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 23-year-old female patient with no significant past medical history presented to the hospital complaining of acute shortness of breath, abdominal pain, and severe left lower extremity pain. The patient was in her usual state of health until the evening of her symptoms, when she suddenly turned in her bed and began to experience numbness, tingling, and purplish discoloration of her left lower extremity. On arrival to the emergency department, the patient was in respiratory distress and had bilateral swelling of her lower extremities, the left side larger than the right. A bilateral lower extremity duplex ultrasound revealed a deep vein thrombosis (DVT) in the left lower extremity, the popliteal, and the femoral veins. In addition a CT of the chest utilizing our pulmonary embolism protocol delineated two pulmonary emboli in the first order pulmonary arteries and multiple segmental emboli located in the right upper and right lower lobes. She was subsequently started on a heparin drip.\nThe patient denied any tobacco use, recent immobilization, or travel. She reported the use of an estrogen vaginal delivery device (ethinyl estradiol vaginal ring) for the previous 6 months. Her hypercoagulable workup was revealing for heterozygosity at C677T for factor V Leiden. It should be noted that heterozygous carriers of FVL have been shown to have an overall 3- to 7-fold increased risk of venous thrombosis, while homozygotes to C677T have a 50- to 100-fold increased risk. []\nDue to the acute presentation of her venous thromboembolism, a left pelvic and lower extremity venous thrombectomy was performed. This was followed by stenting of a popliteal venous occlusion, and subsequent thrombolysis with tissue plasminogen activator. Surprisingly, a left lower extremity venogram revealed bilateral inferior vena cavas.\nIn our patient, the left-sided duplicated IVC and iliac veins were found to be thrombosed. This was marked by the stippled appearance of the duplicated left IVC vessel seen in Figure . The decision was made to stent the duplicated IVC given the anatomic irregularity and increased risk of repeat thrombosis. Two wall stents (Figure ) were deployed at the proximal end at the level of the left sided (duplicated) IVC. Next a balloon was used to angioplasty the entire length of the stented segment of the duplicated IVC (Figure ). Figure depicts the duplicated left IVC with wall-stent draining into the left renal vein with a non-occlusive thrombus within it. The orthotopic IVC remained patent. The patient was kept on heparin for 24-hours and then started on Coumadin.