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) ().
Our patient was an 18-year-old girl with recent onset right leg pain and swelling with extension to her inguinal area. She also had dyspnea with respiratory distress. At the time of presentation, she was ill and febrile. She also had pitting edema of right leg and significant size difference between circumferences of her two legs. On the day of admission, she suddenly presented with dyspnea and severe thoracic pain on the right side. All other physical examination was normal.\nShe had no predisposing factor for venous thrombosis. Besides, she had no known a history of DVT, clotting disorders, recurrent abortion, peripheral vascular disease, non-healing ulcerations on the extremities, cerebrovascular accidents or taking oral contraceptive pills.\nHer laboratory data showed only mild normochromic, normocytic anemia, elevated erythrocyte sedimentation rate (ESR) to 75 (normal range less than 25) and CRP = 16 (normal less than 8). Other laboratory test including renal, electrolytes, liver, and urine analysis and culture were normal.\nColor duplex ultrasound study demonstrated deep venous thrombi in the right popliteal, superficial and common femoral veins, with external iliac vein.\nIn addition, hypercoagulable workup was revealed no abnormal finding and also negative for antiphospholipid syndrome and lupus anticoagulant antibodies.\nA multi-detector computed tomography (CT) pulmonary angiography of the chest defined pulmonary emboli in the territory of right main and segmental branch pulmonary artery and suggesting extensive infarction of the right middle pulmonary lobe. She was subsequently started on a low molecular weight heparin (Clexane®: 60 mg, every 12 h SC). Subsequently, CT of the abdomen and CT angiography with IV contrast injection carried out after the procedure confirmed duplication of the IVC []. Both two IVC originate in the pelvis, run parallel to each other, bordering the aorta and left-sided IVC drained into the left renal vein. There was no other pathologic finding in thoracic and abdominopelvic CT studying.\nAfter fully anticoagulated with low molecular weight heparin for 5 days and starting warfarin international normalized ratio (INR) range was between 2 and 3, she was discharged from hospital and was not symptomatic in her follow-up until next 3 months. According to the previous studies, for this patient we planned to continue anticoagulant therapy for 6 months.[]