing pulmonary vascular resistance. Method. We performed a single-center retrospective review of Fontan patients who were placed on pulmonary vasodilator therapy with prehemodynamic and posthemodynamic, MR elastography, and histologic assessments. Results. A total of 125 patients with Fontan circulation underwent surveillance with cardiac catheterization during the review period. Fifty-three (42%) patients who did not have increased end-diastolic pressures at the time of cardiac catheterization were started on phosphodiesterase type 5 inhibitor therapy. Nine patients (17%) underwent posttherapy follow-up catheterization. The mean Fontan pressure decreased from 15.4 ± 3.3 mmHg to 13.3 ± 2.5 mmHg ( p = 0.026 ), after initiation of pulmonary vasodilatory therapy. There was no change in end-diastolic pressure, transpulmonary gradient, wedge pressure, pulmonary vascular resistance, cardiac index, or saturation. Eleven patients (21%) underwent pretherapy MR elastography testing with posttherapy follow-up MR elastography. We found no improvement in liver stiffness score following the application of pulmonary vasodilators. Three patients underwent pretherapy and posttherapy liver biopsies, with variable histological changes observed within the hepatic parenchyma. Conclusions. These data demonstrate indeterminate results for the selective use of pulmonary vasodilators but highlight the need for large prospective randomized control trials of pulmonary vasodilator therapies to fully assess the benefit of such therapies in Fontan-associated liver disease.
Van Praagh (VP) A3 variant of truncus arteriosus (or common arterial trunk) is defined by only one pulmonary artery (usually the right) originating from the common trunk, while the other lung is supplied either by collaterals or a pulmonary artery arising from the aortic arch. This report describes a staged approach to manage a VP-A3 variant truncus arteriosus with ductal origin of the left pulmonary artery (LPA), a hypoplastic right pulmonary artery, and cyanosis. Initially, the ductal portion of the proximal LPA was stented with a Resolute Onyx drug-eluting stent. The pulmonary arteries grew and at four months of age had an acceptable McGoon ratio and Nakata index. The patient then underwent repair which included unifocalization of the branch pulmonary arteries, closure of the ventricular septal defect, and placement of a right ventricle-to-pulmonary artery homograft conduit.
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