No abstract

Intravascular leiomyomatosis (IVL) is a benign smooth muscle tumor that evolves from the pelvic veins and can spread to the central veins and heart. Cardiac involvement is the most commonly reported presentation. Initial diagnosis is difficult, and IVL is commonly misdiagnosed as thrombus or atrial myxoma. Appropriate imaging and a high clinical suspicion are required for accurate diagnosis. We report a rare case of IVL in the external iliac vein that recurred 4 years after hysterectomy. Only four cases have been reported in the literature to involve the external iliac vein as it has no direct connection to pelvic venous drainage.

Endovascular aneurysm repair (EVAR) has quickly outpaced open treatment of infrarenal abdominal aortic aneurysm (AAA) and iliac artery aneurysms, relegating most open AAA repair for either young patients with long life expectancy or patients with extreme anatomic constraints. Typically, open repair involves opening the aneurysm sac with suture ligation of back-bleeding vessels. However, in situations where an aortobifemoral repair is performed, proximal and distal ligation can be performed leaving behind a “remnant” aorta and iliac arteries. Usually, major palpable vessels are ligated and small lumbars spontaneously thrombose. However, failure of this to occur can lead to a rare situation in which there is persistent filling of a remnant aorta and aneurysm sac leading to a situation similar to a type II endoleak after EVAR. Typically, this leak has been repaired by open ligation. We present a technique for endovascular coiling and thrombin injection to correct a “type II endoleak” from a back-bleeding lumbar artery after open aortoiliac and femoral aneurysm repair.

Objective(s): Thoracic aortic stent graft (TASG) collapse is a complication of thoracic endovascular aortic repair, occurring most commonly after treatment of traumatic aortic transection, and may cause reperfusion of the injured aortic segment or malperfusion of distal organs, or both. We used computational modeling to explore the hypothesis that poor apposition of the proximal end of the TASG to the lesser curvature of the aortic arch and associated proximal TASG protrusion can result in increased transmural pressure of sufficient magnitude to cause graft collapse and occlusion. Quantification of transmural pressure may help to identify patients with malapposition of the endograft who will eventually develop collapse.Methods: One-way coupled fluid-solid interaction analyses were performed to investigate the flow-induced hemodynamic and structural loads exerted on the TASG protrusion. Three-dimensional geometries of the aortic arch and graft were reconstructed from computed tomography images of a representative patient after TASG repair. TASG geometry was characterized by the protrusion extension (PE), defined as the length of the TASG not in contact with the aortic wall and by the angle () between the aortic wall and the protruded segment of the TASG. To explore the effect of , we evaluated three models with PE fixed at a value of 5 mm: ϭ 10°, 20°, and 30°. The effect of PE was explored with three models with fixed at 10°: PE ϭ 5, 10, and 20 mm.Results: The transmural pressure across the TASG wall protrusion increases as both PE and increase (Fig. 1). A reduced pressure was found near the TASG protrusion (eg, 85 mm Hg for the PE ϭ 20 mm and ϭ 10°m odel), which could result in malperfusion of the distal organs. In general, for higher or PE values, the blood flow loses its parallel pattern and enters between the aortic wall and the TASG, possibly leading to endoleak or collapse. In all cases, TASG wall stress did not change markedly.Conclusions: Excessive endograft angle (PE ϭ 20 mm and ϭ 10°) markedly increases the transmural pressure across the TASG wall, a load that would portend TASG collapse. Computational modeling may allow for identification of patients with high probability of TASG collapse and preventative intervention, and may aid in design and development of next generation TASG.