Vascular, congenital, and other interventional complications

A Dual-Snare Percutaneous Retrieval of Venous Stent Embolization to the Right Side of the Heart

Ajay K. Sharma, MD

Sarju Ganatra, MD

James Hansen, MD

Neil Yager, DO

Thomas Piemonte, MD

Gautam Gadey, MD

Michael S. Levy, MPH, MD

A 57-year-old man with a medical history of asthma was transferred from an outside hospital for evaluation of cardiac mass where he was treated for extensive right lower extremity iliofemoral deep venous thrombosis with catheter-directed thrombolytic therapy and thrombectomy. Due to concern of compressive physiology at the site of thrombosis, two overlapping self-expanding WALLSTENT endoprostheses (Boston Scientific, Marlborough, Massachusetts) (two 10 mm ×60 mm and one 10 mm ×40 mm) were placed in the iliofemoral system. Shortly after the procedure, an incidental transthoracic echocardiogram noted a right atrial mass ( Fig. 6.1 ). A transesophageal echocardiogram revealed a cylindrical foreign body extending from the inferior vena cava to the right atrium and across the tricuspid valve into the right ventricle. This was suspected to be a migrated venous stent ( Fig. 6.2 A–B). This was confirmed by a computed tomography scan of the chest, abdomen, and pelvis ( Fig. 6.3 ). Percutaneous access was obtained in the right internal jugular vein (6F sheath) and through the right common femoral vein for a 14F Dexterity catheter (Spirus Medical, Stoughton, Massachusetts), which has the advantage of being a steerable catheter. A dual-snare approach was used: 25-mm snare from the groin and an EN Snare 18-30 (Merit Medical, South Jordan, Utah) from the right internal jugular vein. Fluoroscopy identified that two of three stents had embolized into the right atrium and right ventricle ( Fig. 6.4 ). These were removed separately by snaring them proximally and distally and ultimately stretching and compressing the diameter of the stent so it would fit into the 14F Dexterity catheter ( Fig. 6.5 , Online Video 6.1 ). At the end of the procedure, the femoral sheath was withdrawn and a previously placed Perclose closure (Abbott Vascular, Santa Clara, California) was used for hemostasis. The patient had an uneventful recovery and was discharged on rivaroxaban for follow-up with vascular medicine.

With the advent of self-expanding venous stents, there has been a growing enthusiasm in treating iliofemoral venous thrombosis with angioplasty and stenting when compressive physiology is suspected. This is most commonly considered in May-Thurner syndrome. Several case reports ^, describe embolization of these stents, highlighting the need to ensure adequate oversizing in the iliofemoral vessels. Additionally, there are several cases in the literature describing various approaches to stent.

A Unique Case of May-Thurner Syndrome: Extrinsic Compression of the Common Iliac Vein After Iliac Artery Stenting

Paul L. Hermany, MD

Apurva O. Badheka, MBBS

Carlos I. Mena-Hurtado, MD

Robert R. Attaran, MBBS

A 75-year-old woman with peripheral artery disease presented with left leg discomfort and edema shortly after undergoing bilateral common iliac artery stenting. Examination revealed palpable pedal pulses, small varicose veins, and peripheral edema, most notably in the left leg. A venous duplex ultrasound ruled out lower extremity deep vein thrombosis.

The patient underwent invasive aortoiliac angiography and bilateral iliac venography ( Figs. 6.6 and 6.7 ). Iliac artery stents were patent. Intravascular ultrasound (Volcano, San Diego, California) revealed extrinsic compression of the proximal left common iliac vein ( Figs. 6.8 , 6.9 , and 6.10 ). A 14 × 60-mm WALLSTENT (Boston Scientific, Marlborough, Massachusetts) was deployed within the vein at the level of compression ( Fig. 6.11 ). Subsequent intravascular ultrasound demonstrated improved luminal gain. At 2-week and 6-month follow-up visits, she reported complete resolution of her presenting symptoms and significant improvement in her lower extremity edema.

Iliac vein compression as a consequence of arterial intervention is a rare and likely underreported entity. ^, These images demonstrate venous outflow obstruction due to extrinsic compression from previous arterial stenting, which responded dramatically to subsequent venous stenting.

Acute Pseudoaneurysm After Carotid Artery Stenting

Fabrizio Tomai, MD

Giovanni De Persio, MD

Alessandro Petrolini, MD

Luca Altamura, MD

Nicola Corcione, MD

Raoul Borioni, MD

A 73-year-old man with multidistrict artery disease was referred to our hospital for carotid artery stenting of an 85% stenosis of the right internal carotid artery ( Fig. 6.12 A). Protected carotid artery stenting of the right internal carotid artery was performed with a 7 × 40-mm carotid WALLSTENT (Boston Scientific, Natick, Massachusetts), postdilated with a 5 ×20-mm balloon ( Fig. 6.12 B). Seven days later, the patient exhibited a pulsatile neck mass and underwent computed tomography showing two large pseudoaneurysms at both proximal and distal stent edges ( Fig. 6.12 C), requiring urgent endovascular treatment. After diagnostic angiography ( Fig. 6.12 D), a 0.014-inch guidewire was positioned in the distal tract of the right internal carotid artery to facilitate distal positioning of a 0.035-inch wire. Then two overlapping, covered BeGraft stents (Bentley Innomed GmbH, Hechingen, Germany) were implanted with complete exclusion of the pseudoaneurysms ( Fig. 6.12 E), without any complication. Extracranial carotid artery pseudoaneurysm is an infrequent lesion most commonly traumatic, spontaneous, or iatrogenic in origin. Iatrogenic lesions include complications of carotid endarterectomy or central venous catheterization. The incidence of pseudoaneurysm formation secondary to carotid stenting is extremely rare. To the best of our knowledge, this is the first case of pseudoaneurysm formed at both proximal and distal carotid stent edges a few days after the procedure, successfully treated with implantation of covered stents.

An Unusual Cause of Iatrogenic Hypertension

Shikhar Agarwal, MD, MPH

Maya Serhal, MD

Daniel Shivapour, MD

John R. Bartholomew, MD

Christopher Bajzer, MD

A 26-year-old woman was referred for management of resistant hypertension after admission for hypertensive emergency. Her medical history was notable for attention deficit hyperactivity disorder and a motor vehicle accident 6 years before presentation that was complicated by subdural hematoma and provoked deep venous thrombosis requiring placement of an inferior vena cava (IVC) filter. During her hospital admission, the patient was found to have a headache, acute kidney injury, and proteinuria in the setting of hypertensive emergency. In addition, the patient was found to be hypokalemic. Her antihypertensive agents were progressively titrated to include labetalol, amlodipine, and spironolactone. Renal artery ultrasound revealed normal velocities in the right renal artery, with dampened, monophasic, and turbulent Doppler waveforms suggestive of renal artery atherosclerotic disease. The patient was observed by the Nephrology Department as an outpatient and was found to have elevated plasma renin of 32.8 mg/L per hour (normal range, 0.8–5.8 mg/L per hour). Because of suspicion for renovascular hypertension, magnetic resonance angiography was pursued, which demonstrated severe stenosis of the mid portion of the right renal artery with associated atrophy of the kidney ( Fig. 6.13 ). The left renal arterial system was normal. Invasive angiography was pursued and demonstrated a high-grade stenosis in the mid portion of the right renal artery ( Figs. 6.14 and 6.15 ). Stenosis was found to be secondary to extrinsic compression by a prong of the IVC filter ( Fig. 6.15 ). Intravascular ultrasound imaging demonstrated that the prong of the IVC filter had migrated into the media of the renal artery with resultant high-grade stenosis due to marked intimal proliferation ( Fig. 6.16 ). The patient was subsequently referred for surgical removal of the filter and vascular reconstruction of the renal artery.

Bail-out Technique for Pulmonary Artery Rupture With a Covered Stent in Balloon Pulmonary Angioplasty for Chronic Thromboembolic Pulmonary Hypertension

Kentaro Ejiri, MD

Aiko Ogawa, MD, PhD

Hiromi Matsubara, MD, PhD

A 76-year-old male patient with inoperable chronic thromboembolic pulmonary hypertension was referred to our hospital for treatment with balloon pulmonary angioplasty (BPA). He was in World Health Organization functional class III and pulmonary artery pressure was 69/6 (34) mm Hg. We performed BPA in a staged fashion and at the fourth BPA session, we targeted the left upper lobe A1+2. Pulmonary angiography showed the ringlike stenotic lesion ( arrowhead in Fig. 6.17 A), and we evaluated the lumen size of the vessel with intravascular ultrasound. We then expanded the vessel with a balloon (5.0 × 20 mm; Bandicoot RX, Kaneka Medix, Osaka, Japan) ( Fig. 6.17 B). However, immediately after deflation of the balloon, severe hemosputum occurred. Pulmonary angiography showed extravasation of contrast medium ( Fig. 6.17 C, Online Video 6.2 ). We recognized that a pulmonary artery rupture had occurred and tried to stop the bleeding by balloon occlusion. However, we failed and deployed a covered stent of 3.0 × 16 mm (JOSTENT GraftMaster, Abbott Vascular, Santa Clara, California) to the rupture site. We inflated the balloon (5.0 ×20 mm) inside the stent, and pulmonary angiography showed the disappearance of extravasation of contrast medium ( Fig. 6.17 D, Online Video 6.3 ). Repeated pulmonary angiography 2 weeks later revealed no extravasation. In-stent restenosis does not occur for 2 years ( Fig. 6.17 E–F, Online Video 6.4 ).

Although pulmonary artery rupture is a rare complication during BPA, it can cause lethal bleeding. Therefore it is essential for operators of BPA to know how to handle this complication. The efficacy of coil embolization for pulmonary artery rupture was reported ^, ; however, the embolized vessel could never be reperfused. Treatment with a covered stent could maintain the perfusion of the treated artery. Although the utility of a covered stent for pulmonary artery stenosis and aneurysm has been reported, ^, this is the first report to describe the management of pulmonary artery rupture by a covered stent.

Case of Percutaneous Extracorporeal Femorofemoral Bypass for Acute Limb Ischemia From Large-Bore Access

Saurav Chatterjee, MD

Riyaz Bashir, MD, RVT

Vladimir Lakhter, DO

Brian O’Murchu, MD

Brian O’Neill, MD

Vikas Aggarwal, MD, MPH, RPVI

An 80-year-old man presented with acute inferior ST-segment elevation myocardial infarction and cardiogenic shock. Cardiac catheterization revealed 99% stenosis in the mid right coronary artery, a 95% focal severe stenosis in mid left anterior descending coronary artery, and a 60% to 70% stenosis in the proximal circumflex artery. Given advanced age and unstable hemodynamics, emergent multivessel percutaneous coronary intervention (PCI) with complete revascularization was performed. An intraaortic balloon pump was initially placed, but cardiogenic shock persisted despite this and multiple vasopressors. His femoral arteries were <5 mm bilaterally. Despite borderline access vessels, hemodynamic support with an Impella CP heart pump (Abiomed, Danvers, Massachusetts) was instituted via left common femoral access. The patient was only 4 feet 9 inches tall, weighed 50 kg, and had a body surface area of 1.4 m ² . Lack of flow distal to the common femoral arteriotomy was confirmed on duplex ultrasound examination. The patient was, however, completely dependent on the Impella CP and could not be weaned off despite maximal doses of four vasopressors. ^,

It had already been established noninvasively and with a lower extremity angiogram ( Fig. 6.18 ) that the patient had no antegrade distal flow beyond the site of insertion of the cannula, hence conservative management could threaten the viability of the limb. We thus decided to proceed with percutaneous temporary femorofemoral bypass establishment by placing an antegrade sheath in the left superficial femoral artery and connecting it male-to-male with the contralateral common femoral sheath. This was achieved via careful antegrade access in the left superficial femoral artery, distal to the common femoral arteriotomy, and placement of a 6F BRITE TIP Cordis sheath (Cordis Corporation, Milpitas, California). This sheath was then connected male-to-male with the contralateral 6F right common femoral artery retrograde sheath ( Fig. 6.19 ), thereby creating a temporary, novel percutaneous femorofemoral bypass circuit. Subsequently, the left popliteal pulse was confirmed on physical examination, and duplex ultrasound suggested flow reestablishment in the left lower extremity.