Portal Vein Pull-Through Technique and Thrombectomy for Extensive Portal Vein Thrombosis.

BACKGROUND: Herein, a different technique is presented describing complete dissection of the entire portal vein (PV), superior mesenteric vein (SMV), and splenic vein, thus enabling a complete thrombectomy without the risk of uncontrolled hemorrhage due to blind thrombectomy. METHODS: In cases where a thrombectomy would not be an option because of extensive thrombosis involving the confluence of the PV and SMV, small branches of the SMV, including the inferior mesenteric vein, were divided. Both the SMV and splenic vein were encircled separately. Then, the side branches of the PV above the pancreas, left gastric vein on the left side, and superior pancreatoduodenal vein on the right side were divided. The lateral and posterior part of the PV were dissected within the pancreas both from above and below, allowing the main PV completely free from attachments. At this point, the splenic vein and SMV were clamped, and the main PV was divided above the pancreas and then pulled back through the pancreatic tunnel. The thrombus was easily dissected of the vein under direct visualization, and afterward the PV was redirected to its original position. Then, the liver transplant was carried out in a regular fashion. RESULTS: This technique was applied to 2 patients. The first was a 43-year-old man who underwent a right lobe living donor liver transplant because of hepatitis B virus-related cirrhosis. The patient is still alive and well with stable liver function after 15 years of follow-up. The second was a 69-year-old woman who underwent a right lobe living donor liver transplant because of hepatitis C virus and hepatocellular carcinoma. She survived the procedure and her liver function was entirely normal afterward. She died of pneumonia and sepsis 5 months after transplant. CONCLUSIONS: This technique enables complete dissection of the entire PV, SMV, and splenic vein. Thus, complete thrombectomy under direct visualization without the risk of uncontrolled hemorrhage can be performed.

Late gadolinium enhancement CMR in patients with tachycardia-induced cardiomyopathy caused by idiopathic ventricular arrhythmias.

BACKGROUND: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia-induced cardiomyopathy (TICMP). The aim of this study was to determine the prevalence of late gadolinium enhancement (LGE) in patients with TICMP caused by idiopathic ventricular arrhythmias. METHODS: The study population consisted of 298 consecutive patients (174 F/124 M; mean age 45±17 years) with frequent PVCs and/or VT. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF≥15% after effective treatment of index ventricular arrhythmia. RESULTS: Twenty-seven (9.1%) patients found to have LVEF≤50% and diagnosed as presumptive TICMP. Improvement in LVEF after effective treatment of index ventricular arrhythmia was observed in 22 of 27 patients (TICMP group; mean PVC burden of 30.8±9.9%). LVEF did not improve in five of 27 patients (primary cardiomyopathy group; mean PVC burden of 28.8±10.1%). LGE-cardiac magnetic resonance (CMR) imaging was performed in 19 of 22 patients with TICMP and one patient (5%) had LGE. All five patients with primary cardiomyopathy underwent LGE-CMR imaging and four patients (80%) had LGE. CONCLUSIONS: LGE is a rare finding in patients with TICMP caused by idiopathic ventricular arrhythmias. LGE-CMR can be used in the diagnostic work-up of patients with TICMP. Further prospective studies are required to determine the role of LGE-CMR in predicting the recovery of left ventricular systolic dysfunction in patients with presumptive TICMP.