Endovascular Rehabilitation of Acutely Thrombosed Fontan Conduit in a Patient With Multiorgan Failure

A 32-year-old man with history of hypoplastic left heart syndrome status post-Fontan palliation (20-mm aortic homograft conduit) had previously undergone Fontan conduit (FC) and left pulmonary artery (LPA) stenting to relieve conduit obstruction. The patient developed COVID-19-associated acute thrombotic obstruction of the FC with cardiogenic shock. Thrombolytics were attempted without success. He was deemed non-operative and referred for emergent cardiac catheterization for planned thrombectomy.

Vascular access was obtained in the left internal jugular vein (LIJV) and right common femoral vein (RCFV). Pre-procedure inferior venacava (IVC) mean pressure was 30 mm Hg (in the setting of decompressing veno-venous collaterals) with a superior venacava (SVC) mean pressure of 15 mm Hg consistent with severe FC obstruction. Intracardiac echocardiogram demonstrated widely patent renal veins and infrahepatic IVC with thrombotic occlusion of the FC (Figure, A; Video).

A glide wire was utilized to pass through the thrombus for LIJV-RCFV wire rail creation. A catheter was passed over the wire for placement of a second wire (0.035” Amplatz Superstiff [Boston Scientific]) in the right pulmonary artery (RPA). Thrombectomy utilizing a 12 French Lightning catheter (Penumbra) was performed. Thrombus was removed from the FC, RPA, and from the prior LPA stent. Repeat FC angiography demonstrated improved luminal diameter with evidence of residual well-organized thrombus within the FC (Figure, B & C). A Palmaz XL P3110 stent (Cordis) was placed in the prior PA stent with 18-mm high-pressure dilation (Figure, D). Two Palmaz XL P5010 stents x2 and a 36-mm Ev3 Intrastent LD Max stent (Medtronic) were placed across the FC with 22-mm high pressure dilation (Figure, E-G).

Repeat angiogram demonstrated a widely patent FC conduit and LPA stent with no residual gradient from IVC to the SVC (Figure, H-K). This case highlights the role of percutaneous rehabilitation in the setting of acute thrombotic occlusion of an FC, an etiology historically felt to be lethal.

Affiliations and Disclosures

From the ¹Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA; ²Department of Radiology, Mayo Clinic, Rochester, Minnesota, USA.

Disclosures: The authors report no financial relationships or conflicts of interest regarding the content herein.

Address for correspondence: Jason H. Anderson, MD, 200 1st St SW, Rochester, MN 55905, USA. Email: anderson.jason@mayo.edu