A 54-year-old male patient with long standing history of type II DM, dyslipidemia and hypertension, with medical therapy of bisoprolol 10 mg daily, valsartan 160 mg daily, HCTZ 25 mg daily, atorvastatin 20 mg nocturnally, insulin and metformin was admitted to a peripheral hospital with bronchopneumonia requiring high dependency unit admission. This was complicated by a transient ischemic attack. Brain computed tomography (CT) was normal. On the second day of admission, he had a significant episode of chest pain. Electrocardiogram (ECG) showed transient ST-segment elevation with spontaneous resolution in the inferior lead. There was mild troponin leak. He was later referred to our center for further workup. His physical exam revealed oxygen saturation at 98% on room air, pulse 70 bpm, BP both upper limb 155/65 mm Hg, and BP lower limb 105/45 mm Hg. There was a brachio-femoral delay. Apex was mildly displaced; he had S1+ S2+ S4 and a systolic murmur at the tip of left scapula; no clicks were appreciated on auscultation.\nECG showed sinus rhythm and left ventricular hypertrophy (LVH) with strain pattern. A 24-h Holter came back with normal sinus rhythm, no atrial fibrillation, no heart blocks or arrhythmia. Transthoracic echocardiogram revealed concentric LVH, borderline left ventricular function of 45-50%, mild to moderate aortic regurgitation, bicuspid aortic valve and a coarctation of the aorta with a 70 mm Hg gradient across it. Brain MRI demonstrated lacunar infarcts and no AV-malformations. Both carotid arteries were free of atherosclerosis on Doppler. Coronary CT angiogram not only demonstrated the tight coarctation but also showed a rare anomaly of a PLSVC draining into the left atrium (). Anomalous pulmonary drainage and pulmonary arteriovenous malformation were excluded. The approach to management of this patient was discussed in a heart team meeting. It was decided to proceed percutaneously.\nThe patient was brought to the catheterization laboratory. Coronary angiography showed normal coronaries. He did have a significant coarctation with a pressure gradient of 40 mm Hg. Angiographic confirmation of the PLSVC draining into the left superior pulmonary vein was confirmed. A 40 mm CP stent mounted on a 20 × 45 mm BIB balloon was deployed successfully (), guided by fluoroscopy and overdrive pacing. There was complete abolition of the gradient. At a later date, the patient was brought for PLSVC exclusion therapy. Selective angiography of the PLSVC was performed to delineate vessel course and venous drainage (). Using a marker pigtail measurement of the vessel was obtained. The PLSVC measured 9 mm proximally, 10.5 mm at its mid-point and 8 mm near the entrance to the left upper pulmonary vein. The PLSVC was then temporarily occluded with an 8 mm peripheral balloon to make sure that the patient would tolerate closure of the vessel. There was no significant change in the patient’s hemodynamic measurements, and the decision was made to proceed with transcatheter occlusion of the PLSVC which was achieved using a 12 mm Amplatzer vascular plug II (AGA Medical Corporation, Golden Valley, MN) ().
A 67-year-old woman with hepatitis C was found to have a liver tumor located in segment 8 during follow-up computed tomography (CT) for pyogenic spondylitis. She also had a past medical history of cirrhosis due to hepatitis C infection and diabetes mellitus. Laboratory examination showed normal levels of carcinoembryonic antigen, carbohydrate antigen 19–9, and α-fetoprotein but elevated protein induced by vitamin K antagonist-II at a level of 106 mAU/mL. Other laboratory studies showed the following: total bilirubin 0.6 mg/dL, albumin 3.2 g/dL, prothrombin time 13.7 s, aspartate aminotransferase 28 IU/L, alanine aminotransferase 22 IU/L, blood urea nitrogen 16 mg/dL, and creatinine 0.54 mg/dL. The Child-Pugh score was grade A (6 points), and the indocyanine green retention rate at 15 min was 16.6%. A diagnosis of hepatocellular carcinoma (HCC) located in segment 8 was indicated by CT (Fig. ), magnetic resonance imaging (Fig. ), and ultrasonography. The tumor was attached to the MHV. CT scans also showed multiple varices (Fig. ). MHV resection was necessary to obtain sufficient surgical margins. Central bisectionectomy (S4, S5, and S8 resection) was suggested but could not be tolerated because of her poor liver function and low future liver remnant volume, which preoperatively was only 56% by CT volumetry. Therefore, we decided to perform partial hepatectomy with MHV resection. Preoperative CT scans revealed the existence of duplicated IVC (Fig. ), so we chose to use the left IVC as the graft for reconstructing the MHV.\nThe surgery started with an inverted L-shaped incision. Intraoperative ultrasonography confirmed a 3.5-cm tumor that was touching the MHV. After mobilization of the right lobe, the liver parenchyma was transected, preserving the right hepatic vein and right anterior glissonian pedicle. A 3-cm portion of the MHV was resected around the tumor to obtain sufficient surgical margins. Immediately before resecting the MHV, we harvested the left IVC for use as the graft. After incising the retroperitoneum beside the Treitz ligament, the LRV, which had ramified from the IVC, was detected. The left IVC, which had ramified 3 cm peripherally from the origin of the LRV, was then isolated and harvested for 5 cm from the confluence of the LRV. The cut ends of the left IVC were closed with 4–0 polypropylene running sutures. The venous graft was anastomosed first to the proximal end of the MHV and then to the distal end using 6–0 polypropylene (Fig. ). A good Doppler flow through the graft was confirmed after the reconstruction. The operation required 394 min, and the estimated blood loss was 1,894 mL.\nMacroscopic evaluation showed a 35-mm bile-stained tumor (Fig. ). Histologic examination revealed moderately differentiated HCC without direct invasion of the MHV and a tumor-free surgical margin (Fig. ). The tumor was classified as stage II (T2N0M0) according to the TNM staging system for HCC. The patient recovered uneventfully and was discharged on postoperative day 12.\nThe patency of the reconstructed MHV was confirmed postoperatively by ultrasonography and dynamic CT (Fig. ). Laboratory examination 2 years after surgery showed normal levels of total bilirubin (0.6 mg/dL), albumin (4.0 g/dL), aspartate aminotransferase (24 IU/L), alanine aminotransferase (24 IU/L), prothrombin time of 13.5 s, blood urea nitrogen (15 mg/dL), and creatinine (0.46 mg/dL).\nNew lesions were found in the left lobe of the liver 4 months after surgery and in the right lobe 26 months after surgery. Both lesions were treated using transabdominal catheter embolization.