Successful Treatment of Placental Chorangiomas by Ultrasound-Guided Percutaneous in utero Microcoil Embolization.

Placental chorangiomas can cause a high-output fetal state and increase neonatal morbidity and mortality. There is a paucity of data published describing the optimal treatment of these cases, and methods for occlusion to date include placement of vascular clips, bipolar cautery, injection of alcohol or surgical glue, interstitial laser, and microcoil embolization. We report 2 cases of prenatally diagnosed chorangiomas that caused a high-output fetal state and were successfully treated with microcoil embolization. This case series describes our technique and supports microcoil embolization as a potentially safe and effective antenatal treatment option in symptomatic chorangiomas.

Use of the Protrieve sheath to trap embolizing thrombus during a complex mechanical thrombectomy procedure with a thrombosed inferior vena cava filter.

Removal of thrombosed inferior vena cava (IVC) filters can be complicated by the risk of thrombus embolization. A 67-year-old patient presented for temporary IVC filter retrieval with complaints of worsening lower extremity swelling. Diagnostic imaging identified significant filter thrombosis and bilateral lower extremity deep vein thrombosis (DVT). In the present case, the novel Protrieve sheath was used to successfully remove the IVC filter and thrombus, with an estimated blood loss of 100 mL. The intraprocedurally generated embolus was trapped and removed without complication. This approach could mitigate embolization risks when removing thrombosed IVC filters or complex DVT.

Subsolid pulmonary nodules: CT-pathologic correlation using the 2011 IASLC/ATS/ERS classification.

Adenocarcinoma is the most common histologic subtype of lung cancer. Recent advances in oncology, molecular biology, pathology, imaging, and treatment have led to an increased understanding of this disease. In 2011, the International Association for the Study of Lung Cancer, the American Thoracic Society, and the European Respiratory Society published a new international multidisciplinary classification. Using this taxonomy, we review the spectrum of subsolid pulmonary nodules seen on computed tomography together with their histopathologic correlates and current management guidelines.

Catheter-directed interventions for acute iliocaval deep vein thrombosis.

Acute deep vein thrombosis (DVT) is associated with significant morbidity in the form of acute limb-threatening compromise from phlegmasia cerulea dolens, development of the postthrombotic syndrome (PTS), and even death secondary to pulmonary embolism. Initial therapy for DVT is anticoagulation, which inhibits thrombus propagation but lacks the thrombolytic properties to facilitate active thrombus removal. The existing thrombus burden can cause increased venous hypertension from occlusion as well as damage to venous valves by initiating an inflammatory response, which can ultimately result in PTS in up to half of patients on anticoagulation. The manifestations of PTS include leg pain, swelling, lifestyle-limiting venous claudication, skin hyperpigmentation, venous varicosities, and, in rare cases, venous stasis ulcers. Furthermore, patients with iliocaval DVT and large, free-floating thrombus are at an increased risk for pulmonary embolism despite adequate anticoagulation. Early attempts at thrombus removal with surgical thrombectomy or systemic thrombolysis or both demonstrated reductions in the incidence of PTS but were of limited utility owing to their invasiveness and increased risk of bleeding complications. New minimally invasive endovascular therapies, such as pharmacomechanical catheter-directed thrombolysis, have been proposed, which focus on rapid thrombus removal while decreasing the rate of bleeding complications associated with systemic therapy. This article provides an overview of the current pharmacomechanical catheter-directed thrombolysis protocol utilized at the Mount Sinai Hospital for acute iliocaval DVT.

The histone deacetylase inhibitor vorinostat selectively sensitizes fibrosarcoma cells to chemotherapy.

Soft tissue sarcoma (STS) is a rare malignancy that is generally resistant to chemotherapy. We investigated the ability of the histone deacetylase inhibitor vorinostat to sensitize STS cells versus normal fibroblasts to chemotherapy. Fibrosarcoma, leiomyosarcoma, and liposarcoma cells and normal fibroblasts were treated with vorinostat to determine effects on proliferation and basal apoptosis as measured by total cell number and cleaved caspase 3 staining. Effects on histone deacetylases (HDAC) activity were confirmed by Western blotting for acetylated histone H3. A clinically relevant dose of vorinostat that had no effect on basal apoptosis was selected to examine altered sensitivity to doxorubicin. The effects of vorinostat, doxorubicin, or the combination on fibrosarcoma growth in vivo were determined in a xenograft model. Tumor volume was measured biweekly and HDAC activity and cell death were assessed by immunohistochemical analysis of acetylated histone H3, cleaved caspase 3, and TUNEL staining. Vorinostat inhibited proliferation and induced histone acetylation without affecting basal apoptosis levels. Combined treatment with vorinostat and doxorubicin synergistically induced apoptosis in vitro in fibrosarcoma but not leiomyosarcoma, liposarcoma, or normal fibroblasts. In nude mice, the combination of vorinostat and doxorubicin inhibited fibrosarcoma xenograft growth further than either agent alone. Cell death, as measured by cleaved caspase 3 and TUNEL staining, was greatest in xenografts from mice treated with vorinostat and doxorubicin. Vorinostat inhibits growth and induces chemosensitivity in fibrosarcoma cells in vitro and in vivo, suggesting that the combination of vorinostat and chemotherapy may represent a novel treatment option for this STS subtype. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:623-632, 2011.

Genotype-phenotype aspects of type 2 long QT syndrome.

OBJECTIVES: The purpose of this study was to investigate the effect of location, coding type, and topology of KCNH2(hERG) mutations on clinical phenotype in type 2 long QT syndrome (LQTS). BACKGROUND: Previous studies were limited by population size in their ability to examine phenotypic effect of location, type, and topology. METHODS: Study subjects included 858 type 2 LQTS patients with 162 different KCNH2 mutations in 213 proband-identified families. The Cox proportional-hazards survivorship model was used to evaluate independent contributions of clinical and genetic factors to the first cardiac events. RESULTS: For patients with missense mutations, the transmembrane pore (S5-loop-S6) and N-terminus regions were a significantly greater risk than the C-terminus region (hazard ratio [HR]: 2.87 and 1.86, respectively), but the transmembrane nonpore (S1-S4) region was not (HR: 1.19). Additionally, the transmembrane pore region was significantly riskier than the N-terminus or transmembrane nonpore regions (HR: 1.54 and 2.42, respectively). However, for nonmissense mutations, these other regions were no longer riskier than the C-terminus (HR: 1.13, 0.77, and 0.46, respectively). Likewise, subjects with nonmissense mutations were at significantly higher risk than were subjects with missense mutations in the C-terminus region (HR: 2.00), but that was not the case in other regions. This mutation location-type interaction was significant (p = 0.008). A significantly higher risk was found in subjects with mutations located in alpha-helical domains than in subjects with mutations in beta-sheet domains or other locations (HR: 1.74 and 1.33, respectively). Time-dependent beta-blocker use was associated with a significant 63% reduction in the risk of first cardiac events (p < 0.001). CONCLUSIONS: The KCNH2 missense mutations located in the transmembrane S5-loop-S6 region are associated with the greatest risk.