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 28-year-old man, with a history of CoA repair using Dacron patch aortoplasty at the age of 10 years, presented with shortness of breath and sudden, severe central chest pain that radiated across his chest and back. The patient had been lost to clinical follow-up over the last 15 years. He was conscious, hypotensive (90/60 mmHg on both arms), and in distress with tachycardia (120 BPM) and relatively weak pedal pulses with cold distal extremities. A chest X-ray (CXR) demonstrated the widening of the upper mediastinum (Figure ).\nHe underwent emergency CT angiography, which demonstrated extensive mediastinal hematoma and contrast leaking from a 4x12 cm complex pseudoaneurysm of the proximal thoracic descending aorta (Figure ).\nThe intimal disruption started about 2 cm distal to the origin of the left subclavian artery (LSCA), which was probably the site of the patch repair. The aortic diameter just prior to the disruption was 2.5 cm, and the normal distal thoracic aortic diameter was 2 cm. Of note, there was compression to the distal aorta by the pseudoaneurysm, leading to significant narrowing, which explained the weak distal pulses and cold extremities. After the heart-team discussion, the decision was made to proceed with transcatheter endograft implantation. The transcatheter approach was deemed more feasible and safer than a surgical one, especially in the presence of a good landing zone for endograft placement (away from the LSCA) (Figure ).\nThe patient was taken to cardiac catheterization laboratory and, under general anesthesia, we implanted a tapered (28 mm - 26 mm) x 150 mm Valiant Thoracic Stent Graft with the Captivia Delivery System (Medtronic Vascular, Santa Rosa, CA). The endograft was implanted successfully with complete exclusion of the pseudoaneurysm and excellent flow distally (Figure ).\nThe access site (right femoral artery) was secured successfully with two Perclose ProGlide™ devices (Abbott Laboratories, Abbott Park, IL). The patient did very well and was discharged home after three days. A follow-up CT angiography revealed a widely patent stent graft with no endoleaks.