A 52-year-old male patient underwent surgical correction of interrupted CoA at the age of 20 years using EABG from the LSCA to the descending aorta. He presented with transient sudden central chest pain with sweating. He is a known smoker for more than 30 years and hypertensive for almost 10 years, on losartan 100 mg once daily. The blood pressure (BP) was 140/90 mmHg, equal in four limbs with no brachiofemoral delay. There was no ischemic electrocardiography (ECG) changes or rise in cardiac biomarkers. His transthoracic echocardiography (TTE) revealed normal left ventricular (LV) function, mild bicuspid aortic valve (BAV) regurgitation, and dilated aortic root. The patient was taken to the cardiac catheterization laboratory and underwent coronary and aortic angiography, which revealed normal coronaries, dilated ascending aorta (3.8 cm), post-ductal aortic interruption, and patent EABG with complex pseudoaneurysm at the distal anastomosis site measuring 2x2.5 cm (Figure ).\nAfter the heart team discussion, endovascular treatment was deemed more feasible and safer than redo-surgery. We implanted two overlapped Valiant Thoracic Stent Graft (Medtronic Vascular, Santa Rosa, CA) proximally 22 mm X 100 mm and distally 28 mm X 100 mm. The aortic angiography revealed complete exclusion of the pseudoaneurysm and patent stent graft with no gradient (Figure ).\nThe patient did very well and was discharged home after two days. A follow-up computed tomographic (CT) angiography revealed a widely patent stent graft with no endoleaks (Figure ).
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) ().